NDLI: Synaptic activation of mGluR1 generates persistent depression of a fast after-depolarizing potential in CA3 pyramidal neurons

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Synaptic activation of mGluR1 generates persistent depression of a fast after-depolarizing potential in CA3 pyramidal neurons

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Brown, Jon T. Booth, Clair A. Randall, Andrew D.
Description	Country affiliation: United kingdom Author Affiliation: Brown JT ( Pfizer Applied Neurophysiology Group, MRC Centre for Synaptic Plasticity, School of Physiology and Pharmacology, University of Bristol, University Walk, Bristol BS8 1TD, UK.)
Abstract	Burst firing is an important property of hippocampal pyramidal neurons. Group I metabotropic glutamate receptors (mGluRs) produce a multitude of effects on both the synaptic and intrinsic properties of neurons. We investigated whether brief activation of these receptors results in persistent modifications to the intrinsic excitability of rat hippocampal CA3 pyramidal cells (CA3-PCs). In whole-cell current-clamp recordings, current stimuli consisting of filtered, pseudo-random noise produced action potential firing with a mean frequency of ∼1.5–2 Hz. Analysis of spike intervals revealed that this firing included a substantial component (∼20%) of high-frequency (∼100 Hz) bursting activity. Activation of group I mGluRs with (S)-3,5-dihydroxyphenylglycine [(S)-DHPG] selectively eliminated the high-frequency bursts, an effect that persisted > 30 min after (S)-DHPG washout. The fast after-depolarizing potential (ADP) of CA3-PCs is known to be important for generating high-frequency action potential bursting. This ADP was persistently depressed following a short application of (S)-DHPG. This effect was blocked by the mGluR1 antagonist, (S)-(+)-α-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385). In contrast, the depression was resistant to the mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine hydrochloride (MPEP) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate, N-methyl-d-aspartate (NMDA) and γ-aminobutyric acid $(GABA)_{A}$ antagonists. Unlike other manipulations that generate persistent depression of the ADP in CA3-PCs, DHPG-mediated ADP depression was insensitive to the Kv7 channel inhibitor 10,10-bis(4-Pyridinylmethyl)-9(10H)-anthracenone dihydrochloride (XE991) and strong intracellular $Ca^{2+}$ buffering by 1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA). Synaptic activation of mGluRs in the associational-commissural pathway also resulted in persistent depression of the ADP in postsynaptic CA3-PCs, which was blocked by LY367385. These data represent the first evidence that synaptic activation of mGluR1 can modulate the intrinsic excitability properties of hippocampal neurons.
File Format	HTM / HTML
ISSN	0953816X
Issue Number	5
Volume Number	33
e-ISSN	14609568
Journal	European Journal of Neuroscience
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2011-03-01
Publisher Place	France
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Neuroscience Action Potentials Physiology Hippocampus Cytology Neurons Receptors, Metabotropic Glutamate Metabolism Synapses Drug Effects Animals Benzoates Pharmacology Excitatory Amino Acid Antagonists Glycine Analogs & Derivatives Male Patch-clamp Techniques Rats Rats, Wistar Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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