Induction of giant depolarizing potentials by zinc in area CA1 of the rat hippocampus does not result from block of GABAB receptors

Nevin A Lambert, M. Levitin, N. L. Harrison

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The possibility that zinc (Zn2+) induces giant depolarizing potentials (GDPs) by blocking pre- and postsynaptic γ-aminobutyric acidB (GABAB) receptors in area CAl of rat hippocampal slices was investigated. Monosynaptic GABAA receptor-mediated fast and GABAB receptor-mediated late inhibitory postsynaptic potentials (IPSPs) were evoked in the presence of the excitatory amino acid (EAA) receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and d,l-2-amino-5-phosphonovalerate (APV). Addition of Zn2+ (0.3 mM) resulted in the appearance of long-lasting GDPs which obscured monosynaptic late IPSPs. The GABAA receptor antagonist bicuculline methiodide (BMI; 30 μM) blocked fast monosynaptic IPSPs and GDPs, revealing a monosynaptic late IPSP that was prolonged in the presence of Zn2+ and blocked by the GABAB receptor antagonist CGP 35 348 (100 μM). The selective GABAB receptor agonist baclofen (10 μM) depressed monosynaptic IPSPs and population excitatory postsynaptic potentials (pEPSPs) by acting at presynaptic GABAB receptors. Depression of synaptic potentials by baclofen was unaffected by Zn2+. These results suggest that induction of GDPs in area CAl does not result from an action of Zn2+ at GABAB receptors. We suggest instead that Zn2+ induces GDPs by inducing synchronized discharge of GABAergic interneurons.

Original languageEnglish (US)
Pages (from-to)215-218
Number of pages4
JournalNeuroscience Letters
Volume135
Issue number2
DOIs
StatePublished - Feb 3 1992
Externally publishedYes

Fingerprint

Inhibitory Postsynaptic Potentials
Zinc
Hippocampus
GABA-B Receptors
2-Amino-5-phosphonovalerate
Presynaptic Receptors
GABA-A Receptor Antagonists
Excitatory Amino Acid Antagonists
Synaptic Potentials
Baclofen
Excitatory Postsynaptic Potentials
Glutamate Receptors
Interneurons
GABA-A Receptors
Population

Keywords

  • Baclofen
  • CGP 35 348
  • Giant depolarizing potential
  • Interneuron

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Induction of giant depolarizing potentials by zinc in area CA1 of the rat hippocampus does not result from block of GABAB receptors. / Lambert, Nevin A; Levitin, M.; Harrison, N. L.

In: Neuroscience Letters, Vol. 135, No. 2, 03.02.1992, p. 215-218.

Research output: Contribution to journalArticle

@article{7279832cf7034b3c946996aed2d14ea8,
title = "Induction of giant depolarizing potentials by zinc in area CA1 of the rat hippocampus does not result from block of GABAB receptors",
abstract = "The possibility that zinc (Zn2+) induces giant depolarizing potentials (GDPs) by blocking pre- and postsynaptic γ-aminobutyric acidB (GABAB) receptors in area CAl of rat hippocampal slices was investigated. Monosynaptic GABAA receptor-mediated fast and GABAB receptor-mediated late inhibitory postsynaptic potentials (IPSPs) were evoked in the presence of the excitatory amino acid (EAA) receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and d,l-2-amino-5-phosphonovalerate (APV). Addition of Zn2+ (0.3 mM) resulted in the appearance of long-lasting GDPs which obscured monosynaptic late IPSPs. The GABAA receptor antagonist bicuculline methiodide (BMI; 30 μM) blocked fast monosynaptic IPSPs and GDPs, revealing a monosynaptic late IPSP that was prolonged in the presence of Zn2+ and blocked by the GABAB receptor antagonist CGP 35 348 (100 μM). The selective GABAB receptor agonist baclofen (10 μM) depressed monosynaptic IPSPs and population excitatory postsynaptic potentials (pEPSPs) by acting at presynaptic GABAB receptors. Depression of synaptic potentials by baclofen was unaffected by Zn2+. These results suggest that induction of GDPs in area CAl does not result from an action of Zn2+ at GABAB receptors. We suggest instead that Zn2+ induces GDPs by inducing synchronized discharge of GABAergic interneurons.",
keywords = "Baclofen, CGP 35 348, Giant depolarizing potential, Interneuron",
author = "Lambert, {Nevin A} and M. Levitin and Harrison, {N. L.}",
year = "1992",
month = "2",
day = "3",
doi = "10.1016/0304-3940(92)90439-E",
language = "English (US)",
volume = "135",
pages = "215--218",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

TY - JOUR

T1 - Induction of giant depolarizing potentials by zinc in area CA1 of the rat hippocampus does not result from block of GABAB receptors

AU - Lambert, Nevin A

AU - Levitin, M.

AU - Harrison, N. L.

PY - 1992/2/3

Y1 - 1992/2/3

N2 - The possibility that zinc (Zn2+) induces giant depolarizing potentials (GDPs) by blocking pre- and postsynaptic γ-aminobutyric acidB (GABAB) receptors in area CAl of rat hippocampal slices was investigated. Monosynaptic GABAA receptor-mediated fast and GABAB receptor-mediated late inhibitory postsynaptic potentials (IPSPs) were evoked in the presence of the excitatory amino acid (EAA) receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and d,l-2-amino-5-phosphonovalerate (APV). Addition of Zn2+ (0.3 mM) resulted in the appearance of long-lasting GDPs which obscured monosynaptic late IPSPs. The GABAA receptor antagonist bicuculline methiodide (BMI; 30 μM) blocked fast monosynaptic IPSPs and GDPs, revealing a monosynaptic late IPSP that was prolonged in the presence of Zn2+ and blocked by the GABAB receptor antagonist CGP 35 348 (100 μM). The selective GABAB receptor agonist baclofen (10 μM) depressed monosynaptic IPSPs and population excitatory postsynaptic potentials (pEPSPs) by acting at presynaptic GABAB receptors. Depression of synaptic potentials by baclofen was unaffected by Zn2+. These results suggest that induction of GDPs in area CAl does not result from an action of Zn2+ at GABAB receptors. We suggest instead that Zn2+ induces GDPs by inducing synchronized discharge of GABAergic interneurons.

AB - The possibility that zinc (Zn2+) induces giant depolarizing potentials (GDPs) by blocking pre- and postsynaptic γ-aminobutyric acidB (GABAB) receptors in area CAl of rat hippocampal slices was investigated. Monosynaptic GABAA receptor-mediated fast and GABAB receptor-mediated late inhibitory postsynaptic potentials (IPSPs) were evoked in the presence of the excitatory amino acid (EAA) receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and d,l-2-amino-5-phosphonovalerate (APV). Addition of Zn2+ (0.3 mM) resulted in the appearance of long-lasting GDPs which obscured monosynaptic late IPSPs. The GABAA receptor antagonist bicuculline methiodide (BMI; 30 μM) blocked fast monosynaptic IPSPs and GDPs, revealing a monosynaptic late IPSP that was prolonged in the presence of Zn2+ and blocked by the GABAB receptor antagonist CGP 35 348 (100 μM). The selective GABAB receptor agonist baclofen (10 μM) depressed monosynaptic IPSPs and population excitatory postsynaptic potentials (pEPSPs) by acting at presynaptic GABAB receptors. Depression of synaptic potentials by baclofen was unaffected by Zn2+. These results suggest that induction of GDPs in area CAl does not result from an action of Zn2+ at GABAB receptors. We suggest instead that Zn2+ induces GDPs by inducing synchronized discharge of GABAergic interneurons.

KW - Baclofen

KW - CGP 35 348

KW - Giant depolarizing potential

KW - Interneuron

UR - http://www.scopus.com/inward/record.url?scp=0026597454&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026597454&partnerID=8YFLogxK

U2 - 10.1016/0304-3940(92)90439-E

DO - 10.1016/0304-3940(92)90439-E

M3 - Article

C2 - 1352630

AN - SCOPUS:0026597454

VL - 135

SP - 215

EP - 218

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 2

ER -