Author:
Antzoulatos Evangelos G.,Cleary Leonard J.,Eskin Arnold,Baxter Douglas A.,Byrne John H.
Abstract
Withdrawal reflexes of Aplysia are mediated in part by a
monosynaptic circuit of sensory (SN) and motor (MN) neurons. A brief
high-frequency burst of spikes in the SN produces excitatory postsynaptic
potentials (EPSPs) that rapidly decrease in amplitude during the burst of
activity. It is generally believed that this and other (i.e., low-frequency)
forms of homosynaptic depression are entirely caused by presynaptic mechanisms
(e.g., depletion of releasable transmitter). The present study examines the
contribution that desensitization of postsynaptic glutamate receptors makes to
homosynaptic depression. Bath application of cyclothiazide, an agent that
reduces desensitization of non-NMDA glutamate receptors, reduced high-, but
not low-frequency synaptic depression. Thus, a postsynaptic mechanism,
desensitization of glutamate receptors, can also contribute to homosynaptic
depression of sensorimotor synapses.
Publisher
Cold Spring Harbor Laboratory
Subject
Cellular and Molecular Neuroscience,Cognitive Neuroscience,Neuropsychology and Physiological Psychology
Cited by
17 articles.
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