Abstract
1. Rats receiving (+)-amphetamine (either 0·3 or 0·2 mg/kg, i.v.) are anorexic. Only the former dose increases their motor activity. Both doses fail to change dopamine (DM) and noradrenaline (NA) concentrations in striatum and teldiencephalon. The turnover rate of striatal DM is increased only by 0·3 mg/kg of (+)-amphetamine; neither dose changes NA turnover rate in teldiencephalon.
2. (-)-Amphetamine (1 mg/kg, i.v.) causes anorexia and hyperthermia in rats but it changes neither the steady-state concentration nor the turnover rate of striatal DM and tel-diencephalic NA. Motor activity is not increased by this dose of (-)-amphetamine.
3. Cocaine (3 mg/kg, i.v.) increases motor activity and accelerates the turnover rate of striatal DM. This drug neither accelerates turnover rate of teldiencephalic NA nor causes anorexia.
4. These observations suggest that the acceleration of striatal DM turnover rate elicited by (+)-amphetamine and cocaine may be associated with an effect on motor activity. In contrast, the increase of motor activity seems unrelated to the effects of these drugs on noradrenergic tracts of the teldiencephalon.
Full text
PDF
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- Glowinski J., Axelrod J., Iversen L. L. Regional studies of catecholamines in the rat brain. IV. Effects of drugs on the disposition and metabolism of H3-norepinephrine and H3-dopamine. J Pharmacol Exp Ther. 1966 Jul;153(1):30–41. [PubMed] [Google Scholar]
- Groppetti A., Costa E. Tissue concentrations of p-hydroxynorephedrine in rats injected with d-amphetamine: effect of pretreatment with desipramine. Life Sci. 1969 Jun 1;8(11):653–665. doi: 10.1016/0024-3205(69)90027-7. [DOI] [PubMed] [Google Scholar]
- Hanson L. C. Evidence that the CCENTRAL ACTION OF (+)-amphetamine is mediated via catecholamines. Psychopharmacologia. 1967;10(4):289–297. doi: 10.1007/BF00403897. [DOI] [PubMed] [Google Scholar]
- Hanson L. C. Evidence that the central action of amphetamine is mediated via catecholamines. Psychopharmacologia. 1966;9(1):78–80. doi: 10.1007/BF00427706. [DOI] [PubMed] [Google Scholar]
- Neff N. H., Spano P. F., Groppetti A., Wang C. T., Costa E. A simple procedure for calculating the synthesis rate of norepinephrine, dopamine and serotonin in rat brain. J Pharmacol Exp Ther. 1971 Mar;176(3):701–710. [PubMed] [Google Scholar]
- Randrup A., Munkvad I. Role of catecholamines in the amphetamine excitatory response. Nature. 1966 Jul 30;211(5048):540–540. doi: 10.1038/211540a0. [DOI] [PubMed] [Google Scholar]
- Randrup A., Scheel-Krüger J. Diethyldithiocarbamate and amphetamine stereotype behavior. J Pharm Pharmacol. 1966 Nov;18(11):752–752. doi: 10.1111/j.2042-7158.1966.tb07799.x. [DOI] [PubMed] [Google Scholar]
- SMITH C. B. EFFECTS OF D-AMPHETAMINE UPON BRAIN AMINE CONTENT AND LOCOMOTOR ACTIVITY OF MICE. J Pharmacol Exp Ther. 1965 Jan;147:96–102. [PubMed] [Google Scholar]
- SMITH C. B. ENHANCEMENT BY RESERPINE AND ALPHA-METHYL DOPA OF THE EFFECTS OF D-AMPHETAMINE UPON THE LOCOMOTOR ACTIVITY OF MICE. J Pharmacol Exp Ther. 1963 Dec;142:343–350. [PubMed] [Google Scholar]
- Ungerstedt U., Arbuthnott G. W. Quantitative recording of rotational behavior in rats after 6-hydroxy-dopamine lesions of the nigrostriatal dopamine system. Brain Res. 1970 Dec 18;24(3):485–493. doi: 10.1016/0006-8993(70)90187-3. [DOI] [PubMed] [Google Scholar]
- Weissman A., Koe B. K., Tenen S. S. Antiamphetamine effects following inhibition of tyrosine hydroxylase. J Pharmacol Exp Ther. 1966 Mar;151(3):339–352. [PubMed] [Google Scholar]
- van ROSSUM J., van der SCHOOT J., HURKMANS J. A. Mechanism of action of cocaine and amphetamine in the brain. Experientia. 1962 May 15;18:229–231. doi: 10.1007/BF02148316. [DOI] [PubMed] [Google Scholar]