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Molecular Pharmacology

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Research ArticleArticle

Supersensitivity in Rat Cerebral Cortex: Pre- and Postsynaptic Effects of 6-Hydroxydopamine at Noradrenergic Synapses

JONATHAN R. SPORN, BARRY B. WOLFE, T. KENDALL HARDEN and PERRY B. MOLINOFF
Molecular Pharmacology November 1977, 13 (6) 1170-1180;
JONATHAN R. SPORN
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80262
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BARRY B. WOLFE
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80262
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T. KENDALL HARDEN
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80262
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PERRY B. MOLINOFF
Department of Pharmacology, University of Colorado Medical Center, Denver, Colorado 80262
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Abstract

The intraventricular administration of 6-hydroxydopamine resulted in the destruction of noradrenergic nerve terminals in the rat cerebral cortex and a 90% decrease in norepinephrine content. The time courses of the effects of this treatment on catecholamine-stimulated cyclic 3',5'-AMP accumulation in slices of cerebral cortex and on beta adrenergic receptors were determined to investigate the mechanisms underlying supersensitivity in this system. The EC50 for norepinephrine stimulation of cyclic AMP accumulation decreased following 6-hydroxydopamine administration. This decrease was apparent within 1 day and was probably due to the loss of the presynaptic uptake system for norepinephrine. The density of beta adrenergic receptors, as determined by measuring the binding of the high-affinity beta adrenergic receptor antagonist [125I]iodohydroxybenzylpindolol, and maximal levels of catecholamine-stimulated cyclic AMP accumulation increased with a slower time course, reaching peak levels approximately 16 days after treatment with 6-hydroxydopamine. The maximal increase in the density of beta adrenergic receptors was 50%, while maximal levels of cyclic AMP accumulation in treated rats were approximately twice those measured in control animals. The KD of [125I]iodohydroxybenzylpindolol for beta adrenergic receptors and the EC50 of isoproterenol for stimulation of cyclic AMP accumulation were unchanged following 6-hydroxydopamine administration, suggesting that the intrinsic properties of the postsynaptic receptor were not affected by denervation. The administration of 6-hydroxydopamine did not affect fluoride-sensitive adenylate cyclase activity. The results are consistent with the idea that the supersensitivity to catecholamines that occurs in the cerebral cortex following 6-hydroxydopamine administration had both pre- and postsynaptic components. The slowly developing postsynaptic component can be at least partially explained by an increase in the density of beta adrenergic receptors.

ACKNOWLEDGMENT Ms. Jane Andrews provided excellent technical assistance.

  • Copyright © 1977 by Academic Press, Inc.

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Molecular Pharmacology
Vol. 13, Issue 6
1 Nov 1977
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Research ArticleArticle

Supersensitivity in Rat Cerebral Cortex: Pre- and Postsynaptic Effects of 6-Hydroxydopamine at Noradrenergic Synapses

JONATHAN R. SPORN, BARRY B. WOLFE, T. KENDALL HARDEN and PERRY B. MOLINOFF
Molecular Pharmacology November 1, 1977, 13 (6) 1170-1180;

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Research ArticleArticle

Supersensitivity in Rat Cerebral Cortex: Pre- and Postsynaptic Effects of 6-Hydroxydopamine at Noradrenergic Synapses

JONATHAN R. SPORN, BARRY B. WOLFE, T. KENDALL HARDEN and PERRY B. MOLINOFF
Molecular Pharmacology November 1, 1977, 13 (6) 1170-1180;
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