Metabotropic glutamate receptors modify ionotropic glutamate responses in neocortical pyramidal cells and interneurons

Citation
Ae. Bandrowski et al., Metabotropic glutamate receptors modify ionotropic glutamate responses in neocortical pyramidal cells and interneurons, EXP BRAIN R, 136(1), 2001, pp. 25-40
Citations number
81
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL BRAIN RESEARCH
ISSN journal
00144819 → ACNP
Volume
136
Issue
1
Year of publication
2001
Pages
25 - 40
Database
ISI
SICI code
0014-4819(200101)136:1<25:MGRMIG>2.0.ZU;2-0
Abstract
In neocortex glutamate activates ionotropic and metabotropic receptors (mGl uRs). Whole-cell current-clamp recordings in the in vitro rat auditory cort ex at 32 degreesC were used to explore the role that mGluRs have in regulat ion of AMPA/kainate, NMDA, and GABA receptor-mediated synaptic transmission . Our findings are: (a) The fast EPSP (AMPA/kainate), slow EPSP (NMDA), and IPSPs (GABA(A), GABA(B)), elicited in pyramidal neurons are reduced in the presence of (1S,3R)- ACPD (mGluR agonist) with greatest effect on the slow IPSP>fast IPSP>>fast EPSP. The effect is likely the result of ACPD acting at presynaptic mGluRs because the probability of release of glutamate and G ABA is reduced in the presence of ACPD, intracellular infusion of a G prote in antagonist (GDP betaS) did not block the effect of ACPD, nor were iontop horetic kainic acid or NMDA-induced depolarizations reduced by ACPD. (b) Th e slow EPSP is enhanced following washout of ACPD and enhancement is not du e to disinhibition because it is present in the absence of IPSPs, but if IP SPs are present, its magnitude can be influenced. Iontophoretic NMDA respon ses are enhanced in the presence of ACPD, an effect blocked by GDP betaS an d heparin (intracellular inositol 1,4,5-trisphosphate receptor antagonist). Taken together, this evidence suggests that enhancement is a result of gro up I postsynaptic mGluR activation. (c) In fast-spiking cells ACPD reduces the EPSP (AMPA/kainate and NMDA-mediated). This action is likely presynapti c because it persists when GDP betaS is in the cells. (d) The rate of spike discharge recorded from fast-spiking cells is accelerated in ACPD but does not change in the presence of GDP betaS, suggesting a postsynaptic effect. Our data indicate that mGluRs can influence neocortical synaptic transmiss ion in complex ways by acting presynaptically and postsynaptically.