Abstract
The retinogeniculate synapse conveys visual information from the retina to thalamic relay neurons. Here, we examine the mechanisms of short-term plasticity that can influence transmission at this connection in mouse brain slices. Our studies show that synaptic strength is modified by physiological activity patterns due to marked depression at high frequencies. Postsynaptic mechanisms of plasticity make prominent contributions to this synaptic depression. During trains of retinal input stimulation, receptor desensitization attenuates the AMPA EPSC while the NMDA EPSC saturates. This differential plasticity may help explain the distinct roles of these receptors in shaping the relay neuron response to visual stimulation with the AMPA component being important for transient responses, while sustained high frequency responses rely more on the NMDA component.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Benzothiadiazines / pharmacology
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Biphenyl Compounds / pharmacology
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / physiology
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Geniculate Bodies / cytology
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Geniculate Bodies / drug effects
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Geniculate Bodies / physiology*
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In Vitro Techniques
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Mice
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Neuronal Plasticity / physiology*
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Patch-Clamp Techniques
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Propionates / pharmacology
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Receptors, AMPA / metabolism*
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Synapses / physiology*
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Valine / analogs & derivatives*
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Valine / pharmacology
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Visual Pathways / physiology*
Substances
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Benzothiadiazines
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Biphenyl Compounds
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Excitatory Amino Acid Antagonists
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Propionates
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Receptors, AMPA
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Receptors, N-Methyl-D-Aspartate
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alpha-amino-2'-chloro-5-(phosphonomethyl)(1,1'-biphenyl)-3-propanoic acid
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2-amino-5-phosphopentanoic acid
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Valine
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cyclothiazide