By Kenneth Blum
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Additional resources for Alcohol and Opiates. Neurochemical and Behavioral Mechanisms
In ETHANOL DEPENDENCE 26. 27. 28. 29. press. Neff, Ν· H. and Tozer, T. : In Vivo measurement of brain serotonin turnover. Adv. In Pharmacol. 31. 32. 33. peripheral noradrenergic neurons. J. Pharm. Exp. 36. 37. 38. Ther. 159:380-391 (1974). Ahtee, L. : Effect of ethanol dependence and withdrawal on the catecholamines in rat Pharm. et Toxicol. 56:289-298 (1975). , Sjoerdsma, A. : Elucidation of the rate-limiting step in norepine phrine biosynthesis in the perfused guine pig heart. J. Pharm. Exp.
Acta. 225:185-193 (1971). Ross, D. , Medina, M. A. and Cardenas, H. : Morphine and ethanol: Selective depletion of regional brain calcium. Science 256:63-65 (1974). : Physiology of the choroid plexus. Physiol. Rev. 51:273-311 (1971). , Ritzmann, R. F. and Boggan, W. : Inhibition of the transport of 5-hydroxyindoleacetic acid from brain by ethanol. J. Neurochem. 24:10431051 (1975). , Bulat, M. and Anderson, R. : Ethanol inhibition of transport of 5-hydroxyindoleactic acid from cerebrospinal fluid.
In examining the published results on the effects of ethanol on trasmitter turnover, one area of agreement does, however, become evident. An acute dose of ethanol decreases the turnover of norepinephrine (NE) in brain while chronic ethanol administration produces increases in NE turnover which are evident throughout the period of withdrawal (see Tables 3 and 4 ) . An initial increase in turnover of NE seen after an acute dose of ethanol by Hunt and Majchrowicz (28) (Table 3) may be a result of the early excitant, disinhibiting effects of ethanol in the CNS (29) or possibly due to the release of catecholamines in the CNS (30) by an early infiltration of brain tissue with acetaldehyde.
Alcohol and Opiates. Neurochemical and Behavioral Mechanisms by Kenneth Blum