Abstract: Inhalation anesthetics, such as diethyl ether, halo‐thane, and enflurane, increase 36C1− uptake into rat cerebral cortical synaptoneurosomes in a concentration‐dependent, picrotoxin‐sensitive fashion. At concentrations consistent with those that stimulate 36C1− uptake, inhalation anesthetics also inhibit the binding of t‐[35S]butylbicyclophosphoro‐thionate ([35S]TBPS) to well‐washed cortical membranes. Scatchard analysis of [35S]TBPS binding indicates that these agents reduce the apparent affinity of this radioligand and have little effect on the Bmax. The ability of inhalation anesthetics to directly stimulate 36C1− uptake and inhibit [35S]TBPS binding is a property shared by nonvolatile anesthetics. Nonetheless, there are differences between nonvolatile agents (such as barbiturates and alcohols) and in halation anesthetics, because the former compounds augment muscimol (a GABAmimetic) stimulated 36C1− uptake, whereas the latter group (such as ether and enflurane) inhibit this effect. These findings demonstrate that therapeutically relevant concentrations of inhalation anesthetics perturb the benzodiazepine/γ‐aminobutyric acid receptor chloride channel complex, and suggest this oligomeric protein may be a common mediator of some aspects of anesthetic action.
|Number of pages||8|
|Journal||Journal of Neurochemistry|
|State||Published - Nov 1988|
- Chloride uptake
- γ‐Aminobutyric acid