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Alcohol Withdrawal and Noradrenergic Function
- MARKKU LINNOILA, M.D., Ph.D.;
- IVAN MEFFORD, Ph.D.;
- DAVID NUTT, M.D., P.h.D.; and
- BRYON ADINOFF, M.D.
Abstract
Alcohol withdrawal syndrome is characterized by signs of overactivity of the sympathetic nervous system. Biochemical studies indicate that increased release of norepinephrine is associated with certain symptoms of alcohol withdrawal, and the severity of the withdrawal symptoms correlates positively with the amount of norepinephrine released. In the rat, the brain epinephrine concentration is reduced by alcohol, a phenomenon probably associated with both the intoxicating and rewarding effects of alcohol intake. Furthermore, intoxicating effects of alcohol can be reversed by inhibiting epinephrine synthesis in the rat brain. In this species, alcohol withdrawal is associated with profound depletion of epinephrine in the hypothalamus. When Clonidine, a norepinephrine alpha-2-receptor agonist, was infused in alcoholics, these receptors were found to be subsensitive during alcohol withdrawal, and this subsensitivity may contribute to the syndrome. Repeated withdrawals may lead to "kindling" and thus further enhancement of noradrenergic overactivity. Pituitary responsiveness to corticotropin-releasing hormone, which is a central regulator of stress responses and increases the firing rate of brain noradrenergic neurons, is altered during alcohol withdrawal.
- alcohol, ethyl
- alcohol withdrawal delirium
- clonidine
- corticotropin releasing hormone
- epinephrine
- GABA
- hypothalmus
- methoxyhydroxyphenylglycol
- norepinephrine
- receptors, adrenergic
- sympathetic nervous system
- vanillylmandelic acid
- DHPG
- dopaminergic system
- kindling
- noradrenergic function
- alcohol, ethyl
- alcohol withdrawal delirium
- clonidine
- corticotropin releasing hormone
- epinephrine
- GABA
- hypothalmus
- methoxyhydroxyphenylglycol
- norepinephrine
- receptors, adrenergic
- sympathetic nervous system
- vanillylmandelic acid
- DHPG
- dopaminergic system
- kindling
- noradrenergic function
Article and Author Information
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▸An edited summary of a combined Clinical Staff Conference held 14 January 1987 at the Amphitheatre, Building 10, Bethesda, Maryland, sponsored by the National Institutes of Health, U. S. Department of Health and Human Services.
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▸Authors who wish to cite a section of the conference and specifically indicate its author can use this example for the form of reference:
MEFFORD I. Ethanol and brain epinephrine, pp 877-880. In: LINNOILA M, moderator. Alcohol withdrawal and noradrenergic function. Ann Intern Med. 1987;107:875-889.
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▸Requests for reprints should be addressed to Markku Linnoila, M.D., Ph.D.: LCS, DICBR, National Institute on Alcohol Abuse and Alcoholism, Building 10, Room 3B19, 9000 Rockville Pike; Bethesda, MD 20892.
