Unique ionotropic receptors for D-aspartate are a target for serotonin-induced synaptic plasticity in Aplysia californica

Stephen L. Carlson, Lynne A. Fieber

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

The non-l-glutamate (l-Glu) receptor component of d-aspartate (d-Asp) currents in Aplysia californica buccal S cluster (BSC) neurons was studied with whole cell voltage clamp to differentiate it from receptors activated by other well-known agonists of the Aplysia nervous system and investigate modulatory mechanisms of d-Asp currents associated with synaptic plasticity. Acetylcholine (ACh) and serotonin (5-HT) activated whole cell excitatory currents with similar current voltage relationships to d-Asp. These currents, however, were pharmacologically distinct from d-Asp. ACh currents were blocked by hexamethonium (C6) and tubocurarine (d-TC), while d-Asp currents were unaffected. 5-HT currents were blocked by granisetron and methysergide (MES), while d-Asp currents were unaffected. Conversely, while (2S,3R)-1-(Phenanthren- 2-carbonyl)piperazine-2,3-dicarboxylic acid(PPDA) blocked d-Asp currents, it had no effect on ACh or 5-HT currents. Comparison of the charge area described by currents induced by ACh or 5-HT separately from, or with, d-Asp suggests activation of distinct receptors by all 3 agonists. Charge area comparisons with l-Glu, however, suggested some overlap between l-Glu and d-Asp receptors. Ten minute exposure to 5-HT induced facilitation of d-Asp-evoked responses in BSC neurons. This effect was mimicked by phorbol ester, suggesting that protein kinase C (PKC) was involved.

Original languageEnglish (US)
Pages (from-to)151-159
Number of pages9
JournalComparative Biochemistry and Physiology - C Toxicology and Pharmacology
Volume155
Issue number1
DOIs
StatePublished - Jan 2012

Keywords

  • 5-HT
  • Electrophysiology
  • NMDA
  • Patch clamping
  • Plasticity
  • Protein kinase C

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Physiology
  • Health, Toxicology and Mutagenesis
  • Toxicology

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