PMID- 21497673 OWN - NLM STAT- MEDLINE DCOM- 20120305 LR - 20211020 IS - 1532-0456 (Print) IS - 1532-0456 (Linking) VI - 155 IP - 1 DP - 2012 Jan TI - Unique ionotropic receptors for D-aspartate are a target for serotonin-induced synaptic plasticity in Aplysia californica. PG - 151-9 LID - 10.1016/j.cbpc.2011.04.001 [doi] AB - 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. CI - Copyright (c) 2011 Elsevier Inc. All rights reserved. FAU - Carlson, Stephen L AU - Carlson SL AD - University of Miami Rosenstiel School of Marine and Atmospheric Science, Division of Marine Biology and Fisheries, Miami, FL 33149, USA. FAU - Fieber, Lynne A AU - Fieber LA LA - eng GR - P40 OD010952/OD/NIH HHS/United States GR - P40 RR010294/RR/NCRR NIH HHS/United States GR - P40 RR010294-11/RR/NCRR NIH HHS/United States GR - P40RR01029/RR/NCRR NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20110409 PL - United States TA - Comp Biochem Physiol C Toxicol Pharmacol JT - Comparative biochemistry and physiology. Toxicology & pharmacology : CBP JID - 100959500 RN - 0 (Diazonium Compounds) RN - 0 (Pyridines) RN - 0 (Receptors, Ionotropic Glutamate) RN - 117141-32-9 (4-(2'-pyridyldithio)benzyldiazoacetate) RN - 333DO1RDJY (Serotonin) RN - 3C9PSP36Z2 (Hexamethonium) RN - 3KX376GY7L (Glutamic Acid) RN - 4SR0Q8YD1X (D-Aspartic Acid) RN - N9YNS0M02X (Acetylcholine) RN - W9YXS298BM (Tubocurarine) SB - IM MH - Acetylcholine/pharmacology MH - Animals MH - Aplysia/*drug effects/metabolism/physiology MH - D-Aspartic Acid/metabolism/*pharmacology MH - Diazonium Compounds/pharmacology MH - Ganglia, Invertebrate/drug effects/metabolism MH - Glutamic Acid/pharmacology MH - Hexamethonium/pharmacology MH - Nervous System Physiological Phenomena MH - Neurons/drug effects MH - Patch-Clamp Techniques MH - Pyridines/pharmacology MH - Receptors, Ionotropic Glutamate/*metabolism/physiology MH - Serotonin/*pharmacology MH - *Synaptic Transmission MH - Tubocurarine/pharmacology PMC - PMC3155736 MID - NIHMS290214 EDAT- 2011/04/19 06:00 MHDA- 2012/03/06 06:00 PMCR- 2013/01/01 CRDT- 2011/04/19 06:00 PHST- 2011/01/17 00:00 [received] PHST- 2011/03/30 00:00 [revised] PHST- 2011/04/01 00:00 [accepted] PHST- 2011/04/19 06:00 [entrez] PHST- 2011/04/19 06:00 [pubmed] PHST- 2012/03/06 06:00 [medline] PHST- 2013/01/01 00:00 [pmc-release] AID - S1532-0456(11)00059-7 [pii] AID - 10.1016/j.cbpc.2011.04.001 [doi] PST - ppublish SO - Comp Biochem Physiol C Toxicol Pharmacol. 2012 Jan;155(1):151-9. doi: 10.1016/j.cbpc.2011.04.001. Epub 2011 Apr 9.