The present electric shock (ES) schedule followed in these experiments produced different functional changes in endogenous putative opioid agonist- and antagonist-type receptors, depending on the type of receptor: the amount of antagonist binding was increased by ES application, while the amount of agonist binding was decreased. In order to elucidate the mechanism of these changes, we investigated whether ES application was able to affect sulfhydryl-groups and phospholipids of endogenous opioid receptors. In comparison to the control membrane, the increased antagonist binding sites of the ES membrane were liable to be inactivated by the sulfhydryl-modifying reagents, N-ethylmaleimide (NEM) and iodoacetamide. However, in the presence of 100 mM Na, the antagonist binding sites of both the control and ES membranes were inactivated by NEM in the same manner. On the other hand, the agonist binding sites of both membranes were similarly inactivated by NEM regardless of the absence or presence of 100 mM Na. Another sulfhydryl-modifying reagent, such as p-chloromercuriphenylsulfonic acid, did not produce any difference between the control and ES membranes. The increased antagonist binding sites of the ES membrane were also liable to be inactivated by phospholipase A2. These results suggest that the present ES schedule followed in these experiments produces conformational changes in endogenous opioid receptors in the rat brain. As a result of these conformational changes, the amount of binding in the antagonist sites may be increased, while the amount of binding in the agonist sites may be decreased. However, the increased antagonist binding sites may be liable to be inactivated by NEM, iodoacetamide and phospholipase A2.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Neurology
- Developmental Biology