Endogenous Opioids and Their Receptors. Evidence for Involvement in the Postictal Effects of Electroconvulsive Shock. Part 3. Biochemical and Neuroendocrinological Effects 2

摘要

The biological mechanisms responsible for the therapeutic effects of electroconvulsive therapy (ECT) remain to be defined. In experimental animals as well as humans, it has been demonstrated that many neurotransmitter and neuroendocrine substances are profoundly affected by electroconvulsive shock (ECS). Among the classic neurotransmitters, ECS has been shown to affect such ligands as serotonin gamma-aminobutyric acid (GABA) as well as catecholamines. Circulating concentrations of pituitary peptides and target gland hormones are also affected by ECS. Likewise, many of the receptors with which these substances interact are modified following acute or repeated ECS. Ultimately, the therapeutic effects of ECT are probably a result of interactions among these many endogenous ligands and their altered receptors. Since their discovery almost a decade ago, endogenous opioid peptides have been implicated as being either causative or curative in a variety of mental disorders. The following review emphasizes our own results identifying opioid-like behavioral, electroencephalographic, and autonomic effects of acute and repeated ECS in rats. Evidence as to the source of opioid peptides involved in postictal responses as well as the effects of ECS on opiate receptors will also be reviewed. Finally, the role of opioids as endogenous anticonvulsants released by ECS-induced seizures will be presented.