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Title: Effects of cocaine on norepinephrine stimulated phosphoinositide hydrolysis and locomotor activity in rat

Abstract

The function of {alpha}{sub 1}-adrenoceptors was determined by stimulating cortical tissue slices, which were pre-labeled with ({sup 3}H)inositol, with norepinephrine (NE) in the presence of 8 mM LiCl. Results of in vitro studies showed that cocaine 10 {mu}M potentiated maximal NE-stimulated PI hydrolysis by 30%. In addition, the EC{sub 50} was decreased from 3.93 {plus minus} 0.42 to 1.91 {plus minus} 0.31 {mu}M NE. Concentrations of 0.1-100 {mu}M and 0.1-10 {mu}M cocaine enhanced PI hydrolysis stimulated by 0.3 and 3 {mu}M NE, respectively. The concentration-effect curves for NE-stimulated PI hydrolysis were shifted to the right 100-fold in the presence of 0.1 {mu}M prazosin. Cocaine (10 {mu}M) did not potentiate NE-stimulated PI hydrolysis in the presence of 0.1 {mu}M prazosin. ({sup 3}H)Prazosin saturation and NE ({sup 3}H)prazosin competition binding studies using crude membrane preparations showed that 10 {mu}M cocaine did not alter binding parameters B{sub max}, K{sub d}, Hill slope, and IC{sub 50}. Together, these results implied that cocaine in vitro potentiated NE-stimulated PI hydrolysis by blocking NE reuptake. For in vivo studies, the locomotor activity was determined after an acute or chronic injections of either cocaine or saline. Cocaine or saline-treated rats were killed after measurement of the locomotor activity,more » and NE-stimulated PI hydrolysis was measured. Acute administration of cocaine 3.2-42 mg/kg (i.p.) produced an inverted U shaped dose-response curve on locomotor activity. The peak increase in locomotor activity was at 32 mg/kg cocaine. A dose of 42 mg/kg cocaine produced a significant depression of maximal NE-stimulated PI hydrolysis.« less

Authors:
Publication Date:
Research Org.:
Louisiana State Univ., New Orleans, LA (United States). Medical Center
OSTI Identifier:
5476330
Resource Type:
Miscellaneous
Resource Relation:
Other Information: Thesis (Ph. D.)
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; COCAINE; BIOLOGICAL EFFECTS; PHOSPHOLIPIDS; METABOLISM; SYMPATHOMIMETICS; RECEPTORS; BEHAVIOR; BIOCHEMICAL REACTION KINETICS; INOSITOL; NORADRENALINE; RATS; TRACER TECHNIQUES; TRITIUM COMPOUNDS; ADRENAL HORMONES; ALKALOIDS; ANESTHETICS; ANIMALS; ANTIDEPRESSANTS; AUTONOMIC NERVOUS SYSTEM AGENTS; CARBOHYDRATES; CARDIOTONICS; CARDIOVASCULAR AGENTS; CENTRAL NERVOUS SYSTEM AGENTS; CENTRAL NERVOUS SYSTEM DEPRESSANTS; DRUGS; ESTERS; HORMONES; HYDROGEN COMPOUNDS; INOSITOLS; ISOTOPE APPLICATIONS; KINETICS; LIPIDS; MAMMALS; MEMBRANE PROTEINS; MONOSACCHARIDES; NEUROREGULATORS; ORGANIC COMPOUNDS; ORGANIC PHOSPHORUS COMPOUNDS; PROTEINS; PSYCHOTROPIC DRUGS; REACTION KINETICS; RODENTS; SACCHARIDES; VERTEBRATES; 550201* - Biochemistry- Tracer Techniques

Citation Formats

Mosaddeghi, M. Effects of cocaine on norepinephrine stimulated phosphoinositide hydrolysis and locomotor activity in rat. United States: N. p., 1989. Web.
Mosaddeghi, M. Effects of cocaine on norepinephrine stimulated phosphoinositide hydrolysis and locomotor activity in rat. United States.
Mosaddeghi, M. 1989. "Effects of cocaine on norepinephrine stimulated phosphoinositide hydrolysis and locomotor activity in rat". United States.
@article{osti_5476330,
title = {Effects of cocaine on norepinephrine stimulated phosphoinositide hydrolysis and locomotor activity in rat},
author = {Mosaddeghi, M},
abstractNote = {The function of {alpha}{sub 1}-adrenoceptors was determined by stimulating cortical tissue slices, which were pre-labeled with ({sup 3}H)inositol, with norepinephrine (NE) in the presence of 8 mM LiCl. Results of in vitro studies showed that cocaine 10 {mu}M potentiated maximal NE-stimulated PI hydrolysis by 30%. In addition, the EC{sub 50} was decreased from 3.93 {plus minus} 0.42 to 1.91 {plus minus} 0.31 {mu}M NE. Concentrations of 0.1-100 {mu}M and 0.1-10 {mu}M cocaine enhanced PI hydrolysis stimulated by 0.3 and 3 {mu}M NE, respectively. The concentration-effect curves for NE-stimulated PI hydrolysis were shifted to the right 100-fold in the presence of 0.1 {mu}M prazosin. Cocaine (10 {mu}M) did not potentiate NE-stimulated PI hydrolysis in the presence of 0.1 {mu}M prazosin. ({sup 3}H)Prazosin saturation and NE ({sup 3}H)prazosin competition binding studies using crude membrane preparations showed that 10 {mu}M cocaine did not alter binding parameters B{sub max}, K{sub d}, Hill slope, and IC{sub 50}. Together, these results implied that cocaine in vitro potentiated NE-stimulated PI hydrolysis by blocking NE reuptake. For in vivo studies, the locomotor activity was determined after an acute or chronic injections of either cocaine or saline. Cocaine or saline-treated rats were killed after measurement of the locomotor activity, and NE-stimulated PI hydrolysis was measured. Acute administration of cocaine 3.2-42 mg/kg (i.p.) produced an inverted U shaped dose-response curve on locomotor activity. The peak increase in locomotor activity was at 32 mg/kg cocaine. A dose of 42 mg/kg cocaine produced a significant depression of maximal NE-stimulated PI hydrolysis.},
doi = {},
url = {https://www.osti.gov/biblio/5476330}, journal = {},
number = ,
volume = ,
place = {United States},
year = {Sun Jan 01 00:00:00 EST 1989},
month = {Sun Jan 01 00:00:00 EST 1989}
}

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