Cholinergic disinhibition in area CA1 of the rat hippocampus is not mediated by receptors located on inhibitory neurons

Nevin A Lambert, Timothy J. Teyler

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

We studied the effects of carbamylcholine (carbachol; CCh) on monosynaptic inhibitory postsynaptic potentials (IPSPs) evoked in the presence of the excitatory amino acid receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D,L-2-amino-5-phosphonovalerate (APV). CCh (30 μM) blocked late afterhyperpolarizations but did not depress GABAA receptor-mediated fast monosynaptic IPSPs or GABAB receptor-mediated late monosynaptic IPSPs. In the presence of CCh the GABAB receptor agonist ( ± )-baclofen (2 mM) reversibly hyperpolarized pyramidal neurons and depressed monosynaptic IPSPs as under control conditions. Phorbol-12,13-diacetate (PDAc; 10 μM) increased fast and depressed late monosynaptic IPSPs, and prevented depression of IPSPs by baclofen. These results suggest that cholinergic disinhibition in area CA1 of the hippocampus results from decreased synaptic excitation of inhibitory neurons.

Original languageEnglish (US)
Pages (from-to)129-131
Number of pages3
JournalEuropean Journal of Pharmacology
Volume203
Issue number1
DOIs
StatePublished - Oct 2 1991
Externally publishedYes

Fingerprint

Inhibitory Postsynaptic Potentials
Cholinergic Agents
Hippocampus
Neurons
Carbachol
GABA-B Receptors
2-Amino-5-phosphonovalerate
Excitatory Amino Acid Antagonists
Baclofen
Pyramidal Cells
Glutamate Receptors
GABA-A Receptors

Keywords

  • (Disinhibition)
  • Baclofen
  • Carbachol
  • Inhibitory postsynaptic potentials (monosynaptic)
  • Phorbol esters

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

Cholinergic disinhibition in area CA1 of the rat hippocampus is not mediated by receptors located on inhibitory neurons. / Lambert, Nevin A; Teyler, Timothy J.

In: European Journal of Pharmacology, Vol. 203, No. 1, 02.10.1991, p. 129-131.

Research output: Contribution to journalArticle

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