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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Neuronal Nicotinic Acetylcholine Receptor Activation Modulates γ-Aminobutyric Acid Release from CA1 Neurons of Rat Hippocampal Slices

Manickavasagom Alkondon, Edna F. R. Pereira, Catão T. F. Barbosa and Edson X. Albuquerque
Journal of Pharmacology and Experimental Therapeutics December 1997, 283 (3) 1396-1411;
Manickavasagom Alkondon
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Edna F. R. Pereira
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Catão T. F. Barbosa
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Edson X. Albuquerque
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Abstract

In the present study we investigated electrophysiologically the nicotinic responses of pyramidal neurons and interneurons visualized by infrared-assisted videomicroscopy and fluorescence in the CA1 field of hippocampal slices obtained from 8- to 24-day-old rats. Application of nicotinic agonists to CA1 neurons evoked at least four types of nicotinic responses. Of major interest was the ability of these agonists to induce the release of γ-aminobutyric acid (GABA) from interneurons. Slowly decaying ACh whole-cell currents and GABA-mediated postsynaptic currents could be recorded from pyramidal neurons and interneurons, whereas fast-decaying nicotinic currents and fast current transients were recorded only from interneurons. Nicotinic responses were sensitive to blockade by d-tubocurarine (10 μM), which indicated that they were mediated by nicotinic acetylcholine receptors (nAChRs). The slowly decaying currents, the postsynaptic currents and the fast current transients were insensitive to blockade by the α-7 nAChR-specific antagonist methyllycaconitine (up to 1 μM) or α-bungarotoxin (100 nM). On the other hand, the slowly decaying nicotinic currents recorded from the interneurons were blocked by the α4β2 nAChR-specific antagonist dihydro-β-erythroidine, and the fast-desensitizing nicotinic currents were evoked by the α-7 nAChR-specific agonist choline. In experimental conditions similar to those used to record nicotinic responses from neurons in slice (i.e., in the absence of tetrodotoxin), we observed that nicotinic agonists can also induce the release of GABA from hippocampal neurons in culture. In summary, these results provide direct evidence for more than one subtype of functional nAChR in CA1 neurons and suggest that activation of nAChRs present in GABAergic interneurons can evoke inhibitory activity in CA1 pyramidal neurons, thereby modulating processing of information in the hippocampus.

Footnotes

  • Send reprint requests to: Dr. Edson X. Albuquerque, Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201.

  • ↵1 This study was supported by US Public Health Service Grant NS25296 and Programa de Apoio a Núcleos de Excelência (PRONEX, Brazil).

  • Abbreviations:
    nAChR
    nicotinic acetylcholine receptor
    CNS
    central nervous system
    α-BGT
    α-bungarotoxin
    MLA
    methyllycaconitine
    α-CTX-ImI
    α-conotoxin-ImI
    DHβE
    dihydro-β-erythroidine
    LTP
    long-term potentiation
    PSC
    postsynaptic current
    GABA
    γ-aminobutyric acid
    ACSF
    artificial cerebrospinal fluid
    DIC
    differential interference contrast
    HEPES
    N-[2-hydroxyethyl]piperazine-N′-[2-ethanesulfonic acid]
    EGTA
    ethyleneglycoltetraacetic acid
    TTX
    tetrodotoxin
    MPSCs
    miniature postsynaptic currents
    CNQX
    6-cyano-7-nitroquinoxaline-2,3-dione
    NMDA
    N-methyl-d-aspartate
    ACh
    acetylcholine
    DMPP
    dimethyl phenyl piperazinium
    AnTX
    (+)-anatoxin-a
    d-TC
    d-tubocurarine
    PSP
    postsynaptic potential
    IR
    infrared
    DIC.
    • Received July 28, 1997.
    • Accepted October 21, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 283, Issue 3
1 Dec 1997
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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Neuronal Nicotinic Acetylcholine Receptor Activation Modulates γ-Aminobutyric Acid Release from CA1 Neurons of Rat Hippocampal Slices

Manickavasagom Alkondon, Edna F. R. Pereira, Catão T. F. Barbosa and Edson X. Albuquerque
Journal of Pharmacology and Experimental Therapeutics December 1, 1997, 283 (3) 1396-1411;

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OtherCELLULAR AND MOLECULAR PHARMACOLOGY

Neuronal Nicotinic Acetylcholine Receptor Activation Modulates γ-Aminobutyric Acid Release from CA1 Neurons of Rat Hippocampal Slices

Manickavasagom Alkondon, Edna F. R. Pereira, Catão T. F. Barbosa and Edson X. Albuquerque
Journal of Pharmacology and Experimental Therapeutics December 1, 1997, 283 (3) 1396-1411;
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