ALCOHOL WITHDRAWAL REACTIONS IN MICE: EFFECTS OF DRUGS THAT MODIFY NEUROTRANSMISSION
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TL;DR
Both γ-aminobutyric acid and catecholamine pathways tend to suppress the hyperexcitability of the alcohol withdrawal state, apparently both of which are observed in mice made physically dependent on ethanol.
Abstract
Mice were made physically dependent on ethanol by a three-day period of alcohol inhalation with small daily injections of pyrazole to stabilize the blood alcohol levels. The severity of the withdrawal reaction was measured by repeatedly scoring the characteristic convulsions that could be elicited by handling. The effects of neuropharmacological agents on the withdrawal seizures were observed. Drugs that affect cholinergic systems (atropine, dihydro-β-erythroidine or physostigmine) had little or no effect. Similarly, attempts to modify serotonergic neurons with p -chlorophenylalanine, tryptophan or 5-hydroxytryptophan did not affect the withdrawal reaction. However, agents directed at γ-aminobutyric acid neurons modified the seizures; picrotoxin facilitated and aminooxyacetic acid suppressed the convulsions. Drugs that interfere with catecholamine pathways (reserpine, α-methyltyrosine, phentolamine or propranolol) aggravated the withdrawal seizures. Reserpine had the strongest and most prolonged effect. Apparently both γ-aminobutyric acid and catecholamine pathways tend to suppress the hyperexcitability of the alcohol withdrawal state.