Previous work has demonstrated that thyrotropin releasing hormone (TRH) and its β alanine analogue (β ala TRH) are potent antagonists of barbiturate induced sedation. This study sought to determine the effects of these oligopeptides on the anticonvulsant properties of phenobarbital in the maximal electroshock seizure (MES) test. Pro leu gly NH 2, another hypothalamic peptide, was also examined. None of the peptides studied had any anticonvulsant properties of their own, but TRH and β ala TRH, though not pro leu gly NH 2, potentiated the anticonvulsant potency of phenobarbital. Thyrotropin (TSH) and triiodothyronine (T 3) were ineffective, suggesting that the effects observed with TRH are not mediated via the pituitary thyroid axis. Since phenobarbital treatment of grand mal epilepsy is often limited by sedation and since TRH antagonizes sedation and enhances anticonvulsant effects of the barbiturate, the hormone or a congener may find value as an adjunct in therapy.
|Title of host publication||PSYCHOPHARM.COMMUN.|
|Number of pages||13|
|State||Published - Dec 1 1975|
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