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2013

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

November

Date: November 2nd

Time: 09:30 am

Place : Gonda 2303

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

Speaker: Thomas Rogerson

Summary: ICLM Junior Scientist Lecture Series


Date: November 9th

Time: 09:30 am

Place : Gonda 2303

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

Speaker: Tristan Shuman

Abstract: Lateral prefrontal and posterior parietal cortical areas exhibit task-dependent activation during working memory tasks in humans and monkeys. Neurons in these regions become synchronized during attention-demanding tasks, but the contribution of these interactions to working memory is largely unknown. Using simultaneous recordings of neural activity from multiple areas in both regions, we find widespread, task-dependent, and content-specific synchronization of activity across the fronto-parietal network during visual working memory. The patterns of synchronization are prevalent among stimulus-selective neurons and are governed by influences arising in parietal cortex. These results indicate that short-term memories are represented by large-scale patterns of synchronized activity across the fronto-parietal network.


Date: November 16th

Time: 09:30 am

Place : Gonda 2303

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

Speaker: Denise Cai

Abstract: The origin of the spatial receptive fields of hippocampal place cells has not been established. A hippocampal CA1 pyramidal cell receives thousands of synaptic inputs, mostly from other spatially tuned neurons; however, how the postsynaptic neuron’s cellular properties determine the response to these inputs during behavior is unknown. We discovered that, contrary to expectations from basic models of place cells and neuronal integration, a small, spatially uniform depolarization of the spatially untuned somatic membrane potential of a silent cell leads to the sudden and reversible emergence of a spatially tuned subthreshold response and place-field spiking. Such gating of inputs by postsynaptic neuronal excitability reveals a cellular mechanism for receptive field origin and may be critical for the formation of hippocampal memory representations.


Date: November 30th

Time: 09:30 am

Place : Gonda 2303

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

Speaker: Kelsey Martin

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?”

Speaker: Dr. Michel Baudry

Summary:

In 1984, Gary Lynch and Michel Baudry proposed the hypothesis that the calcium-dependent protease, calpain, plays an important role in LTP and in learning and memory. Dr. Baudry will review the evidence accumulated over the last 2 years that argues the importance of calpain in synaptic plasticity and identifies critical targets for calpain, thus supporting its role in regulating structural organization and function of synaptic contacts.

May

Date: May 4th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Generation of a synthetic memory trace"

Speaker: Don Julien

Summary:

We investigated the effect of activating a competing, artificially generated, neural representation on encoding of contextual fear memory in mice. We used a c-fos?based transgenic approach to introduce the hM3Dq DREADD receptor (designer receptor exclusively activated by designer drug) into neurons naturally activated by sensory experience. Neural activity could then be specifically and inducibly increased in the hM3Dq-expressing neurons by an exogenous ligand. When an ensemble of neurons for one context (ctxA) was artificially activated during conditioning in a distinct second context (ctxB), mice formed a hybrid memory representation. Reactivation of the artificially stimulated network within the conditioning context was required for retrieval of the memory, and the memory was specific for the spatial pattern of neurons artificially activated during learning. Similar stimulation impaired recall when not part of the initial conditioning.

Relevant Reading Material:

Science. 2012 Mar 23;335(6075):1513-6. Generation of a synthetic memory trace. Garner AR, Rowland DC, Hwang SY, Baumgaertel K, Roth BL, Kentros C, Mayford M.


Date: May 11th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: David Glanzman

Summary:

Mushroom bodies are a well-known site for associative learning in insects. Yet the precise mechanisms that underlie plasticity there and ensure their specificity remain elusive. In locusts, the synapses between the intrinsic mushroom body neurons and their postsynaptic targets obey a Hebbian spike-timing-dependent plasticity (STDP) rule. Although this property homeostatically regulates the timing of mushroom body output, its potential role in associative learning is unknown. Here we show in vivo that pre-post pairing causing STDP can, when followed by the local delivery of a reinforcement-mediating neuromodulator, specify the synapses that will undergo an associative change. At these synapses, and there only, the change is a transformation of the STDP rule itself. These results illustrate the multiple actions of STDP, including a role in associative learning, despite potential temporal dissociation between the pairings that specify synaptic modification and the delivery of reinforcement-mediating neuromodulator signals.

Relevant Reading Material:

Nature. 2012 Jan 25;482(7383):47-52. doi: 10.1038/nature10776. Conditional modulation of spike-timing-dependent plasticity for olfactory learning. Cassenaer S, Laurent G.


Date: May 18th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Lisa Moore

Summary:

The ability to learn new skills and perfect them with practice applies not only to physical skills but also to abstract skills, like motor planning or neuroprosthetic actions. Although plasticity in corticostriatal circuits has been implicated in learning physical skills, it remains unclear if similar circuits or processes are required for abstract skill learning. Here we use a novel behavioural task in rodents to investigate the role of corticostriatal plasticity in abstract skill learning. Rodents learned to control the pitch of an auditory cursor to reach one of two targets by modulating activity in primary motor cortex irrespective of physical movement. Degradation of the relation between action and outcome, as well as sensory-specific devaluation and omission tests, demonstrate that these learned neuroprosthetic actions are intentional and goal-directed, rather than habitual. Striatal neurons change their activity with learning, with more neurons modulating their activity in relation to target-reaching as learning progresses. Concomitantly, strong relations between the activity of neurons in motor cortex and the striatum emerge. Specific deletion of striatal NMDA receptors impairs the development of this corticostriatal plasticity, and disrupts the ability to learn neuroprosthetic skills. These results suggest that corticostriatal plasticity is necessary for abstract skill learning, and that neuroprosthetic movements capitalize on the neural circuitry involved in natural motor learning.Relevant Reading Material:

Nature. 2012 Mar 4;483(7389):331-5. doi: 10.1038/nature10845. Corticostriatal plasticity is necessary for learning intentional neuroprosthetic skills.

April

Date: Apr 20th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Alexander Reeves

Summary:

A specific memory is thought to be encoded by a sparse population of neurons. These neurons can be tagged during learning for subsequent identification and manipulation. Moreover, their ablation or inactivation results in reduced memory expression, suggesting their necessity in mnemonic processes. However, the question of sufficiency remains: it is unclear whether it is possible to elicit the behavioural output of a specific memory by directly activating a population of neurons that was active during learning. Here the authors show in mice that optogenetic reactivation of hippocampal neurons activated during fear conditioning is sufficient to induce freezing behavior. The authors labelled a population of hippocampal dentate gyrus neurons activated during fear learning with ChR2 and later optically reactivated these neurons in a different context. The mice showed increased freezing only upon light stimulation, indicating light-induced fear memory recall. This freezing was not detected in non-fear-conditioned mice expressing ChR2 in a similar proportion of cells, nor in fear-conditioned mice with cells labelled by eYFP instead of ChR2. Finally, activation of cells labelled in a context not associated with fear did not evoke freezing in mice that were previously fear conditioned in a different context, suggesting that light-induced fear memory recall is context specific. Together, their findings indicate that activating a sparse but specific ensemble of hippocampal neurons that contribute to a memory engram is sufficient for the recall of that memory. Moreover, their experimental approach offers a general method of mapping cellular populations bearing memory engrams.

Relevant Reading Material:

Optogenetic stimulation of a hippocampal engram activates fear memory recall. Liu X, Ramirez S, Pang PT, Puryear CB, Govindarajan A, Deisseroth K, Tonegawa S. Nature. 2012 Mar 22. doi: 10.1038/nature11028. [Epub ahead of print]


Date: Apr 13th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Activity Recall in a Visual Cortical Ensemble"

Speaker: Weixiang Chen

Summary:

Cue-triggered recall of learned temporal sequences is an important cognitive function that has been attributed to higher brain areas. Here recordings in both anesthetized and awake rats demonstrate that after repeated stimulation with a moving spot that evoked sequential firing of an ensemble of primary visual cortex (V1) neurons, just a brief flash at the starting point of the motion path was sufficient to evoke a sequential firing pattern that reproduced the activation order evoked by the moving spot. The speed of recalled spike sequences may reflect the internal dynamics of the network rather than the motion speed. In awake rats, such recall was observed during a synchronized ('quiet wakeful') brain state having large-amplitude, low-frequency local field potential (LFP) but not in a desynchronized ('active') state having low-amplitude, high-frequency LFP. Such conditioning-enhanced, cue-evoked sequential spiking of a V1 ensemble may contribute to experience-based perceptual inference in a brain state?dependent manner.

Relevant Reading Material:

Nat Neurosci. 2012 Jan 22;15(3):449-55, S1-2. doi: 10.1038/nn.3036. Activity recall in a visual cortical ensemble. Xu S, Jiang W, Poo MM, Dan Y.


Date: Apr 6th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : "Dynamics of Retrieval Strategies for Remote Memories"

Speaker: Thomas Rogerson

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)

Relevant Information:

Paper

Supp



March

Mar 4th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : Maladaptive Cortical Plasticity and Plasticity

Speaker: Dean Buonomano

Summary: Engineer ND, Riley JR, Seale JD, Vrana WA, Shetake JA, Sudanagunta SP, Borland MS, Kilgard MP (2011) Nature 470:101-104. Reversing pathological neural activity using targeted plasticity

Relevant Information:

Paper


Mar 11th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : Memory enhancement and PKM Zeta

Speaker: Yong-Seok Lee

Summary: Yong-Seok Lee will present the newest paper from the Dudai Lab regarding overexpression of PKM in the neocortex and its enhancement of LTM.


Relevant Information:

Paper


Mar 18th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

Title : Notch Signaling

Speaker: Kelsey Martin

Summary: Notch signaling plays critical roles during the development of the nervous system. Several studies have suggested that Notch signaling in neurons is also involved in learning and memory and synaptic plasticity in the mature brain. However, these studies have been suggestive rather than conclusive. Moreover, studies from Ben Barres indicate that Notch receptor and ligands are expressed at very low levels in mature neurons, and at very high levels in glia. I will present a paper from Nick Gaiano's lab that argues that Notch signals from synapse to nucleus in mature hippocampal neurons and that this signaling is required for long-term potentiation and memory acquisition. Gaiano's data further indicates that the immediate early gene arc regulates Notch signaling in neurons.

The reference for the primary paper is:

Activity-induced notch signaling in neurons requires arc/arg3.1 and is essential for synaptic plasticity in hippocampal networks.

Relevant Information:

Paper

Review


April

01st Apr


Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Ravi Ponnusamy

Summary: not provided

Relevant Information:

Paper


08th Apr


Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Walter Babiec

Summary: The late-phase of long-term potentiation (L-LTP), the cellular correlate of long-term memory, induced at some synapses facilitates L-LTP expression at other synapses receiving stimulation too weak to induce L-LTP by itself. Using glutamate uncaging and two-photon imaging, we demonstrate that the efficacy of this facilitation decreases with increasing time between stimulations, increasing distance between stimulated spines and with the spines being on different dendritic branches. Paradoxically, stimulated spines compete for L-LTP expression if stimulated too closely together in time. Furthermore, the facilitation is temporally bidirectional but asymmetric. Additionally, L-LTP formation is itself biased toward occurring on spines within a branch. These data support the Clustered Plasticity Hypothesis, which states that such spatial and temporal limits lead to stable engram formation, preferentially at synapses clustered within dendritic branches rather than dispersed throughout the dendritic arbor. Thus, dendritic branches rather than individual synapses are the primary functional units for long-term memory storage

Relevant Information:

Paper

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

Summary: This paper from Coleen Murphy's lab at Princeton describes a novel assay for short and long-term associative memory in the worm c. elegans. Using this assay, the authors show that long-term memory declines very early in c elegans, before any deficits in chemotaxis or motility. Analysis of genetic mutants identifies a specific role for CREB during long-term memory, and further reveals that long-term memory is differentially regulated by the insulin/IGF-1 and dietary restriction longevity pathways.

Relevant Information:

Paper


July

Date: Jul 08th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Michael A. Long

Summary: Not Provided

Relevant Information:

Lab Homepage



Date: Jul 22nd

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Alcino J Silva and Anthony Landreth

Summary: The increasing volume and complexity of published studies in neuroscience have made it difficult to determine what is known, what is uncertain, and how to contribute effectively to one’s field. Therefore, there is a pressing need for strategies to derive simplified useful representations (i.e. maps) of previous findings and to help experiment planning. Toward these goals, we introduce a framework for classifying experiments and an approach for integrating experimental results based on implicit and explicit research practices in molecular and cellular studies of cognitive function. The development and explicit use of approaches like this one will enable researchers to systematically identify convergent evidence critical for assembling maps of published information. These maps will not only provide succinct summaries of published information, they will also be invaluable during experiment planning.

Relevant Information:

Internally circulated PDF (check your LMP email)


Date: Jul 29th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Dean Buonomano

Summary: A discussion on the following paper:

A cortical neural prosthesis for restoring and enhancing memory.

Berger TW, Hampson RE, Song D, Goonawardena A, Marmarelis VZ, Deadwyler SA, Journal of Neural Engineering 8:046017 (2011).

Relevant Information:

http://iopscience.iop.org/1741-2552/8/4/046017/pdf/1741-2552_8_4_046017.pdf


August

Date: Aug 05th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: Walter Babiec

Summary: clark et al., have developed a behavioral paradigm for the rat that makes it possible to separate the evaluation of memory functions from the evaluation of perceptual functions. Animals were given extensive training on an automated two-choice discrimination task and then maintained their memory performance at a high level while interpolated probe trials tested visual perceptual ability. The probe trials systematically varied the degree of feature ambiguity between the stimuli. As feature ambiguity increased, performance declined in an orderly, monotonic manner. Bilateral lesions of the perirhinal cortex fully spared the capacity to make feature-ambiguous discriminations and the performance of lesioned and intact animals was indistinguishable at every difficulty level. In contrast, the perirhinal lesions did impair recognition memory. The findings suggest that the perirhinal cortex is important for memory and not for perceptual functions.


Relevant Information:

http://www.cell.com/neuron/abstract/S0896-6273(11)00197-8?switch=standard


Date : Aug 12th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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

Speaker: David Glanzman

Summary: In this paper Preat and colleagues identify specific neurons in the fly's brain that are essential for the retrieval of a conditioned olfactory memory. These neurons (MB-V2) are found in the mushroom bodies of the Drosophila brain, an area previously identified as critical for olfactory conditioning, during which flies learn to avoid an odor that is paired with shock. Interestingly, the MB-V2 neurons, although essential for the retrieval of both short-term and long-lasting memory, are not required for either memory formation or memory consolidation. The authors propose that MB-V2 neurons recruit the olfactory pathway involved in innate odor avoidance during memory retrieval.

Relevant Information:

Nat. Neurosci. (2011) vol. 14 (7) pp. 903-10



Date: Aug 19th

Time: 09:30 am

Place : 2nd Floor Conference Room, Gonda building.

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 "

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 Semesters

2011

Winter 2010

Fall 2010

Summer 2010

Spring 2010

Fall 2009