Long-lasting facilitation of 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release from rat hippocampal slices by nicotinic receptor activation

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Abstract

In this study we explored the effect of the stimulation of nicotinic acetylcholine receptors located on interneurons by measuring 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release and monitoring [Ca 2+](i) in superfused hippocampal slices. In the presence of 6-cyano-7-nitroquinoxaline-2,3-dione, (±)-2-amino-5-phosphonopentanoic acid, and atropine, i.e., under the blockade of N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate and muscarinic receptors, nicotine did not alter the spontaneous outflow of [3H]GABA, but significantly increased the stimulation-evoked [3H]GABA efflux. This effect of nicotine depended on the time interval between nicotine treatment and electrical stimulus, the concentration of nicotine (1-100 μM), and the parameters of electrical depolarization. Acetylcholine (0.03-3 mM), and the α7 subtype-selective agonist choline (0.1-10 mM), also potentiated stimulus-evoked release of [3H]GABA, whereas 1,1-dimethyl-4-phenilpiperazinium iodide failed to increase the tritium outflow significantly. The effect of nicotine treatment was prevented by tetrodotoxin (1 μM) and by the nicotinic acetylcholine receptor antagonist mecamylamine (10 μM), and the α7 subtype-selective antagonists α-bungarotoxin (100 nM) and methyllycaconitine (10 nM), whereas dihidro-β-erythroidine (20 nM) was without effect. Perfusion of 100 μM nicotine caused a [Ca2+](i) transient in about one-third of the tested interneurons; however, the response to subsequent electrical stimulation remained unchanged. Inhibition of the GABA transporter system by nipecotic acid (1 mM) or by decreasing the bath temperature to 12°C abolished completely the effect of nicotine to potentiate the stimulation-evoked release of GABA. These findings indicate that the activation of α7-type nicotinic receptors of hippocampal interneurons results in a long-lasting ability of these cells to respond to depolarization with an increased release of GABA mediated by the transporter system.

Original languageEnglish
Pages (from-to)453-462
Number of pages10
JournalJournal of Pharmacology and Experimental Therapeutics
Volume295
Issue number2
Publication statusPublished - 2000

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Butyric Acid
Nicotinic Receptors
Nicotine
gamma-Aminobutyric Acid
Interneurons
GABA Plasma Membrane Transport Proteins
6-Cyano-7-nitroquinoxaline-2,3-dione
2-Amino-5-phosphonovalerate
Mecamylamine
D-Aspartic Acid
Bungarotoxins
Tritium
Tetrodotoxin
Glutamate Receptors
Cholinergic Antagonists
Iodides
Muscarinic Receptors
N-Methylaspartate
Choline
Baths

ASJC Scopus subject areas

  • Pharmacology

Cite this

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title = "Long-lasting facilitation of 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release from rat hippocampal slices by nicotinic receptor activation",
abstract = "In this study we explored the effect of the stimulation of nicotinic acetylcholine receptors located on interneurons by measuring 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release and monitoring [Ca 2+](i) in superfused hippocampal slices. In the presence of 6-cyano-7-nitroquinoxaline-2,3-dione, (±)-2-amino-5-phosphonopentanoic acid, and atropine, i.e., under the blockade of N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate and muscarinic receptors, nicotine did not alter the spontaneous outflow of [3H]GABA, but significantly increased the stimulation-evoked [3H]GABA efflux. This effect of nicotine depended on the time interval between nicotine treatment and electrical stimulus, the concentration of nicotine (1-100 μM), and the parameters of electrical depolarization. Acetylcholine (0.03-3 mM), and the α7 subtype-selective agonist choline (0.1-10 mM), also potentiated stimulus-evoked release of [3H]GABA, whereas 1,1-dimethyl-4-phenilpiperazinium iodide failed to increase the tritium outflow significantly. The effect of nicotine treatment was prevented by tetrodotoxin (1 μM) and by the nicotinic acetylcholine receptor antagonist mecamylamine (10 μM), and the α7 subtype-selective antagonists α-bungarotoxin (100 nM) and methyllycaconitine (10 nM), whereas dihidro-β-erythroidine (20 nM) was without effect. Perfusion of 100 μM nicotine caused a [Ca2+](i) transient in about one-third of the tested interneurons; however, the response to subsequent electrical stimulation remained unchanged. Inhibition of the GABA transporter system by nipecotic acid (1 mM) or by decreasing the bath temperature to 12°C abolished completely the effect of nicotine to potentiate the stimulation-evoked release of GABA. These findings indicate that the activation of α7-type nicotinic receptors of hippocampal interneurons results in a long-lasting ability of these cells to respond to depolarization with an increased release of GABA mediated by the transporter system.",
author = "A. Kofalvi and B. Sperl{\'a}gh and T. Zelles and E. V{\'i}zi",
year = "2000",
language = "English",
volume = "295",
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journal = "Journal of Pharmacology and Experimental Therapeutics",
issn = "0022-3565",
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T1 - Long-lasting facilitation of 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release from rat hippocampal slices by nicotinic receptor activation

AU - Kofalvi, A.

AU - Sperlágh, B.

AU - Zelles, T.

AU - Vízi, E.

PY - 2000

Y1 - 2000

N2 - In this study we explored the effect of the stimulation of nicotinic acetylcholine receptors located on interneurons by measuring 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release and monitoring [Ca 2+](i) in superfused hippocampal slices. In the presence of 6-cyano-7-nitroquinoxaline-2,3-dione, (±)-2-amino-5-phosphonopentanoic acid, and atropine, i.e., under the blockade of N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate and muscarinic receptors, nicotine did not alter the spontaneous outflow of [3H]GABA, but significantly increased the stimulation-evoked [3H]GABA efflux. This effect of nicotine depended on the time interval between nicotine treatment and electrical stimulus, the concentration of nicotine (1-100 μM), and the parameters of electrical depolarization. Acetylcholine (0.03-3 mM), and the α7 subtype-selective agonist choline (0.1-10 mM), also potentiated stimulus-evoked release of [3H]GABA, whereas 1,1-dimethyl-4-phenilpiperazinium iodide failed to increase the tritium outflow significantly. The effect of nicotine treatment was prevented by tetrodotoxin (1 μM) and by the nicotinic acetylcholine receptor antagonist mecamylamine (10 μM), and the α7 subtype-selective antagonists α-bungarotoxin (100 nM) and methyllycaconitine (10 nM), whereas dihidro-β-erythroidine (20 nM) was without effect. Perfusion of 100 μM nicotine caused a [Ca2+](i) transient in about one-third of the tested interneurons; however, the response to subsequent electrical stimulation remained unchanged. Inhibition of the GABA transporter system by nipecotic acid (1 mM) or by decreasing the bath temperature to 12°C abolished completely the effect of nicotine to potentiate the stimulation-evoked release of GABA. These findings indicate that the activation of α7-type nicotinic receptors of hippocampal interneurons results in a long-lasting ability of these cells to respond to depolarization with an increased release of GABA mediated by the transporter system.

AB - In this study we explored the effect of the stimulation of nicotinic acetylcholine receptors located on interneurons by measuring 4-amino-n-[2,3-3H]butyric acid ([3H]GABA) release and monitoring [Ca 2+](i) in superfused hippocampal slices. In the presence of 6-cyano-7-nitroquinoxaline-2,3-dione, (±)-2-amino-5-phosphonopentanoic acid, and atropine, i.e., under the blockade of N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate and muscarinic receptors, nicotine did not alter the spontaneous outflow of [3H]GABA, but significantly increased the stimulation-evoked [3H]GABA efflux. This effect of nicotine depended on the time interval between nicotine treatment and electrical stimulus, the concentration of nicotine (1-100 μM), and the parameters of electrical depolarization. Acetylcholine (0.03-3 mM), and the α7 subtype-selective agonist choline (0.1-10 mM), also potentiated stimulus-evoked release of [3H]GABA, whereas 1,1-dimethyl-4-phenilpiperazinium iodide failed to increase the tritium outflow significantly. The effect of nicotine treatment was prevented by tetrodotoxin (1 μM) and by the nicotinic acetylcholine receptor antagonist mecamylamine (10 μM), and the α7 subtype-selective antagonists α-bungarotoxin (100 nM) and methyllycaconitine (10 nM), whereas dihidro-β-erythroidine (20 nM) was without effect. Perfusion of 100 μM nicotine caused a [Ca2+](i) transient in about one-third of the tested interneurons; however, the response to subsequent electrical stimulation remained unchanged. Inhibition of the GABA transporter system by nipecotic acid (1 mM) or by decreasing the bath temperature to 12°C abolished completely the effect of nicotine to potentiate the stimulation-evoked release of GABA. These findings indicate that the activation of α7-type nicotinic receptors of hippocampal interneurons results in a long-lasting ability of these cells to respond to depolarization with an increased release of GABA mediated by the transporter system.

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