Shandra A A, Godlevskii L S, Mazarati A M, Oleshko A A, Mikhaleva I I
Department of Normal Physiology of the N. I. Pirogov Medical Institute, Odessa.
Neurosci Behav Physiol. 1993 Sep-Oct;23(5):480-5. doi: 10.1007/BF01183011.
Data are presented in this paper on the influence of the delta-sleep-inducing peptide (DSIP) on various forms of convulsive activity. The capacity of this peptide to suppress convulsive activity in foci created in the cerebral cortex by the application of strychnine has been demonstrated in experiments on cats. It has been established in experiments on rats that DSIP determines the later development of the convulsive kindling syndrome, and prevents the development of convulsions in mice induced by bicuculline, picrotoxin, and corazol, but is devoid of such action in relation to thiosemicarbazide and strychnine. It was demonstrated that the anticonvulsant action of DSIP is associated with its influence on the reticular portion of the substantia nigra. The lowest level of this peptide itself has been discovered, in the reticular portion of the substantia nigra at the late stages of pharmacological kindling. It is inferred that DSIP may represent one of the factors of the endogenous control of the excitability of the brain.
本文给出了有关δ-睡眠诱导肽(DSIP)对各种惊厥活动形式影响的数据。在猫身上进行的实验已证明,该肽抑制因应用士的宁在大脑皮层产生的病灶中惊厥活动的能力。在大鼠实验中已确定,DSIP决定惊厥点燃综合征的后期发展,并预防由荷包牡丹碱、印防己毒素和戊四氮诱导的小鼠惊厥的发展,但对氨基硫脲和士的宁没有这种作用。已证明DSIP的抗惊厥作用与其对黑质网状部的影响有关。在药理学点燃后期,在黑质网状部发现了该肽本身的最低水平。据推测,DSIP可能是大脑兴奋性内源性控制的因素之一。