Delta-sleep-inducing peptide and its analogs and the serotoninergic system in the development of anticonvulsive influences

Abstract

Experiments on rats were carried out to study the effects of administration of delta-sleep-inducing peptide (DSIP) and its analogs (9-14) into the reticular part of the substantia nigra and ventral hippocampus on picrotoxin- and kainate-induced epileptic activity. Additionally, the uptake of [3H]tryptophan by brain structures was studied. Intranigral and intrahippocampal microinjections of peptide and its analogs were found to have anticonvulsant effects against both picrotoxin- and kainate-induced epileptic activity. Studies of the effects of DSIP and its structural analogs on the uptake of tryptophan by brain structures showed that peptides predominantly increased uptake of this amino acid. It is suggested that brain structures which modulate tryptophan uptake are largely responsible for the anticonvulsant actions of DSIP and its analogs. The results obtained here provide evidence that the serotoninergic system is not of key importance in mediating the anticonvulsant effects of DSIP and its analogs.

Synthesis of tritium labelled delta sleep‐inducing peptide

“…1 It exhibits a wide range of modulatory effects, it has an effect on circadian rhythms by interacting with serotonin and melatonin, 2,3 on temperature regulation [4][5][6] and on resistance against acute emotional stress. 7 It is also connected with inhibition of histamine and activation of GABA-ergic systems 8,9 and with inducing cerebral monoamine oxidase activity. [10][11][12] Finally, it has been postulated that DSIP modulates endogenous opioid-peptidergic systems and exogenous intracerebrally or systemically administered morphine.…”

Концептуальний Доказ Ефективності Сумісного Введення Вортіоксетину З Протиепілептичними Препаратами При Експериментальному Хронічному Судомному Синдромі: Позитивний Вплив Комплексної Патогенетичної Фармакокорекції На Вираженість Процесів Пам’яті Та Навчан

“…поведінки за умов різних моделей хронічного судомного синдрому [23][24][25][26][27]. Проте, патогенетичні механізми вказаних розладів поведінки залишаються неостаточно дослідженими в динаміці формування хронічного епілептогенезу [5][6][7][28][29][30][31], а питання стосовно патогенетично обумовленої корекції несудомних епілептиформних розладів поведінки не розглядається в аспекті комплексного лікування хронічного судомного синдрому [1, 14,32].…”