Abstract
The GABA synapse plays an important role in the pharmacologic effects of barbiturates and the mechanisms involved in barbiturate tolerance and dependence. A synopsis of the effects which have been reported to date is found in Tables 1 and 2. Although the acute changes in neurotransmitter uptake and release are nonselective, a lag in the ability of the GABA synapse to compensate for discontinuation of barbiturate exposure may be important in the symptoms of withdrawal. Barbiturates cause changes in the properties of many receptors, but manipulations of the GABAA receptor in vivo correlate with changes in the therapeutic and toxicologic responses to barbiturates, indicating that the GABAA receptor complex plays a pivotal role in the effects of barbiturates. Experiments done in several laboratories show that barbiturate tolerance and dependence cause subtle changes in the properties of the GABAA receptor complex. These observations suggest that decreased GABA-stimulated chloride channel activity and reduced ability to modulate it may be important in causing barbiturate tolerance and the symptoms observed in withdrawal. Selection of drug-resistant rodent strains suggests that there may be genetic factors involved in drug tolerance and dependence. The complexity of the responses of the GABA synapse to both acute and prolonged exposure to barbiturates indicates that it is a valuable model for understanding how the central nervous system responds to drugs and the mechanisms involved in drug addiction.
Published Version
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