Desensitization of postsynaptic glutamate receptors contributes to high-frequency homosynaptic depression of aplysia sensorimotor connections.
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.
Antzoulatos
Evangelos G
EG
Department of Neurobiology and Anatomy, W M Keck Center for the Neurobiology of Learning and Memory, The University of Texas-Houston Medical School, Houston, Texas 77030, USA.
Cleary
Leonard J
LJ
Eskin
Arnold
A
Baxter
Douglas A
DA
Byrne
John H
JH
D000818:Animals; D001048:Aplysia; D001581:Benzothiadiazines / Q000494:pharmacology; D015536:Down-Regulation; D004558:Electric Stimulation; D004594:Electrophysiology; D019706:Excitatory Postsynaptic Potentials; D036881:Long-Term Synaptic Depression; D009046:Motor Neurons / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology*; D017729:Presynaptic Terminals; D018091:Receptors, AMPA / Q000502:physiology*; D017470:Receptors, Glutamate / Q000502:physiology; D012018:Reflex / Q000502:physiology*; D009435:Synaptic Transmission
D001581:Benzothiadiazines; D018091:Receptors, AMPA; D017470:Receptors, Glutamate; C004639:cyclothiazide