Work

Desensitization of Postsynaptic Glutamate Receptors Contributes to High-Frequency Homosynaptic Depression of Aplysia Sensorimotor Connections

Year: 2003

Type: preprint

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.

Source: Learning & Memory

DOI: 10.1101/lm.61403

Authors: Evangelos G. Antzoulatos, Leonard J. Cleary, Arnold Eskin, Douglas A. Baxter, John H. Byrne

Institutions: The University of Texas Health Science Center at Houston, University of Houston

Language: English

Topic: Neuroscience and Neuropharmacology Research

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

Open Access status: diamond

Funders: National Institutes of Health, National Institute of Neurological Disorders and Stroke

Awards: G2017213778, MORPHOLOGICAL CORRELATES OF LEARNING, G6677619958, G883240435, LONG-TERM REGULATION OF GLUTAMATE UPTAKE IN APLYSIA