Difference between revisions of "Previous weeks"
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<h4> "The Death of the Subunit-Specific Rules Hypothesis of AMPA Receptor Trafficking?"</h4> | <h4> "The Death of the Subunit-Specific Rules Hypothesis of AMPA Receptor Trafficking?"</h4> | ||
| − | '''Summary of the Talk''' | + | '''Summary of the Talk:''' |
For many years the prevailing view regarding the mechanisms of AMPA receptor trafficking at excitatory synapses has held that the subunit composition of AMPA receptors has a crucial role. Via mechanisms dependent on the intracellular c-termini of the subunits, GluR2/GluR3 subunit containing receptors were thought to form a stable, continuously recycling pool of AMPA receptors at the synapse while GluR1/GluR2 subunit containing receptors were only trafficking into synapses in an activity-dependent manner. Once inserted into synapses, GluR1/GluR2 containing receptors were then thought to be gradually replaced by GluR2/GluR3 containing receptors. Along with other studies, recent work from the Nicoll laboratory using a single-cell “knockout” approach shows that there is very little role for GluR2/GluR3 containing receptors. Instead, 80% of all synaptic receptors (and 95% of all extrasynaptic receptors) are GluR1/GluR2 heteromers. | For many years the prevailing view regarding the mechanisms of AMPA receptor trafficking at excitatory synapses has held that the subunit composition of AMPA receptors has a crucial role. Via mechanisms dependent on the intracellular c-termini of the subunits, GluR2/GluR3 subunit containing receptors were thought to form a stable, continuously recycling pool of AMPA receptors at the synapse while GluR1/GluR2 subunit containing receptors were only trafficking into synapses in an activity-dependent manner. Once inserted into synapses, GluR1/GluR2 containing receptors were then thought to be gradually replaced by GluR2/GluR3 containing receptors. Along with other studies, recent work from the Nicoll laboratory using a single-cell “knockout” approach shows that there is very little role for GluR2/GluR3 containing receptors. Instead, 80% of all synaptic receptors (and 95% of all extrasynaptic receptors) are GluR1/GluR2 heteromers. | ||
'''Relevant Papers:''' | '''Relevant Papers:''' | ||
| + | |||
[[:Image:19thFeb09_1.pdf | Paper_1]] | [[:Image:19thFeb09_1.pdf | Paper_1]] | ||
Revision as of 19:36, 23 February 2010
Spring 2010:
January
Jan 15th
Speaker : John Guzowski of UC Irvine.
"Immediate-Early Gene Expression in Hippocampus: A Window into the Cellular Mechanisms & Neural Circuit Dynamics of Memory"
Summary of Talk:
The ability of neurons to change gene expression patterns in response to synaptic input is critical for cellular mechanisms underlying learning and memory. Following behavioral experience, expression of specific "immediate-early genes (IEGs)" is dramatically increased in discrete populations of neurons in hippocampus, neocortex, and subcortical brain regions. IEGs such as /Arc/ and /Homer 1a/ encode proteins capable of modifying synaptic function and are required for converting experience into lasting memory (i.e., memory consolidation). I will discuss past and ongoing research using sophisticated IEG imaging methods to study neural ensemble dynamics during learning and memory retrieval. In combining these imaging approaches with lesion, neuropharmacological, and vector-mediated gene knockdown/mutation methods, we are address long-standing and fundamental questions about the role of the hippocampus and associated neocortical regions in memory encoding, consolidation, and retrieval.
Jan 29th
Speaker : Dean Buonomano
"What is the Neural Basis of Priming "
Papers Covered:
Grill-Spector K, Henson R, Martin A (2006) Repetition and the brain: neural models of stimulus-specific effects. Trends in Cognitive Sciences 10:14-23.
Li L, Miller EK, Desimone R (1993) The representation of stimulus familiarity in anterior inferior temporal cortex. J Neurophysiol 69:1918-1929.
McMahon DBT, Olson CR (2007) Repetition Suppression in Monkey Inferotemporal Cortex: Relation to Behavioral Priming. J Neurophysiol 97:3532-3543.
February
Feb 05th
Speaker: Thomas W. Abrams, from Dept of Pharmacology, University of Maryland School of Medicine, Baltimore, MD.
"Molecular Mechanisms of Sensory Gating in Aplysia as a Model of Attention"
Summary of the Talk:
Sensory gating enables nervous systems to select which environmental stimuli receive attention. The sensory neuron-to-motor neuron synapse in the defensive withdrawal reflexes of the marine snail /Aplysia/ undergoes rapid and dramatic synaptic depression with low frequency activity. Although this phenomenon has been known for four decades, the underlying molecular mechanism has remained obscure. Our recent analysis suggests that synaptic depression in this system mediates a form of synaptic gating related to stimulus salience, rather than mediating a type of learning, habituation, based on familiarity with a stimulus. In my talk, I will discuss two opposing, calcium-dependent processes that flip these synapses between bistable states during sensory gating. The molecular elements in this switch include protein kinase C and the small G protein Arf. The ubiquitous presence of these highly conserved proteins among metazoans suggest that a similar sensory gating mechanism may operate in mammalian sensory systems, where it could contribute to attention.
Feb 19th
Speaker: Tom O'Dell
"The Death of the Subunit-Specific Rules Hypothesis of AMPA Receptor Trafficking?"
Summary of the Talk:
For many years the prevailing view regarding the mechanisms of AMPA receptor trafficking at excitatory synapses has held that the subunit composition of AMPA receptors has a crucial role. Via mechanisms dependent on the intracellular c-termini of the subunits, GluR2/GluR3 subunit containing receptors were thought to form a stable, continuously recycling pool of AMPA receptors at the synapse while GluR1/GluR2 subunit containing receptors were only trafficking into synapses in an activity-dependent manner. Once inserted into synapses, GluR1/GluR2 containing receptors were then thought to be gradually replaced by GluR2/GluR3 containing receptors. Along with other studies, recent work from the Nicoll laboratory using a single-cell “knockout” approach shows that there is very little role for GluR2/GluR3 containing receptors. Instead, 80% of all synaptic receptors (and 95% of all extrasynaptic receptors) are GluR1/GluR2 heteromers.
Relevant Papers:
