Blockade of methamphetamine-induced depression of tyrosine hydroxylase by GABA transaminase inhibitors

doi:10.1016/0014-2999(80)90143-0

European Journal of Pharmacology

Volume 66, Issues 2–3, 29 August 1980, Pages 201-205

https://doi.org/10.1016/0014-2999(80)90143-0 Get rights and content

Abstract

Tyrosine hydroxylase (TH) levels in the rat neostriatum are decreased by chronic treatment with methamphetamine. GABAergic neurons could potentially interact with the nigrostriatal dopaminergic neurons in either the neostriatum or the substantia nigra; therefore, the GABA transaminase inhibitors, amino-oxyacetic acid, γ-acetylenic GABA and ethanolamine-O-sulfate, were evaluated for possible influences on the methamphetamine-induced decrease in TH. TH was measured by the procedure of Nagatsu et al. (1964). Methamphetamine (10 mg/ kg, s.c) was given every 6 h for 24 h. Thirty-six h after initiation of the methamphetamine treatment, neostriatal TH activity was approximately 70% of control. Concurrent administration of amino-oxyacetic acid (20 mg/kg, i.p.) or γ-acetylenic GABA (15 mg/kg, i.p.) with methamphetamine completely blocked the TH depression. Dose-response curves were constructed for amino-oxyacetic acid and γ-acetylenic GABA. A single intraventricular injection of ethanolamine-O-sulfate (400 μg/rat), 2–6 h before initiating the methamphetamine regimen, also completely blocked the TH depression. These data suggest that the striatonigral or other GABAergic systems are involved in the regulation of the functional state of the nigrostriatal dopaminergic neurons, and that enhanced GABAergic function will antagonize the effects of high doses of methamphetamine.

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^∗: Present address: Laboratory of Clinical Science, National Institute of Mental Health, Building 10, Room 2D47, Bethesda, Maryland 20014, U.S.A.

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Blockade of methamphetamine-induced depression of tyrosine hydroxylase by GABA transaminase inhibitors

Abstract

European J. Pharmacol.

Brain Res.

Brain Res.

Anal. Biochem.

Brain Res.

Brain Res.

Biochem. Pharmacol.

Dopaminergic influence in the basal ganglia: Evidence for a striatonigral feedback regulation