α2-Adrenoceptors are not involved in the regulation of striatal glutamate release

Comparison to dopaminergic inhibition

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Striatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) and superfused in order to measure release of radioactivity at rest and during potassium-evoked depolarization. Addition of KCl (22-40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration-dependent manner, and this release was abolished by omission of CaCl2. High-performance liquid chromatography (HPLC) separation coupled with radiochemical detection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respectively, was due to [3H]Glu. At the end of the superfusion about 63% of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCl excess was significantly higher from striatum dissected from 6-hydroxydopamine-pretreated rats. Apomorphine decreased the KCl-evoked release of [3H]Glu, and haloperidol exerted the opposite effect. Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD-1015 and γ-butyrolactone-pretreated rat caudate nucleus, also reversed the apomorphine inhibition of the release of [3H]Glu evoked by depolarization. The selective α2-adrenoceptor antagonist CH-38083, however, did not modify the apomorphine inhibition of [3H]Glu release or dopa accumulation, and the α2-adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2-adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rather than α2-adrenoceptor blocking effect.

Original languageEnglish
Pages (from-to)376-381
Number of pages6
JournalJournal of Neuroscience Research
Volume28
Issue number3
Publication statusPublished - 1991

Fingerprint

Corpus Striatum
Adrenergic Receptors
Glutamic Acid
Tritium
Apomorphine
Dihydroxyphenylalanine
Yohimbine
Potassium
Perfusion
Xylazine
Caudate Nucleus
Oxidopamine
Haloperidol
Radioactivity
Dopamine
High Pressure Liquid Chromatography
Neurons

Keywords

  • CH-38083
  • high-performance liquid chromatography
  • rat striatum

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

@article{99c5904d9d104d16a042e2aa4e206179,
title = "α2-Adrenoceptors are not involved in the regulation of striatal glutamate release: Comparison to dopaminergic inhibition",
abstract = "Striatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) and superfused in order to measure release of radioactivity at rest and during potassium-evoked depolarization. Addition of KCl (22-40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration-dependent manner, and this release was abolished by omission of CaCl2. High-performance liquid chromatography (HPLC) separation coupled with radiochemical detection revealed that 23{\%} and 41{\%} of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respectively, was due to [3H]Glu. At the end of the superfusion about 63{\%} of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCl excess was significantly higher from striatum dissected from 6-hydroxydopamine-pretreated rats. Apomorphine decreased the KCl-evoked release of [3H]Glu, and haloperidol exerted the opposite effect. Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD-1015 and γ-butyrolactone-pretreated rat caudate nucleus, also reversed the apomorphine inhibition of the release of [3H]Glu evoked by depolarization. The selective α2-adrenoceptor antagonist CH-38083, however, did not modify the apomorphine inhibition of [3H]Glu release or dopa accumulation, and the α2-adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2-adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rather than α2-adrenoceptor blocking effect.",
keywords = "CH-38083, high-performance liquid chromatography, rat striatum",
author = "L. H{\'a}rsing and E. V{\'i}zi",
year = "1991",
language = "English",
volume = "28",
pages = "376--381",
journal = "Journal of Neuroscience Research",
issn = "0360-4012",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - α2-Adrenoceptors are not involved in the regulation of striatal glutamate release

T2 - Comparison to dopaminergic inhibition

AU - Hársing, L.

AU - Vízi, E.

PY - 1991

Y1 - 1991

N2 - Striatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) and superfused in order to measure release of radioactivity at rest and during potassium-evoked depolarization. Addition of KCl (22-40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration-dependent manner, and this release was abolished by omission of CaCl2. High-performance liquid chromatography (HPLC) separation coupled with radiochemical detection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respectively, was due to [3H]Glu. At the end of the superfusion about 63% of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCl excess was significantly higher from striatum dissected from 6-hydroxydopamine-pretreated rats. Apomorphine decreased the KCl-evoked release of [3H]Glu, and haloperidol exerted the opposite effect. Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD-1015 and γ-butyrolactone-pretreated rat caudate nucleus, also reversed the apomorphine inhibition of the release of [3H]Glu evoked by depolarization. The selective α2-adrenoceptor antagonist CH-38083, however, did not modify the apomorphine inhibition of [3H]Glu release or dopa accumulation, and the α2-adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2-adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rather than α2-adrenoceptor blocking effect.

AB - Striatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) and superfused in order to measure release of radioactivity at rest and during potassium-evoked depolarization. Addition of KCl (22-40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration-dependent manner, and this release was abolished by omission of CaCl2. High-performance liquid chromatography (HPLC) separation coupled with radiochemical detection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respectively, was due to [3H]Glu. At the end of the superfusion about 63% of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCl excess was significantly higher from striatum dissected from 6-hydroxydopamine-pretreated rats. Apomorphine decreased the KCl-evoked release of [3H]Glu, and haloperidol exerted the opposite effect. Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD-1015 and γ-butyrolactone-pretreated rat caudate nucleus, also reversed the apomorphine inhibition of the release of [3H]Glu evoked by depolarization. The selective α2-adrenoceptor antagonist CH-38083, however, did not modify the apomorphine inhibition of [3H]Glu release or dopa accumulation, and the α2-adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2-adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rather than α2-adrenoceptor blocking effect.

KW - CH-38083

KW - high-performance liquid chromatography

KW - rat striatum

UR - http://www.scopus.com/inward/record.url?scp=0025908095&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025908095&partnerID=8YFLogxK

M3 - Article

VL - 28

SP - 376

EP - 381

JO - Journal of Neuroscience Research

JF - Journal of Neuroscience Research

SN - 0360-4012

IS - 3

ER -