2014

February

Date: 14 February 2014

Time: 09:30 am

Place : Gonda 2nd Floor Conference Room

Title: Basal ganglia subcircuits distinctively encode the parsing and concatenation of action sequences

Speaker: Kostya Bakhurin

This Valentine's Day, Kostya will be discussing a center of reward and desire while breaking hearts, presenting this paper from an alum of the Silva Lab.

Chunking allows the brain to efficiently organize memories and actions. Although basal ganglia circuits have been implicated in action chunking, little is known about how individual elements are concatenated into a behavioral sequence at the neural level. Using a task in which mice learned rapid action sequences, we uncovered neuronal activity encoding entire sequences as single actions in basal ganglia circuits. In addition to neurons with activity related to the start/stop activity signaling sequence parsing, we found neurons displaying inhibited or sustained activity throughout the execution of an entire sequence. This sustained activity covaried with the rate of execution of individual sequence elements, consistent with motor concatenation. Direct and indirect pathways of basal ganglia were concomitantly active during sequence initiation, but behaved differently during sequence performance, revealing a more complex functional organization of these circuits than previously postulated. These results have important implications for understanding the functional organization of basal ganglia during the learning and execution of action sequences.

Relevant Materials:

Paper

Basal Ganglia Primer

Date: 07 February 2014

Time: 09:30 am

Place : Gonda 2nd Floor Conference Room

Title: Distance-Dependent Scaling of AMPA Receptors: Whatever Happened To That Idea?

Speaker: Walt Babiec

The Super Bowl is over and pitchers and catchers report later this month, so I'll use a baseball metaphor. I'm pinch hitting this week due to a bunch of schedule reshuffles and no one else's interest in taking this week. Magee and Cook (2000) first reported distance-dependent scaling of AMPA receptor synapses strength in hippocampal pyramidal cells, but the origins of this scaling are not well understood. We will discuss a recent paper from the Nicoll Lab that takes on the question of whether this scaling is driven cell autonomously or as a result of extrinsic hippocampal factors.

January

Date: 31 January 2014

Time: 09:30 am

Place : Gonda 2nd Floor Conference Room

Title: LTP requires a reserve pool of glutamate receptors independent of subunit type

Speaker: Tom O'Dell

Long-term potentiation (LTP) of synaptic transmission is thought to be an important cellular mechanism underlying memory formation. A widely accepted model posits that LTP requires the cytoplasmic carboxyl tail (C-tail) of the AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor subunit GluA1. To find the minimum necessary requirement of the GluA1 C-tail for LTP in mouse CA1 hippocampal pyramidal neurons, Granger et al. used a single-cell molecular replacement strategy to replace all endogenous AMPA receptors with transfected subunits. In contrast to the prevailing model, they found no requirement of the GluA1 C-tail for LTP. In fact, replacement with the GluA2 subunit showed normal LTP, as did an artificially expressed kainate receptor not normally found at these synapses. The only conditions under which LTP was impaired were those with markedly decreased AMPA receptor surface expression, indicating a requirement for a reserve pool of receptors. These results suggest a fundamental change in thinking with regard to the core molecular events underlying synaptic plasticity is required.

Relevant Materials:

Paper

Welberg Commentary

Sheng, Malinow, Huganir Commentary

Date: 24 January 2014

Time: 09:30 am

Place : Gonda 2nd Floor Conference Room

Title: A Cholinergic Mechanism for Reward Timing within Primary Visual Cortex

Speaker: Helen Motanis (Buonomano lab)

This week I have chosen a paper entitled ‘A Cholinergic Mechanism for Reward Timing within Primary Visual Cortex’ by Chubykin et al. 2013. Neurons in rodent primary visual cortex (V1) relate operantly conditioned stimulus-reward intervals with modulated patterns of spiking output, but little is known about the locus or mechanism of this plasticity. The authors show that cholinergic basal forebrain projections to V1 are necessary for the neural acquisition, but not the expression, of reward timing in the visual cortex of awake, behaving animals. The authors also mimic reward timing in vitro by pairing white matter stimulation with muscarinic receptor activation at a fixed interval and show that this protocol results in the prolongation of electrically evoked spike train durations out to the conditioned interval. Together, these data suggest that V1 possesses the circuitry and plasticity to support reward time prediction learning and the cholinergic system serves as an important reinforcement signal, which, in vivo, conveys to the cortex the outcome of behavior.

Date: 17 January 2014

Time: 09:30 am

Place : Gonda 1st Floor Conference Room

Title: Long-term potentiation (LTP), from humble beginnings to major significance

Speaker: Terje Lømo (University of Oslo)

2013

December

Date: 13 December 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Attention enhances synaptic efficacy and the signal-to-noise ratio in neural circuits.

Speaker: Michael Einstein (Golshani Lab)

Attention enhances the processing of salient visual stimuli. Despite thirty years of research on the correlates of attention in the visual cortex, the mechanism by which attention boosts the signal of a salient visual stimulus is still of great debate. One argument is that attention depolarizes visual cortical cells, which could increase neuronal gain by raising the probability for inputs to trigger spiking. Others say that attention synchronizes specific neural populations in such a way that their impact on downstream neurons is increased. Briggs et al. (2013) adds a new piece to the puzzle by testing how attention alters synaptic weights between the LGN and primary visual cortex in monkeys. This research suggests that attention primarily synchronizes specific neural populations as a means to increase the signal to noise ratio of attended stimuli. To conclude, I will reflect on the impact of this paper and suggest future directions for the field.

Reference: Briggs F, Mangun GR, Usrey WM (2013) Attention enhances synaptic efficacy and the signal-to-noise ratio in neural circuits. Nature 499: 476-80. http://www.nature.com/nature/journal/v499/n7459/full/nature12276.html

Date: 06 December 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Selection of distinct populations of dentate granule cells in response to inputs as a mechanism for pattern separation in mice.

Speaker: Denise Cai (Silva Lab)

I'd like to present this paper from the Gage/Mayford lab and discuss it in the context of the work from the Tonegawa lab (Liu et al., 2012, Ramirez et al., 2013) with their reactivation of dentate studies.

Gage/Mayford Reference: http://elife.elifesciences.org/content/2/e00312

Tonegawa References: Liu et al., 2012 Ramirez et al., 2013

November

Date: 22 November 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Maturation of silent synapses in amygdala-accumbens projection contributes to incubation of cocaine craving

Speaker: Paul Mathews (Otis Lab)

This week I have chosen to present a paper entitled "Maturation of silent synapses in amygdala-accumbens projections contributes to incubation of cocaine craving," by Lee at al. Previous research has shown that after repeated cocaine exposure there is a rapid "silencing" of dendritic synapses in medium spiny neurons of the nucleus accumbens. These silenced synapses become rapidly (over days) un-silenced through the incorporation of Ca2+ permeable, rather than Ca2+ impermeable AMPA receptors, which normally predominate the synapse. The authors of this paper present experiments that suggest that these newly un-silenced synapses composed of Ca2+ permeable AMPA receptors underlie the cellular basis for incubated cocaine craving. Given the wide range of experimentation, from behavior to cellular physiology I think this paper should have plenty to interest most ICLM journal club participants.

Reference: http://www.nature.com/neuro/journal/v16/n11/full/nn.3533.html

Date: 15 November 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Spatial representations along the longitudinal hippocampal axis: Tradeoff between memory interference and generalization

Speaker: Isabel Muzzio (Dept. of Psychology, University of Pennsylvania)

The hippocampus has long been implicated in contextual gating of aversive events. Lesion and neuroanatomical studies indicate that the dorsal hippocampus specializes in spatial processing while the ventral hippocampus is more involved in emotion and anxiety. However, it is currently unclear if these regions work as independent modules processing distinct types of information or sensory and emotional inputs are integrated along the longitudinal hippocampal axis to provide a comprehensive representation of context. To investigate this question, my lab has conducted in vivo recordings from freely moving mice while animals form and retrieve contextual representations of different emotional valence in the dorsal and ventral hippocampus. We have found evidence that space is faithfully coded in both the dorsal and ventral regions in different manners. In the dorsal hippocampus, sparse finely tuned representations remap in response to the altered valence of a context forming a new stable spatial representation. Conversely, in the ventral hippocampus space is represented through population coding and emotional valence is coded through changes in firing rate. Furthermore, our data show that having a spatial representational gradient along the longitudinal axis favors a tradeoff between memory interference and generalization.

Date: 01 November 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Epigenetics in action: social regulation of microRNAs

Speaker: Stephanie White

My talk with discuss how the speech and language related gene, FoxP2, is regulated 'on line' during social interactions. Relevance to the LMP community is that this occurs within procedural learning circuitry in the basal ganglia. Perhaps not surprisingly, the model system in question is the songbird, especially given that lab rodents do not learn how to squeak.

Relevant Paper: "miR-9 and miR-140-5p Target FoxP2 and Are Regulated as a Function of the Social Context of Singing Behavior in Zebra Finches"

Shi Z, Luo G, Fu L, Fang Z, Wang X, Li X (2013) J Neurosci 33:16510-21.

http://www.jneurosci.org/content/33/42/16510.long

October

Date: 25 October 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Perineuronal Nets and Plasticity

Speaker: Kelsey Martin

I will discuss a recent PNAS paper from Roger Tsien (see below) that is essentially a hypothesis paper about the function of perineuronal nets and long-term plasticity. I will also present work from other research papers on perineuronal nets during developmental and adult plasticity.

"Very long-term memories may be stored in the pattern of holes in the perineuronal net"

Tsien, RY (2013) PNAS 110:12456.

http://www.pnas.org/content/110/30/12456.full?sid=ec9e5dc0-bb51-46f5-b83c-313145c456ee

Date: 11 October 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title: Where in the Cell Is Long-Term Memory?

Speaker: David Glanzman

I will be presenting recent work from my lab.

There are no papers to read specifically for the presentation. But the following provide useful background information:

Cai, D., Pearce, K., Chen, S., and Glanzman, D. L. (2011). Protein kinase M maintains long-term sensitization and long-term facilitation in Aplysia. J. Neurosci. 31, 6421-6431. (http://www.jneurosci.org/content/31/17/6421.long)

Cai, D., Pearce, K., Chen, S., and Glanzman, David L. (2012). Reconsolidation of long-term memory in Aplysia. Curr. Biol. 22, 1783-1788. (http://www.sciencedirect.com/science/article/pii/S0960982212008639)

Date: 04 October 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title : Metabotropic NMDA Receptor Function

Speaker: Walt Babiec

Recently, two laboratories have reported data from hippocampal slice culture that the depression of AMPA receptor mediated transmission by amyloid beta is blocked by competitive NMDA receptor antagonists, e.g., APV, but not non-competitive antagonists, e.g., MK-801. One of these, the Malinow Laboratory, has proposed that NMDA receptors not only display an ionotropic function but a metabotropic function. They suggest that this metabotropic function, which requires NMDA receptor activation but not cation flux, is necessary and sufficient for generating long-term depression (LTD), which they argue mediates this amyloid beta effect. This week, we will review that data offered in support of their metabotropic NMDA hypothesis of LTD, as well as some data we have taken in the O’Dell Laboratory investigating whether such a function persists in adult animals, thus enhancing its potential for relevance to neurological disorders of aging such as Alzheimer’s Disease.

Covering This Week’s Paper: “Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression” PNAS (2013) 110:4027. Sadegh Nabavia, Helmut W. Kessels, Stephanie Alfonso, Jonathan Aow, Rocky Fox, and Roberto Malinow http://www.pnas.org/content/110/10/4027.long

September

Date: 27 September 2013

Time: 09:30 am

Place : Gonda 2303 (2nd Floor Conference Room)

Title : The Value of Messy Neural Responses

Speaker: Dean Buonomano

Covering This Week’s Paper: “The importance of mixed selectivity in complex cognitive tasks” Nature (2013) 497:585-590. Rigotti M, Barak O, Warden MR, Wang X-J, Daw ND, Miller EK, Fusi S http://www.nature.com/nature/journal/v497/n7451/full/nature12160.html

May

Date: May 10th

Time: 09:30 am

Place : Gonda 2nd Floor Conference Room

Title : Hilar Mossy Cell Degeneration Causes Transient Dentate Granule Cell Hyperexcitability and Impaired Pattern Separation

Speaker: Sarah Hersman

Although excitatory mossy cells of the hippocampal hilar region are known to project both to dentate granule cells and to interneurons, it is as yet unclear whether mossy cell activity’s net effect on granule cells is excitatory or inhibitory. To explore their influ- ence on dentate excitability and hippocampal func- tion, we generated a conditional transgenic mouse line, using the Cre/loxP system, in which diphtheria toxin receptor was selectively expressed in mossy cells. One week after injecting toxin into this line, mossy cells throughout the longitudinal axis were degenerated extensively, theta wave power of dentate local field potentials increased during exploration, and deficits occurred in contextual discrimination. By contrast, we detected no epilepti- form activity, spontaneous behavioral seizures, or mossy-fiber sprouting 5–6 weeks after mossy cell degeneration. These results indicate that the net effect of mossy cell excitation is to inhibit granule cell activity and enable dentate pattern separation.

Neuron. 2012 Dec 20;76(6):1189-200. doi: 10.1016/j.neuron.2012.10.036. Hilar mossy cell degeneration causes transient dentate granule cell hyperexcitability and impaired pattern separation. Jinde S, Zsiros V, Jiang Z, Nakao K, Pickel J, Kohno K, Belforte JE, Nakazawa K.

Front Neural Circuits. 2013;7:14. doi: 10.3389/fncir.2013.00014. Epub 2013 Feb 12. Hilar mossy cell circuitry controlling dentate granule cell excitability. Jinde S, Zsiros V, Nakazawa K.

Date: May 3rd

Time: 09:30 am

Place : Gonda ****1st Floor Conference Room****

Title : ICLM Journal Club Special Lecture

Speaker: Yiota Poirazi

The goal of this presentation is to provide a set of predictions generated by biophysical and theoretical neuron models regarding the role of dendrites in information coding across three different brain regions: the hippocampus, the prefrontal cortex and the amygdala. Towards this goal I will present modelling studies –along with supporting experimental evidence- that investigate how dendrites may be used to facilitate the coding of both spatial and temporal information at the single cell, the microcircuit and the neuronal network level. I will first discuss how the dendrites of individual CA1 pyramidal neurons may allow a single cell to discriminate between familiar versus novel memories and propagate this information to down stream cells [1]. I will then discuss how these dendritic nonlinearities may enable stimulus specificity in individual PFC pyramidal neurons during working memory [2] and underlie the emergence of sustained activity at the single cell and the microcircuit level [2,3]. Finally, I will present findings from our ongoing work in collaboration with Alcino Silva regarding the role of dendrites in shaping the formation of fear memory engrams in the amygdala.

1. Pissadaki, E.K., Sidiropoulou K., Reczko M., and Poirazi, P. “Encoding of spatio-temporal input characteristics by a single CA1 pyramidal neuron model” PLoS Comp. Biology, 2010 Dec;6(12): e1001038.

2. Sidiropoulou, K. and Poirazi, P. “Predictive features of persistent activity emergence in regular spiking and intrinsic bursting model neurons” (PLoS Comp. Biology, 2012 April; 8(4): e1002489)

3. Papoutsi, A., Sidiropoulou, K., and Poirazi, P. “PFC microcircuits as tunable and predictive modules of persistent activity.” (submitted)

April

Date: April 12th

Time: 09:30 am

Place : Gonda 2303

Title : Neural mechanisms mediating inferential reasoning in rats.

Speaker: Cynthia Fast

Abstract: Many decisions are made under conditions of uncertainty. We rarely have access to all of the information in our environment that is pertinent to making an important decision. In fact, our lives are replete with ambiguous situations that nonetheless require consideration. Yet it is unclear what cognitive and neural processes enable the distinction between explicit and ambiguous situations. Moreover, it is unknown what processes mediate inferential reasoning when an ambiguous situation has been detected. We have recently discovered that rats are capable of distinguishing between the ambiguous absence of an event and its explicit absence. That is, like humans, rats appear to recognize the conditions under which they should be able to observe an event and those conditions under which the event should be hidden from observation. Interestingly, this ability depends on prior learning. In a series of experiments, we explored the necessary and sufficient features of prior learning that contribute to sensitivity to ambiguity as well as potential underlying neural mechanisms. Specifically, micro-infusions of scopolamine into the dorsal hippocampus appear to eliminate this reasoning ability, suggesting a critical role for hippocampal cholinergic modulation under normal conditions. Additionally, analysis of cfos expression in the brains of reasoning and non-reasoning rats offer further insight into possible neural circuits mediating reasoning about absent events.

Date: April 5th

Time: 09:30 am

Place : Gonda 2303

Title : "Prkcz null mice show normal learning and memory" and "PKM-ζ is not required for hippocampal synaptic plasticity, learning and memory"

Speaker: David Glanzman

Authors: Lee AM, Kanter BR, Wang D, Lim JP, Zou ME, Qiu C, McMahon T, Dadgar J, Fischbach-Weiss SC, Messing RO.

Abstract: Protein kinase M-ζ (PKM-ζ) is a constitutively active form of atypical protein kinase C that is exclusively expressed in the brain and implicated in the maintenance of long-term memory. Most studies that support a role for PKM-ζ in memory maintenance have used pharmacological PKM-ζ inhibitors such as the myristoylated zeta inhibitory peptide (ZIP) or chelerythrine. Here we use a genetic approach and target exon 9 of the Prkcz gene to generate mice that lack both protein kinase C-ζ (PKC-ζ) and PKM-ζ (Prkcz(-/-) mice). Prkcz(-/-) mice showed normal behaviour in a cage environment and in baseline tests of motor function and sensory perception, but displayed reduced anxiety-like behaviour. Notably, Prkcz(-/-) mice did not show deficits in learning or memory in tests of cued fear conditioning, novel object recognition, object location recognition, conditioned place preference for cocaine, or motor learning, when compared with wild-type littermates. ZIP injection into the nucleus accumbens reduced expression of cocaine-conditioned place preference in Prkcz(-/-) mice. In vitro, ZIP and scrambled ZIP inhibited PKM-ζ, PKC-ι and PKC-ζ with similar inhibition constant (K(i)) values. Chelerythrine was a weak inhibitor of PKM-ζ (K(i) = 76 μM). Our findings show that absence of PKM-ζ does not impair learning and memory in mice, and that ZIP can erase reward memory even when PKM-ζ is not present.

Authors: Volk LJ, Bachman JL, Johnson R, Yu Y, Huganir RL.

Abstract: Long-term potentiation (LTP), a well-characterized form of synaptic plasticity, has long been postulated as a cellular correlate of learning and memory. Although LTP can persist for long periods of time, the mechanisms underlying LTP maintenance, in the midst of ongoing protein turnover and synaptic activity, remain elusive. Sustained activation of the brain-specific protein kinase C (PKC) isoform protein kinase M-ζ (PKM-ζ) has been reported to be necessary for both LTP maintenance and long-term memory. Inhibiting PKM-ζ activity using a synthetic zeta inhibitory peptide (ZIP) based on the PKC-ζ pseudosubstrate sequence reverses established LTP in vitro and in vivo. More notably, infusion of ZIP eliminates memories for a growing list of experience-dependent behaviours, including active place avoidance, conditioned taste aversion, fear conditioning and spatial learning. However, most of the evidence supporting a role for PKM-ζ in LTP and memory relies heavily on pharmacological inhibition of PKM-ζ by ZIP. To further investigate the involvement of PKM-ζ in the maintenance of LTP and memory, we generated transgenic mice lacking PKC-ζ and PKM-ζ. We find that both conventional and conditional PKC-ζ/PKM-ζ knockout mice show normal synaptic transmission and LTP at Schaffer collateral-CA1 synapses, and have no deficits in several hippocampal-dependent learning and memory tasks. Notably, ZIP still reverses LTP in PKC-ζ/PKM-ζ knockout mice, indicating that the effects of ZIP are independent of PKM-ζ.

March

Date: March 15th

Time: 09:30 am

Place : Gonda 5303 ***Note Room Change***

Title : Neural signals of extinction in the inhibitory microcircuit of the ventral midbrain

Speaker: Konstantin Bakhurin

Abstract: Midbrain dopaminergic (DA) neurons are thought to guide learning via phasic elevations of firing in response to reward predicting stimuli. The mechanism for these signals remains unclear. Using extracellular recording during associative learning, we found that inhibitory neurons in the ventral midbrain of mice responded to salient auditory stimuli with a burst of activity that occurred before the onset of the phasic response of DA neurons. This population of inhibitory neurons exhibited enhanced responses during extinction and was anticorrelated with the phasic response of simultaneously recorded DA neurons. Optogenetic stimulation revealed that this population was, in part, derived from inhibitory projection neurons of the substantia nigra that provide a robust monosynaptic inhibition of DA neurons. Thus, our results elaborate on the dynamic upstream circuits that shape the phasic activity of DA neurons and suggest that the inhibitory microcircuit of the midbrain is critical for new learning in extinction.

Date: March 8th

Time: 09:30 am

Place : Gonda 2303

Title : Long-term stabilization of place cell remapping produced by a fearful experience

Speaker: Michael Fanselow

Abstract: Fear is an emotional response to danger that is highly conserved throughout evolution because it is critical for survival. Accordingly, episodic memory for fearful locations is widely studied using contextual fear conditioning, a hippocampus-dependent task (Kim and Fanselow, 1992; Phillips and LeDoux, 1992). The hippocampus has been implicated in episodic emotional memory and is thought to integrate emotional stimuli within a spatial framework. Physiological evidence supporting the role of the hippocampus in contextual fear indicates that pyramidal cells in this region, which fire in specific locations as an animal moves through an environment, shift their preferred firing locations shortly after the presentation of an aversive stimulus (Moita et al., 2004). However, the long-term physiological mechanisms through which emotional memories are encoded by the hippocampus are unknown. Here we show that during and directly after a fearful experience, new hippocampal representations are established and persist in the long term. We recorded from the same place cells in mouse hippocampal area CA1 over several days during predator odor contextual fear conditioning and found that a subset of cells changed their preferred firing locations in response to the fearful stimulus. Furthermore, the newly formed representations of the fearful context stabilized in the long term. Our results demonstrate that place cells respond to the presence of an aversive stimulus, modify their firing patterns during emotional learning, and stabilize a long-term spatial representation in response to a fearful encounter. The persistent nature of these representations may contribute to the enduring quality of emotional memories.

Date: March 1st

Time: 09:30 am

Place : Gonda 2303

Title : Mechanisms controlling the gain of the visual cortex neurons during wakefulness

Speaker: Pierre-Olivier Polack

Abstract: Reliable acquisition and amplification of sensory input is the first essential step for learning and memory. During wakefulness the gain of sensory neurons can change with behavior. In particular, visual cortical neurons fire at higher rates to visual stimuli during locomotion than during immobility while maintaining orientation selectivity. The mechanisms underlying this change in gain are not understood. We performed whole cell recordings from layer 2/3 and layer 4 visual cortical excitatory neurons as well as from parvalbumin-positive and somatostatin-positive inhibitory neurons in mice free to rest or run on a spherical treadmill. We found that the membrane potential of all cell types became more depolarized and (with the exception of somatostatin-positive interneurons) less variable during locomotion. Cholinergic input was essential for maintaining the unimodal membrane potential distribution during immobility, while noradrenergic input was necessary for the tonic depolarization associated with locomotion. Our results provide a mechanism for how neuromodulation controls the gain and signal-to-noise ratio of visual cortical neurons during changes in the state of vigilance. We are now investigating whether the same mechanism is responsible for controlling selective attention to visual input during a perceptual learning task.

February

Date: February 21st

Time: 09:30 am

Place : Gonda 2303

Title : FMRP Regulates Neurotransmitter Release and Synaptic Information Transmission by Modulating Action Potential Duration via BK Channels

Speaker: Felix Schweizer

Abstract: Loss of FMRP causes fragile X syndrome (FXS), but the physiological functions of FMRP remain highly debatable. Here we show that FMRP regulates neurotransmitter release in CA3 pyramidal neurons by modulating action potential (AP) duration. Loss of FMRP leads to excessive AP broadening during repetitive activity, enhanced presynaptic calcium influx, and elevated neurotransmitter release. The AP broadening defects caused by FMRP loss have a cell-autonomous presynaptic origin and can be acutely rescued in postnatal neurons. These presynaptic actions of FMRP are translation independent and are mediated selectively by BK channels via interaction of FMRP with BK channel’s regulatory β4 subunits. Information-theoretical analysis demonstrates that loss of these FMRP functions causes marked dysregulation of synaptic information transmission. FMRP-dependent AP broadening is not limited to the hippocampus, but also occurs in cortical pyramidal neurons. Our results thus suggest major translation-independent presynaptic functions of FMRP that may have important implications for understanding FXS neuropathology.

Date: February 1st

Time: 09:30 am

Place : Gonda 2303

Title : Experience-dependent plasticity of Network Dynamics

Speaker: Anubhuthi Goel

Abstract: Cortical computations underlying normal and abnormal brain function are not only dependent on modifications at individual synapses but on the net interaction between many forms of plasticity at the level of the entire network. Together multiple forms of plasticity govern the complex spatio-temporal patterns of activity within local networks – that is, neural dynamics. One particular learning rule that is critical in the development of functional neural dynamics in a controlled fashion is Homeostatic plasticity. We examined plasticity of network dynamics in cortical organotypic slices in response to chronic changes in activity and found that networks rely on a balance between spontaneous and evoked activity in order to drive their average activity levels towards homeostatic set points. Importantly our data highlights the fact that at the network level homeostatic mechanisms are not restricted to simple and traditional synaptic scaling phenomena wherein all the synapses are indiscriminately scaled up or down. Rather homeostatic mechanisms involve multiple forms of plasticity operating in parallel thereby allowing circuits to independently regulate spontaneous, monosynaptic, and polysynaptic activity.

Having gained some insight as to how homeostatic plasticity influences computations in general so that recurrent cortical circuits generate functional dynamic states in a stable fashion we examined one particularly interesting type of computation, namely, how does timing emerge from the plasticity of neural dynamics. Timing is fundamental to learning and behavior, and it is increasingly clear that in many cases timing is an emergent network phenomenon; but almost nothing is known about the neural mechanisms that underlie even the simplest of temporal tasks, such as discriminating a 100 and 200 ms interval. We have recently established that when cortical organotypic slices are chronically presented with specific intervals (using electrical stimulation), the network can in a sense “learn” the trained interval: after training, presentation of a single pulse results in increased neural activity around the expected time of the second pulse—as if the network “expected” the arrival of the second pulse. We view this as an example of an emergent computation in vitro because: First, the changes in the behavior of the network seem to rely on the interaction of many neurons in a circuit rather than the simple amplification of neural responses observed in traditional synaptic plasticity studies. Second, it can be said that a simple computation is taking place because the activity patterns in the trained network provide information about elapsed time. To examine the mechanisms of temporal pattern completion, we combined electrical and optical stimulation to provide “sensory spatio-temporal experience” to cortical organotypic slices. Our data suggests that the observed timing is in part due to evoked patterns of activity—neural trajectories—in which distinct points in time can be encoded by the population of active neurons. Furthermore based on our insights from homeostatic plasticity studies we believe that homeostatic mechanisms aid in the emergence and propagation of these neural trajectories in a stable manner.

January

Date: January 25th

Time: 09:30 am

Place : Gonda 2303

Title : Spatial Regulation of Gene Expression in neurons During Synapse Formation and Synaptic Plasticity

Speaker: Sangmok Kim

Abstract: mRNA localization and regulated translation allow individual neurons to locally regulate the proteome of each of their myriad of subcellular compartments. To determine whether and how synaptogenic signals spatially regulate gene expression, we cultured a bifurcated Aplysia sensory neuron contacting a nontarget motor neuron, with which it did not form chemical synapses, and a target motor neuron, with which it formed glutamatergic synapses, and imaged RNA and protein localization. We find that RNAs and translational machinery are delivered throughout the neuron, but that translation is enriched at sites of synaptic contact. Investigation of the molecular mechanisms that promote local translation revealed a role for netrin-1/DCC signaling. Together, our study indicates that the spatial regulation of gene expression during synapse formation is mediated at the level of translation. This mechanism maximizes neuronal plasticity by rendering each compartment capable of locally changing its proteome in response to local cues.

2012

Abstract: The mammalian brain is composed of thousands of interacting neural cell types. Systematic approaches to establish the molecular identity of functional populations of neurons would advance our under- standing of neural mechanisms controlling behavior. Here, we show that ribosomal protein S6, a structural component of the ribosome, becomes phosphory- lated in neurons activated by a wide range of stimuli. We show that these phosphorylated ribosomes can be captured from mouse brain homogenates, thereby enriching directly for the mRNAs expressed in discrete subpopulations of activated cells. We use this approach to identify neurons in the hypo- thalamus regulated by changes in salt balance or food availability. We show that galanin neurons are activated by fasting and that prodynorphin neu- rons restrain food intake during scheduled feed- ing. These studies identify elements of the neural circuit that controls food intake and illustrate how the activity-dependent capture of cell-type-specific transcripts can elucidate the functional organization of a complex tissue.

October

Date: October 26th

Time: 09:30 am

Place : Gonda 2303

Title : “Why are there so many types of inhibitory neurons”

Speaker: Dr. Dean Buonomano

Related Material:

Division and subtraction by distinct cortical inhibitory networks in vivo

Nathan R. Wilson1*, Caroline A. Runyan1*, Forea L. Wang1 & Mriganka Sur1

Brain circuits process information through specialized neuronal subclasses interacting within a network. Revealing their interplay requires activating specific cells while monitoring others in a functioning circuit. Here we use a new platform for two-way light-based circuit interrogation in visual cortex in vivo to show the computational implications of modulating different subclasses of inhibitory neurons during sensory processing. We find that soma-targeting, parvalbumin-expressing (PV) neurons principally divide responses but preserve stimulus selectivity, whereas dendrite-targeting, somatostatin-expressing (SOM) neurons principally subtract from excitatory responses and sharpen selectivity. Visualized in vivo cell-attached recordings show that division by PV neurons alters response gain, whereas subtraction by SOM neurons shifts response levels. Finally, stimulating identified neurons while scanning many target cells reveals that single PV and SOM neurons functionally impact only specific subsets of neurons in their projection fields. These findings provide direct evidence that inhibitory neuronal subclasses have distinct and complementary roles in cortical computations.

Date: October 5th

Time: 09:30 am

Place : Gonda 2303

Title : “Dissecting spatial knowledge from spatial choice by hippocampal NMDA receptor deletion”

Speaker: Dr. Tom O'Dell

Summary:

Hippocampal NMDA receptors (NMDARs) and NMDAR-dependent synaptic plasticity are widely considered crucial substrates of long-term spatial memory, although their precise role remains uncertain. Here we show that Grin1∆DGCA1 mice, lacking GluN1 and hence NMDARs in all dentate gyrus and dorsal CA1 principal cells, acquired the spatial reference memory water maze task as well as controls, despite impairments on the spatial reference memory radial maze task. When we ran a spatial discrimination water maze task using two visually identical beacons, Grin1∆DGCA1 mice were impaired at using spatial information to inhibit selecting the decoy beacon, despite knowing the platform’s actual spatial location. This failure could suffice to impair radial maze performance despite spatial memory itself being normal. Thus, these hippocampal NMDARs are not essential for encoding or storing long-term, associative spatial memories. Instead, we demonstrate an important function of the hippocampus in using spatial knowledge to select between alternative responses that arise from competing or overlapping memories.

August

Date: August 17th

Time: 09:30 am

Place : ***53-105, CHS.***

Title : “Calpain: a key component of synaptic plasticity and learning & memory?”

Summary:

Prevailing theory suggests that long-term memories are encoded via a two-phase process requiring early involvement of the hippocampus followed by the neocortex. Contextual fear memories in rodents rely on the hippocampus immediately following training but are unaffected by hippocampal lesions or pharmacological inhibition weeks later. With fast optogenetic methods, we examine the real-time contribution of hippocampal CA1 excitatory neurons to remote memory and find that contextual fear memory recall, even weeks after training, can be reversibly abolished by temporally precise optoge- netic inhibition of CA1. When this inhibition is extended to match the typical time course of phar- macological inhibition, remote hippocampus depen- dence converts to hippocampus independence, suggesting that long-term memory retrieval normally depends on the hippocampus but can adaptively shift to alternate structures. Further revealing the plasticity of mechanisms required for memory recall, we confirm the remote-timescale importance of the anterior cingulate cortex (ACC) and implicate CA1 in ACC recruitment for remote recall.

Relevant Reading Material:

Cell. 2011 Oct 28;147(3):678-89. Epub 2011 Oct 20. Dynamics of retrieval strategies for remote memories. Goshen I, Brodsky M, Prakash R, Wallace J, Gradinaru V, Ramakrishnan C, Deisseroth K.

March

Date: Mar 9th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Triggering and degrading associative memory formation"

Speaker: Joshua Johansen PhD

Summary:

Aversive experiences powerfully regulate memory formation by activating ‘teaching signal’ circuits in the brain which can engage neural plasticity in memory storage areas resulting in associative memories. Fear conditioning is a useful paradigm in which to examine the mechanisms by which aversive experiences trigger associative memories because a site of neural plasticity mediating the learning has been identified in the lateral nucleus of the amygdala. Aversive stimuli can either engage or degrade memory formation depending on the temporal placement of aversive stimuli in relation to sensory cues in the environment. Using a combination of optogenetic, electrophysiological and behavioral approaches I examined the neural mechanisms in the lateral amygdala by which aversive experiences trigger or degrade behavioral fear memory formation and neural plasticity. The results of these experiments suggest that combined Hebbian and neuromodulatory mechanisms trigger behavioral fear learning and neural plasticity in the lateral amygdala. In addition, activation of LA pyramidal neurons by aversive stimuli serves as a switch to either induce or degrade fear memory formation depending on the temporal placement of the aversive stimuli during learning.

Date: Mar 2nd

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Heterogeneous reallocation of presynaptic efficacy in recurrent excitatory circuits adapting to inactivity."

Speaker: Anubhuthi Goel, Ph.D.

Homeostatic plasticity is an important negative feedback regulator that maintains stability within networks of neurons. The synaptic basis and mechanisms underlying homeostatic plasticity have been extensively studied, however a large number of these investigations are restricted to understanding homeostatic modifications at feed forward pathways. This paper provides compelling evidence that the rules under which homeostatic plasticity operates are very different for recurrently connected networks and that traditional homogenous homeostatic adaptation is not enforced across all synapses.

Relevant Reading Material:

Nat Neurosci. 2011 Dec 18;15(2):250-7. doi: 10.1038/nn.3004. Heterogeneous reallocation of presynaptic efficacy in recurrent excitatory circuits adapting to inactivity. Mitra A, Mitra SS, Tsien RW.

February

Date: Feb 24th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Inducible and Selective Erasure of Memories in the Mouse Brain via Chemical-Genetic Manipulation"

Speaker: Adam Frank.

Summary:

I will present Joe Tsien's 2008 Neuron paper about a chemical-genetic approach to study CaMKIIa function ("Inducible and Selective Erasure of Memories in the Mouse Brain via Chemical-Genetic Manipulation"). This paper is a continuation of work beginning in 2003, when his lab generated a CaMKIIa overexpressing mouse with a targeted mutation in CaMKIIa that makes it highly susceptible to inhibition by a modified kinase inhibitor (Wang, 2003, PNAS). This story of overexpression and inhibition of wildtype CaMKIIa activity is interesting and provocative and raises as many questions as it answers. I am particularly interested in these results as I have generated a BAC transgenic mouse that overexpresses the same CaMKIIa mutation as that generated in the Tsien lab. I am hopeful we can have a lively discussion about his results and the important questions they raise. Relevant Reading Material:

Neuron. 2008 Oct 23;60(2):353-66. Inducible and selective erasure of memories in the mouse brain via chemical-genetic manipulation. Cao X, Wang H, Mei B, An S, Yin L, Wang LP, Tsien JZ.

Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4287-92. Epub 2003 Mar 19. Inducible protein knockout reveals temporal requirement of CaMKII reactivation for memory consolidation in the brain. Wang H, Shimizu E, Tang YP, Cho M, Kyin M, Zuo W, Robinson DA, Alaimo PJ, Zhang C, Morimoto H, Zhuo M, Feng R, Shokat KM, Tsien JZ.

January

Date: Jan 6th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Practice makes perfect: defining the role of inhibition in vision and sensory learning."

Speaker: Sandra Kuhlman, Ph.D.

GABAergic inhibition is a key mediator of experience-dependent plasticity during postnatal development, and accumulating evidence identifies aberrant GABAergic function in schizophrenia and autism. However, the mechanisms by which inhibition regulates plasticity and learning in-vivo are largely unknown, and by extension it is not well understood how disturbance of cellular signaling pathways within inhibitory interneurons impacts cortical function in-vivo. Using in-vivo targeted electrophysiological recording of an identified inhibitory interneuron cell type, the parvalbumin (PV+) fast-spiking GABAergic interneuron, we found that visual experience uniquely broadens orientation tuning of PV+ interneurons at a time during development when excitatory neurons become more sharply tuned (Kuhlman et al., Nature Neuroscience 2011). Furthermore, we found that inhibitory broadening precedes binocular matching of excitatory orientation tuning, thus establishing that maturation of the recruitment of inhibition is a candidate for initiating binocular plasticity of excitatory neurons during the critical period. These results highlight the need for designing treatment strategies to rescue recruitment of PV+ interneurons in disease, thereby expanding the existing focus which is to enhance GABAergic synaptic output.

Perceptual learning is a progressive process of skill acquisition in which neural response properties are re-shaped by experience, even at the earliest stages of sensory processing. Thus, the very perception of the environment which informs motor output and behavioral action is itself modified during learning. How does recruitment of inhibition regulate sensory learning? Using techniques described above in combination with recent advances in head-fixed mouse behavior, this is now a tractable question in mice. I will outline a strategy to define the unique roles of specific inhibitory interneuron subclasses during ‘practice’, a.k.a. progressive learning.

Date: Jan 13th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Inhibitory Plasticity"

Speaker: Dean Buonomano, Ph.D.

Releavant Reading Material:

Vogels TP, Sprekeler H, Zenke F, Clopath C, Gerstner W (2011) Science 334:1569-1573. Inhibitory Plasticity Balances Excitation and Inhibition in Sensory Pathways and Memory Networks http://www.sciencemag.org/content/334/6062/1569.abstract

Froemke RC, Merzenich MM, Schreiner CE (2007) Nature 450:425-429. A synaptic memory trace for cortical receptive field plasticity. http://www.nature.com/nature/journal/v450/n7168/full/nature06289.html

Date: Jan 20th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "A disinhibitory microcircuit for associative fear learning in the auditory cortex"

Speaker: Walter Babiec, Ph.D.

Summary: Learning causes a change in how information is processed by neuronal circuits. Whereas synaptic plasticity, an important cellular mechanism, has been studied in great detail, we know much less about how learning is implemented at the level of neuronal circuits and, in particular, how interactions between distinct types of neurons within local networks contribute to the process of learning. Here we show that acquisition of associative fear memories depends on the recruitment of a disinhibitory microcircuit in the mouse auditory cortex. Fear-conditioning-associated disinhibition in auditory cortex is driven by foot-shock-mediated cholinergic activation of layer 1 interneurons, in turn generating inhibition of layer 2/3 parvalbumin-positive interneurons. Importantly, pharmacological or optogenetic block of pyramidal neuron disinhibition abolishes fear learning. Together, these data demonstrate that stimulus convergence in the auditory cortex is necessary for associative fear learning to complex tones, define the circuit elements mediating this convergence and suggest that layer-1-mediated disinhibition is an important mechanism underlying learning and information processing in neocortical circuits.

Releavant Reading Material: Johannes J. Letzkus1*, Steffen B. E. Wolff1,2*, Elisabeth M. M. Meyer1,2, Philip Tovote1, Julien Courtin3, Cyril Herry3 & Andreas Lu ̈thi1 (2011) Nature 480:331-335. A disinhibitory microcircuit for associative fear learning in the auditory cortex http://www.nature.com/nature/journal/v480/n7377/full/nature10674.html

2011

January

February

Feb 25th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title :A selective role for dopamine in stimulus–reward learning

Speaker: Michael Faneslow

Summary: Flagel et al Nature 469, 53–57 (06 January 2011)

Supp

Apr 15th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : Mushroom Body Output Neurons Encode Odor-Reward Associations

Speaker: David Glanzman

Summary: The paper describes neural correlates of odor representation and olfactory reward learning in honeybees using both population and single unit recording from the mushroom bodies.

Relevant Information: Paper

Apr 22nd

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title :From Drosophila olfaction to a general circuit model for behavioral habituation.

Speaker: Mani Ramaswami

Summary:

Relevant Information:

Date: Apr 27th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title :The role of Thorase in the surface expression of glutamate receptors and its implications for synaptic plasticity and behavior

Speaker: Adam Roberts

Summary: Zhang et al., 2011 indicate that the AAA+ ATPase Thorase is required for the internalization of AMPARs by dissociating the GRIP1-GluR2 interaction. Genetic manipulation of Thorase expression modifies the surface expression of GluR1 and GluR2 in an ATP-dependent manner. Thorase KO mice have enhanced LTP, deficits in LTD, and larger AMPAR-dependent currents. These alterations in nervous system function result in deficits in learning and memory.

Relevant Information:

Paper

May

Date: May 13th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title :The role of Thorase in the surface expression of glutamate receptors and its implications for synaptic plasticity and behavior

Speaker: Adam Roberts

Summary: Zhang et al., 2011 indicate that the AAA+ ATPase Thorase is required for the internalization of AMPARs by dissociating the GRIP1-GluR2 interaction. Genetic manipulation of Thorase expression modifies the surface expression of GluR1 and GluR2 in an ATP-dependent manner. Thorase KO mice have enhanced LTP, deficits in LTD, and larger AMPAR-dependent currents. These alterations in nervous system function result in deficits in learning and memory.

Relevant Information:

Paper

Date: May 17th

Time 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title: Action-Potential Modulation During Axonal Conduction

Speaker: Besim Ugzil"

Summary: Once initiated near the soma, an action potential (AP) is thought to propagate autoregeneratively and distribute uniformly over axonal arbors. We challenge this classic view by showing that APs are subject to waveform modulation while they travel down axons. Using fluorescent patch-clamp pipettes, we recorded APs from axon branches of hippocampal CA3 pyramidal neurons ex vivo. The waveforms of axonal APs increased in width in response to the local application of glutamate and an adenosine A1 receptor antagonist to the axon shafts, but not to other unrelated axon branches. Uncaging of calcium in periaxonal astrocytes caused AP broadening through ionotropic glutamate receptor activation. The broadened APs triggered larger calcium elevations in presynaptic boutons and facilitated synaptic transmission to postsynaptic neurons. This local AP modification may enable axonal computation through the geometry of axon wiring.

Releavant Information:

Paper

Date: May 17th

Time 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title: Action-Potential Modulation During Axonal Conduction

Speaker: Besim Ugzil"

Summary: Once initiated near the soma, an action potential (AP) is thought to propagate autoregeneratively and distribute uniformly over axonal arbors. We challenge this classic view by showing that APs are subject to waveform modulation while they travel down axons. Using fluorescent patch-clamp pipettes, we recorded APs from axon branches of hippocampal CA3 pyramidal neurons ex vivo. The waveforms of axonal APs increased in width in response to the local application of glutamate and an adenosine A1 receptor antagonist to the axon shafts, but not to other unrelated axon branches. Uncaging of calcium in periaxonal astrocytes caused AP broadening through ionotropic glutamate receptor activation. The broadened APs triggered larger calcium elevations in presynaptic boutons and facilitated synaptic transmission to postsynaptic neurons. This local AP modification may enable axonal computation through the geometry of axon wiring.

Relevant Information:

Paper

Date: May 27th

Time 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title: "What makes a place cell?"

Speaker: Justin Shobe"

Summary: Once initiated near the soma, an action potential (AP) is thought to propagate autoregeneratively and distribute uniformly over axonal arbors. We challenge this classic view by showing that APs are subject to waveform modulation while they travel down axons. Using fluorescent patch-clamp pipettes, we recorded APs from axon branches of hippocampal CA3 pyramidal neurons ex vivo. The waveforms of axonal APs increased in width in response to the local application of glutamate and an adenosine A1 receptor antagonist to the axon shafts, but not to other unrelated axon branches. Uncaging of calcium in periaxonal astrocytes caused AP broadening through ionotropic glutamate receptor activation. The broadened APs triggered larger calcium elevations in presynaptic boutons and facilitated synaptic transmission to postsynaptic neurons. This local AP modification may enable axonal computation through the geometry of axon wiring.

Releavant Information: Paper

June

Date: Jun 17th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age"

Speaker: Kelsey Martin

Speaker: Dean Buonomano

Summary: A discussion on the following paper:

A cortical neural prosthesis for restoring and enhancing memory.

Speaker: Christine Serway

Summary: The interplay between brain anatomy, neural network organization and behavior has been well studied in Drosophila for over three decades. The first experimental evidence implicating the mushroom bodies (MBs) as centers of sensory integration and association in flies came from anatomical and behavioral work on brain structure mutants. Here we present a detailed analysis of three genes using mutant alleles initially described by Martin Heisenberg et al. more than 25 years ago. We characterized the different levels of associative conditioning and mushroom body defects seen in mushroom body miniature B (mbmB), small mushroom bodies (smu) and mushroom bodies reduced (mbr). This work has allowed us to implicate subsets of the MBs in different forms of associative conditioning. Surprisingly most of the mutants created in this screen have yet to be molecularly characterized. Extensive complementation analysis and sequencing revealed mbmB to be synonymous with the Drosophila Importin-2 (Imp-2). We present rescue experiments, western blot analysis, and have demonstrated that all Imp-2 domains are required for normal MB development. In Drosophila, imp-2 mediated nuclear transport is necessary for proper axon guidance, neuronal injury response, synaptic plasticity, cell proliferation and apoptosis, while its role in central brain development has not been investigated until now. This work provides a novel link between Importin--2 and MB development and offers insight on the cell biology of developmental and behavioral plasticity.

September

Date: Sep 02nd

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : ""Prior experience modulates a natural threshold for memory formation ""

Speaker: Kiriana Cowansage

Summary: Our current understanding of the molecular requirements for long–term memory come largely from studies that use experimental manipulations to alter average behavior. Few studies, on the other hand, have investigated the contribution of plasticity-related proteins, like CREB, to existing behavioral differences in memory strength that emerge naturally from genetically diverse populations. In this talk I will begin by presenting work from the labs of Joe LeDoux and Eric Klann (in collaboration with Sheena Josselyn) to identify rats from a normally distributed group that fail to form typical cued fear associations and express reduced baseline levels of phospho-CREB. Memory in this subset of rats was selectively improved by both pre-training exposure to contextual novelty and by virally mediated enhancement of amygdala CREB activity. These results provide some conceptual basis for current plans to investigate the cellular dynamics of weak versus strong associative memory traces in the lab of Mark Mayford, using a novel genetically encoded fluorescent timer expressed in mice under the control of neural activity.

Relevant Information:

Subach et al (2009) Nat. Chem Biol

Date: Sep 23rd

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : " 2½ Short Stories of Pavlov's Flies "

Speaker: Steven de Belle

Summary: Not provided

Date: Sep 30th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : " Talk 1: Grid cells, theta oscillations, and a novel code phase code of the head direction signal Talk 2: Septotemporal variation in theta rhythm dynamics "

Speaker: Mark Brandon and Jake Hinman

Summary: Not provided

Relevant Materials:

http://www.sciencemag.org/content/332/6029/595.full

http://jn.physiology.org/content/105/6/2675.full.pdf+html

October

Date: Oct 14th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : " AMPA receptor trafficking in reconsolidation of context fear memories "

Speaker: Tom O Dell

Summary: Not provided

Relevant Materials:

http://www.nature.com/neuro/journal/v14/n10/full/nn.2907.html

Date: Oct 28th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : " Mental Schema and its Neural Correlates"

Speaker: Balaji

Summary: Not provided

Relevant Materials:

http://www.sciencemag.org/content/333/6044/891.full

November

Date: Nov 04th

Time: 09:00 am

Place : 1st Floor Conference Room, Gonda building.

Title : " The Cytoplasmic Fragile X Mental Retardation Protein1 CYFIP1 is a Key Player in Neurodevelopment: The Link with Autism"

Speaker: Claudia Bagni

Date: Nov 18th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : " The h-currents, LTP,theta oscillations,grid cells and learning"

Speaker: Mayank Mehta

Summary: The hippocampal theta oscillations are thought to be critical for learning and memory and for the formation of entorhinal grid cells. Over the past few years the attention has been focused on the HCN1 channel: HCN1 channel knockout enhances theta rhythm and LTP, and improves spatial learning.

Two recent studies, one in the current issue of Neuron, from the Kandel lab, and another in the upcoming issue of Cell from the Moser lab, have measured the effect of HCN1 knockout on the entorhinal grid cells and hippocampal place cells, with many surprising results that compels us to rethink the cellular mechanisms governing grid cells and place cells.

Releavant Reading Material: http://www.sciencedirect.com/science?_ob=MiamiImageURL&_cid=272195&_user=4423&_pii=S0896627311007938&_check=y&_coverDate=2011-11-17&view=c&_gw=y&wchp=dGLzVlt-zSkzk&md5=9c0fb5a1be9056818c9b1daa13635cdf/1-s2.0-S0896627311007938-main.pdf

December

Date: Dec 9th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Reevaluating the Role of LTD in Cerebellar Motor Learning"

Speaker: Paul Mathews

Summary: It is widely believed that changes in the strength of synapses underlies the cellular changes responsible for memory formation. In the Cerebellum theories regarding the location of the cellular changes necessary for motor learning have recently been of great debate. One particular hypothesis proposed by Marr, Albus and Ito is that errors in motor behavior lead to changes in the strength of parallel fiber (PF) inputs onto Purkinje neurons (PNs). These errors, which are believed to be carried by climbing fiber terminals originating from the inferior olive, are thought to drive long term depressions (LTD) of PF-PN synapses that are activated coincidentally with the error signal. This change in the cerebellar circuit is believed, at least in part to underlie the cellular mechanisms driving motor learning. Supporting this hypothesis are numerous studies in which blocking the pathways responsible for PF-PN LTD leads to a deficit in cerebellar mediated motor behaviors. However, it has been argued that since these manipulations effect targets that often play multiple cellular regulatory roles (mGlur1/PKC, PKG, and αCamKII) the changes observed in motor behavior may be due instead to alterations in processes unrelated to the abolition of LTD. In the paper for discussion this Friday the authors reevaluate the role LTD plays in cerebellar motor learning by disrupting LTD through preventing AMPA receptor endocytosis directly rather than effecting more precocious molecules. Their experiments show that while these manipulations prevent associative PF-PN LTD in vitro numerous tests fail to show any significant behavioral effect of LTD disruption. For LMP this Friday we will examine the previous data suggesting LTD in the cerebellar cortex is critical for motor learning as well as how these new negative findings potentially alter our view of LTD’s role in cerebellar mediated motor learning.

Releavant Reading Material: http://www.sciencedirect.com/science?_ob=MiamiImageURL&_cid=272195&_user=4423&_pii=S0896627311001991&_check=y&_origin=&_coverDate=14-Apr-2011&view=c&wchp=dGLbVlS-zSkzk&md5=b2315bb5e6d206c4b2b051a7e8edf789/1-s2.0-S0896627311001991-main.pdf

Date: Dec 16th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Synaptic Potentiation in the Central Amygdala upon Fear Learning"

Speaker: Ayako M. Watabe, Ph.D.

Previous weeks

Contents

2014

February

January

2013

December

November

October

September

May

April

March

February

January

2012

November

Title : “Memory allocation mechanisms to trap and activate emotional memories”

Title : “Content-Specific Fronto-Parietal Synchronization During Visual Working Memory”

Title : “Hippocampal Place Fields Emerge upon Single-Cell Manipulation of Excitability During Behavior”

Title : “Molecular Profiling of Activated Neurons by Phosphorylated Ribosome Capture”

October

Title : “Why are there so many types of inhibitory neurons”

Title : “Dissecting spatial knowledge from spatial choice by hippocampal NMDA receptor deletion”

August

Title : “Calpain: a key component of synaptic plasticity and learning & memory?”

May

Title : "Generation of a synthetic memory trace"

Title : "Conditional modulation of spike-timing- dependent plasticity for olfactory learning"

Title : "Corticostriatal plasticity is necessary for learning intentional neuroprosthetic skills"

April

Title : "Optogenetic stimulation of a hippocampal engram activates fear memory recall"

Title : "Activity Recall in a Visual Cortical Ensemble"

Title : "Dynamics of Retrieval Strategies for Remote Memories"

March

Title : "Triggering and degrading associative memory formation"

Title : "Heterogeneous reallocation of presynaptic efficacy in recurrent excitatory circuits adapting to inactivity."

February

Title : "Inducible and Selective Erasure of Memories in the Mouse Brain via Chemical-Genetic Manipulation"

January

Title : "Practice makes perfect: defining the role of inhibition in vision and sensory learning."

Title : "Inhibitory Plasticity"

Title : "A disinhibitory microcircuit for associative fear learning in the auditory cortex"

2011

January

February

Title :A selective role for dopamine in stimulus–reward learning

March

Title : Maladaptive Cortical Plasticity and Plasticity

Title : Memory enhancement and PKM Zeta

Title : Notch Signaling

April

Title : A critical role for IGF-II in memory consolidation and enhancement

Title : The dendritic branch is the preferred integrative unit for protein synthesis-dependent LTP.

Title : Mushroom Body Output Neurons Encode Odor-Reward Associations

Title :From Drosophila olfaction to a general circuit model for behavioral habituation.

Title :The role of Thorase in the surface expression of glutamate receptors and its implications for synaptic plasticity and behavior

May

Title :The role of Thorase in the surface expression of glutamate receptors and its implications for synaptic plasticity and behavior

Title: Action-Potential Modulation During Axonal Conduction

Title: Action-Potential Modulation During Axonal Conduction

Title: "What makes a place cell?"

June

Title : "Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age"

July

Title : "The Origin of Time (in the Songbird Motor Pathway)"

Title : ""Maps for navigating published work and informing experiment planning""

Title : ""A neural prosthesis for memory? ""

August

Title : ""Intact Performance on Feature-Ambiguous Discriminations in Rats with Lesions of the Perirhinal Cortex ""

Title : " Mushroom body efferent neurons responsible for aversive olfactory memory retrieval in Drosophila "

Title : " Drosophila mutants undercover functional specificity in mushroom body architecture and a novel role for Importin- (alpha)2 in mushroom body development and classical conditioning "

September

Title : ""Prior experience modulates a natural threshold for memory formation ""

Title : " 2½ Short Stories of Pavlov's Flies "

Title : " Talk 1: Grid cells, theta oscillations, and a novel code phase code of the head direction signal Talk 2: Septotemporal variation in theta rhythm dynamics "

October

Title : " AMPA receptor trafficking in reconsolidation of context fear memories "

Title : " Mental Schema and its Neural Correlates"

November