GABA binding is not known, and an initial decrease of GABA binding may result in later increase of GABA receptors. If this is the case, however, the greater number of receptors cannot be responsible for symptoms of alcohol withdrawal. Some additional differences between the data presented and the results of animal experiments make comparison difficult. It is not clear if the tissue preparation was treated by Triton X-100, because in a paper the authors cite as the source for their method both treated and untreated tissues were studied. However, examination of the results of that paper clearly shows that the Scatchard plot of muscimol binding in the rat brain is curvilineaf in both conditions, indicating the presence of at least two receptor populations. In contrast, the Scatchard plot of muscimol binding in the human brain presented by Tran and co-workers seems to be linear, indicating the presence of only one binding site, and the number of binding sites ( B max) was much lower than observed in animal experiments. Although the difference between muscimol binding in animal and human brain could be due to species differences, it seems possible that postmortem changes prevented detection of one of the muscimol binding sites. The increased number of receptors observed in alcoholics might not be related to the decreased GABA levels during ethanol withdrawal because denervation results in increased affinity and an unchanged number of GABA receptors [ 11. The functional consequences of changes in GABA receptor binding are not clear at present. GABA-induced stimulation of benzodiazepine binding is unchanged by ethanol dependence in rats [21 in spite of a decrease in GABA binding (Volicer and Biagioni, in preparation). It would be valuable to know if GABA-induced stimulation of benzodiazepine binding differed in the brains of alcoholics and control subjects. Possibly only some of the GABA receptors are connected with benzodiazepine receptors and GABA receptors which are affected by chronic alcohol intake are functionally independent.
[1]
S H Snyder,et al.
GABA receptors are increased in brains of alcoholics
,
1981,
Annals of neurology.
[2]
S. Murakami,et al.
Palatal myoclonus responding to carbamazepine
,
1981,
Annals of neurology.
[3]
M. Ticku,et al.
Alterations in γ‐Aminobutyric Acid Receptor Sensitivity Following Acute and Chronic Ethanol Treatments
,
1980,
Journal of neurochemistry.
[4]
F. Bloom,et al.
Benzodiazepine receptors remain unchanged after chronic ethanol administration
,
1980,
Neuropharmacology.
[5]
L. Volicer.
GABA levels and receptor binding after acute and chronic ethanol administration
,
1979,
Brain Research Bulletin.
[6]
L. Wilkins.
Session on Neuropharmacology II Afternoon Meeting Thursday, April 27, 1978
,
1978,
Neurology.
[7]
P. Campochiaro,et al.
GABA receptor binding in rat striatum: Localization and effects of denervation
,
1977,
Brain Research.
[8]
E. Dupont,et al.
PALATAL MYOCLONUS TREATED WITH 5‐HYDROXYTRYPTOPHAN AND A DECARBOXYLASE‐INHIBITOR
,
1977,
Acta neurologica Scandinavica.