PMID- 1675800
OWN - NLM
STAT- MEDLINE
DCOM- 19910722
LR  - 20161018
IS  - 0962-8452 (Print)
IS  - 0962-8452 (Linking)
VI  - 243
IP  - 1308
DP  - 1991 Mar 22
TI  - Glutamate mediates a slow synaptic response in hippocampal slice cultures.
PG  - 221-6
AB  - Glutamate (GLU) mediates its 'fast' excitatory transmitter action in the brain by 
      directly gating cation-selective ion channels ('ionotropic' receptors). However, 
      GLU can also activate another type of receptor, coupled to phospholipase C 
      ('metabotropic' receptor). In hippocampal cells, stimulation of this metabotropic 
      receptor by GLU, or by a racemic mixture of (1S-3R and 1R-3S) 
      1-aminocyclopentyl-1,3-dicarboxylate (ACPD), induces a slower excitation mediated 
      by inhibition of K+ currents. We have assessed whether this slow form of 
      metabotropic receptor excitation can contribute to the effects of synaptically 
      released GLU in hippocampal slice cultures, by recording the responses of CA3 
      pyramidal cells to afferent mossy fibre stimulation. When the fast ionotropic 
      response was blocked pharmacologically, mossy fibre stimulation produced a slow 
      depolarizing postsynaptic potential associated with a decrease in membrane 
      conductance, a depression of the slow after-hyperpolarization following a train 
      of action potentials, and reduced accommodation during the action potential 
      train. Under voltage-clamp, mossy fibre stimulation produced a slow 
      voltage-dependent inward current which resembled that produced by application of 
      exogenous ACPD or quisqualate (QUIS), and which was occluded by these 
      metabotropic agonists. We therefore suggest that synaptically released GLU can 
      induce two types of postsynaptic responses: a fast excitation through activation 
      of ionotropic receptors and a slower excitation associated with inhibition of K+ 
      conductances through activation of metabotropic receptors. This is analogous to 
      the dual action of acetylcholine on ionotropic (nicotinic) and metabotropic 
      (muscarinic) receptors.
FAU - Charpak, S
AU  - Charpak S
AD  - Brain Research Institute, University of Zurich, Switzerland.
FAU - Gahwiler, B H
AU  - Gahwiler BH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Proc Biol Sci
JT  - Proceedings. Biological sciences
JID - 101245157
RN  - 0 (Glutamates)
RN  - 0 (Receptors, Amino Acid)
RN  - 0 (Receptors, Cell Surface)
RN  - 0TQU7668EI (Cycloleucine)
RN  - 111900-32-4 (1-amino-1,3-dicarboxycyclopentane)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 8OC22C1B99 (Quisqualic Acid)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Cycloleucine/analogs & derivatives/pharmacology
MH  - Electric Stimulation
MH  - Electrophysiology
MH  - Glutamates/*pharmacology/physiology
MH  - Glutamic Acid
MH  - Hippocampus/*drug effects/physiology
MH  - In Vitro Techniques
MH  - Potassium/metabolism
MH  - Quisqualic Acid/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Receptors, Amino Acid
MH  - Receptors, Cell Surface/drug effects/physiology
MH  - Synapses/drug effects/physiology
EDAT- 1991/03/22 00:00
MHDA- 1991/03/22 00:01
CRDT- 1991/03/22 00:00
PHST- 1991/03/22 00:00 [pubmed]
PHST- 1991/03/22 00:01 [medline]
PHST- 1991/03/22 00:00 [entrez]
AID - 10.1098/rspb.1991.0035 [doi]
PST - ppublish
SO  - Proc Biol Sci. 1991 Mar 22;243(1308):221-6. doi: 10.1098/rspb.1991.0035.