Effects of ethanol and salsolinol on catecholamine function in LS and SS mice

doi:10.1016/0091-3057(84)90112-6

Pharmacology Biochemistry and Behavior

Volume 20, Issue 1, January 1984, Pages 125-131

https://doi.org/10.1016/0091-3057(84)90112-6 Get rights and content

Abstract

Long Sleep (LS) and Short Sleep (SS) mice differ in duration of ethanol-induced sleep time because of differences in brain sensitivity to the depressant effects of alcohols. These lines of mice also differ in their sensitivity to salsolinol, the condensation product of acetaldehyde with dopamine. These lines of mice also differ in their sensitivity to salsolinol, the condensation product of acetaldehyde with study, the half-lives of salsolinol were found to be 12.8 min (LS) and 12.3 min (SS). Salsolinol administration resulted in a decrease in brain norepinephrine content in LS but not SS mice. Dopamine levels were not altered by salsolinol. Ethanol or salsolinol, in vitro, inhibited dopamine uptake by striatal synaptosomes. The IC₅₀ values for ethanol were 491 mM (LS) and 514 mM (SS), and for salsolinol, 300 μM (LS) and 1000 μM (SS). Thus, the mouse line which is most sensitive to the behavioral effects of salsolinol is also most sensitive to salsolinol's effects on norepinephrine levels and inhibition of dopamine uptake. However, much higher concentrations are required to alter dopamine uptake in vitro than are required to alter behavior in vivo.

References (41)

H.S. Alpers et al.
Inhibition of catecholamine uptake and retention in synaptosomal preparations by tetrahydroisoquinoline and tetrahydroberberine alkaloids
Biochem Pharmacol
(1975)
K. Blum et al.
Alcohol and opiates: A review of common neurochemical and behavioral mechanisms
M.A. Collins
Identification of isoquinoline alkaloids during alcohol intoxication
H. Komiskey et al.
The isomers of cocaine and tropacocaine: Effect on ³H-catecholamine uptake by rat brain synaptosomes
Life Sci
(1977)
O.H. Lowry et al.
Protein measurement with the folin phenol reagent
J Biol Chem
(1951)
D.R. Petersen et al.
Characterization of brain acetaldehyde oxidizing systems in the mouse
Drug Alcohol Depend
(1979)
R.G. Rahwan
Toxic effects of ethanol: Possible role of acetaldehyde, tetrahydroisoquinolines and tetrahydro-β-carbolines
Toxicol Appl Pharmacol
(1975)
N. Awazi et al.
Effects of tetrahydropapaveroline and salsolinol on cerebral monoamine metabolism and their interactions with psychopharmacological drugs
Naunyn Schmiedeberg Arch Pharmacol
(1979)
K. Blum et al.
Putative role of isoquinoline alkaloids in alcoholism:A link to opiates
Alcoholism: Clin Exp Res
(1973)
J.L. Bruning et al.

A. Carlsson et al.

Effect of ethanol on the metabolism of brain catecholim

Phychopharmacology

(1973)

A.C. Church et al.

Behavioral effects of salsolinol and ethanol on mice selected for sensitivity to alcohol-induced sleep time

Drug Alcohol Depend

(1977)

A.C. Church et al.

Salsolinol differentially affects mice selected for sensitivity to alcohol

Psychopharmacology (Berlin)

(1976)

G. Cohen

Interaction of catecholamines with acetaldehyde to form tetrahydroisoquinoline neurotransmitters

G. Cohen et al.

Alkaloids from catecholamines in adrenal tissue: Possible role in alcoholism

Science

(1970)

A.C. Collins et al.

Alterations in catecholamine turnover by ethanol in lines of mice which differ in ethanol sleep time

Behav. Gen.

(1973)

A.C. Collins et al.

Mechanisms that underline sex-linked in sex-linked and genotypicaly determination differences in the depressant actions of alcohol

Ann NY Acad Sci

(1976)

M.A. Collins

Dopamine-related tetrahydroisoquinolines: Significant urinary excretion

Science

(1979)

M.A. Collins et al.

Tetrahydroisoquinolines in vivo. I. Rat brain formation of salsolinol, a condensation produc to dopamine and acetalde hycde under certain

(1975)

V.E. Davis et al.

Alcohol, amines and alkaloids: a possible biochemical basis for alcohol addiction

Science

(1970)

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Attenuation of pulsatile changes in the density of striatal [<sup>3</sup>H]GBR-12935 binding sites during chronic ethanol consumption
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Oxidation: The cornerstone of carcinogenesis: Oxidation and tobacco smoke carcinogenesis. A relationship between cause and effect
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Modulation of dopamine release in the striatum: Physiology, pharmacology and pathology
2005, Advances in Neuroregulation and Neuroprotection

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^☆: Supported in part by grants GM-07305, AA-00029 and AA 003527.

²: Requests for reprints should be addressed to Dr. T. Smolen at her current addressed: Institute for Behavioral Genetics, University of Colorado, East Campus-Box 447, Boulder, CO 80309, Telephone: (303) 492-8844.

³: School of Pharmacy, University of Kansas, Lawrence, KS 66045.

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Effects of ethanol and salsolinol on catecholamine function in LS and SS mice☆

Abstract

Biochem Pharmacol

Life Sci

J Biol Chem

Drug Alcohol Depend

Toxicol Appl Pharmacol

Effects of tetrahydropapaveroline and salsolinol on cerebral monoamine metabolism and their interactions with psychopharmacological drugs

Naunyn Schmiedeberg Arch Pharmacol

Putative role of isoquinoline alkaloids in alcoholism:A link to opiates

Alcoholism: Clin Exp Res

Effect of ethanol on the metabolism of brain catecholim

Phychopharmacology

Behavioral effects of salsolinol and ethanol on mice selected for sensitivity to alcohol-induced sleep time

Drug Alcohol Depend

Salsolinol differentially affects mice selected for sensitivity to alcohol

Psychopharmacology (Berlin)

Interaction of catecholamines with acetaldehyde to form tetrahydroisoquinoline neurotransmitters

Alkaloids from catecholamines in adrenal tissue: Possible role in alcoholism

Science

Alterations in catecholamine turnover by ethanol in lines of mice which differ in ethanol sleep time

Behav. Gen.

Mechanisms that underline sex-linked in sex-linked and genotypicaly determination differences in the depressant actions of alcohol

Ann NY Acad Sci

Dopamine-related tetrahydroisoquinolines: Significant urinary excretion

Science

Tetrahydroisoquinolines in vivo. I. Rat brain formation of salsolinol, a condensation produc to dopamine and acetalde hycde under certain

Alcohol, amines and alkaloids: a possible biochemical basis for alcohol addiction

Science