The activity of glutamate decarboxylase, GABA-, aspartate-and alanine aminotransferases, the content of GABA, glutamate, aspartate and alanine were studied in the brain hemispheres and stem of rats that were undergoing the hypoglycemic coma as well as those rats had undergone 7-9 comas on the second day after the last coma. In hypoglycemia, the brain's content of glutamate, alanine and GABA decreased and content of aspartate increased; the activity of enzymes investigated did not change. On the second day after 7-9th hypoglycemic coma, the decrease of activity of glutamate decarboxylase in hemispheres and the decrease of GABA amount in brain stem were detected. This can be an evidence of decrease of GABA amount produced and secreted by nerve ends of the pathways leading from striata to substantia nigra. The detected changes result from multiple influence of hypoglycemia to the brain and may by important in the development of posthypoglycemic encephalopathy.
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Keywords: Brain metabolism, hypoglycemia, GABA
Citation:
Telushkin P.K., Shidlovskaya T.E. (1996) Enzymatic activity and content of GABA-shunt substrates in rat brain during repeated exposure to hypoglycemic doses of insulin. Voprosy Meditsinskoi Khimii, 42(4), 306-308.
Telushkin P.K. et al. Enzymatic activity and content of GABA-shunt substrates in rat brain during repeated exposure to hypoglycemic doses of insulin // Voprosy Meditsinskoi Khimii. - 1996. - V. 42. -N 4. - P. 306-308.
Telushkin P.K. et al., "Enzymatic activity and content of GABA-shunt substrates in rat brain during repeated exposure to hypoglycemic doses of insulin." Voprosy Meditsinskoi Khimii 42.4 (1996): 306-308.
Telushkin, P. K., Shidlovskaya, T. E. (1996). Enzymatic activity and content of GABA-shunt substrates in rat brain during repeated exposure to hypoglycemic doses of insulin. Voprosy Meditsinskoi Khimii, 42(4), 306-308.
References
Генес СИ. Гипогликемия. Гииогликемическийсимптомокомплекс. — М, 1970. Scholar google search
Лукьянчиков B.C., Балаболкин ММ. Гипогликемический синдром: (Этиология, патогенез, диагностика, лечение). — М., 1987. — Вып. 1. Scholar google search
Auer RN., Siesjo B.K.//BaiUires. Clin. Endocrmol Metab. - 1993. — V. 7. — N. 3. — P. 611-625. Scholar google search
Marks V., Teale J.D. // Baillircs. Clin. Eiidocrinol. Metab. - 1993. -V. 7. - N. 3. - P. 705-729. Scholar google search
Siesjo B.K // Diabetes/Metab. Rev. - 1988. - V. 4. - P. 113-141. Scholar google search
Хухо Ф. Нейрохимия. Основы и принципы. — М , 1990 — С. 229-231. Scholar google search
Промыслов М.Ш., Соловьева ТВ., Аниськина Р.И. // Вопр. мед. химии. —1968. — N 6. — С. 619-622. Scholar google search
Методы биохимических исследований: Липидный и энергетический обмен / Под ред. М.И.Прохоровой. — Л., 1982. - С . 246-250. Scholar google search
Пасхина Т.С. // Современные методы в биохимии / Под ред. В.Н.Ореховича. — М., 1964. — С. 162-180. Scholar google search
Бархатова В.П. Нейротрансмиттеры и экстрапирамидная патология. — М., 1988. Scholar google search
Филиппов С.П. // Вопр. мед. химии. — 1980. — N 4. — С. 455-457. Scholar google search
Wysmyk-Cybula U., Albrecht J. // Neuropatolol. pol. - 1981. - V. 19. - N. 3. - P. 369-376. Scholar google search
Johansen F.F., Christensen Т., Jensen M.S., Valente E. // Exp. Brain. Res. - 1991. - V. 86. — N. 1. — P. 529-537. Scholar google search
Ylinen A.M.A., Miettinen R, Pitkanen A., Gulyas A.J. // Proc. Nat. Acad. Sci. USA. - 1991. - V 88. - N. 17. - P. 7650- 7653. Scholar google search
Телушкин ПК., Потапов Н.П // Пробл. эндокринол. — 1994 — N 5. —С. 53-54. Scholar google search
Moche S.L, Sperber E.R, Velisek L. // Physiol. Res. - 1993. - V. 42 - N. 3. - P 145-154. Scholar google search