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РЖ ВИНИТИ 34 (BI24) 96.06-04М3.114

Ex vivo demonstration of nitric oxide in the rat brain: Effects of intrastriatal endothelin-1 injection [Text] / Andrey V. Kozlov [et al.] // Neurosci. Lett. - 1995. - Vol. 196, N 1-2. - P140-144 . - ISSN 0304-3940
Перевод заглавия: Обнаружение ex vivo оксида азота в головном мозге крыс: эффекты внутристриатного введения эндотелина-1
Аннотация: The aim of the present study was to demonstrate the ex vivo detection of NO{.} in basal conditions and after ET-1 intrastriatal injection by means of electron paramagnetic resonance (EPR) spectroscopy using locally injected hemoglobin (Hb) as a NO{.} trapping agent. The extent of neostriatal damage after Hb and ET-1 injections was assessed by means of immunocytochemistry with a monoclonal antibody against dopamine and cAMP-phosphoprotein M[r]32 (DARPP-32), which is considered a marker of striatal intrinsic neurons. In the absence of local Hb injection, no signal related to endogenous NO{.} was detected in neostriatum, suggesting that endogenous NO{.} trapping agents are not sufficiently concentrated to allow NO{.} detection with the present technique. Instead, 1 h after Hb injection, a clear nitrosyl-Hb signal can be detected in neostriatal homogenates. ET-1, a powerful vasoconstrictor agent, was used to cause neuronal loss in the neostriatum. No change in nitrosyl-Hb signal was observed in neostriata 1 h after ET-1 injection, whereas an almost 3-fold increase in the signal intensity was present 24 h after ET-1 injection. The analysis of neostriatal damage showed that Hb injection did not cause either significant damage of striatal tissue or potentiation of ET-1-induced lesions. In conclusion, the present technique allows ex vivo detection of NO{.} in the brain. The delayed increase in NO{.} observed after ET-1 injection indicates that this molecule may participate in the development of slowly progressive neuronal damage occuring at late post-ischemic times. Библ. 32

ГРНТИ	34.39.15

ВИНИТИ 341.39.15.37.17.19.15
Рубрики: ФИЗИОЛОГИЧЕСКИЕ АКТИВНЫЕ ВЕЩЕСТВА
ОКСИД АЗОТА
ЭНДОТЕЛИН-1
ДОФАМИН
ГЛУТАМАТ
ЦАМФ-РЕГУЛИРУЕМЫЙ ФОСФОПРОТЕИН M[T]32
ИШЕМИЯ МОЗГА
СТРИАТУМ
КРЫСЫ

Доп.точки доступа:
Kozlov, Andrey V.; Biagini, Giuseppe; Tomasi, Aldo; Zini, Isabella

РЖ ВИНИТИ 34 (BI48) 96.06-04Т2.273

Ex vivo demonstration of nitric oxide in the rat brain: Effects of intrastriatal endothelin-1 injection [Text] / Andrey V. Kozlov [et al.] // Neurosci. Lett. - 1995. - Vol. 196, N 1-2. - P140-144 . - ISSN 0304-3940
Перевод заглавия: Обнаружение ex vivo оксида азота в головном мозге крыс: эффекты внутристриатного введения эндотелина-1
Аннотация: The aim of the present study was to demonstrate the ex vivo detection of NO{.} in basal conditions and after ET-1 intrastriatal injection by means of electron paramagnetic resonance (EPR) spectroscopy using locally injected hemoglobin (Hb) as a NO{.} trapping agent. The extent of neostriatal damage after Hb and ET-1 injections was assessed by means of immunocytochemistry with a monoclonal antibody against dopamine and cAMP-phosphoprotein M[r]32 (DARPP-32), which is considered a marker of striatal intrinsic neurons. In the absence of local Hb injection, no signal related to endogenous NO{.} was detected in neostriatum, suggesting that endogenous NO{.} trapping agents are not sufficiently concentrated to allow NO{.} detection with the present technique. Instead, 1 h after Hb injection, a clear nitrosyl-Hb signal can be detected in neostriatal homogenates. ET-1, a powerful vasoconstrictor agent, was used to cause neuronal loss in the neostriatum. No change in nitrosyl-Hb signal was observed in neostriata 1 h after ET-1 injection, whereas an almost 3-fold increase in the signal intensity was present 24 h after ET-1 injection. The analysis of neostriatal damage showed that Hb injection did not cause either significant damage of striatal tissue or potentiation of ET-1-induced lesions. In conclusion, the present technique allows ex vivo detection of NO{.} in the brain. The delayed increase in NO{.} observed after ET-1 injection indicates that this molecule may participate in the development of slowly progressive neuronal damage occuring at late post-ischemic times. Библ. 32

ГРНТИ	34.45.21

ВИНИТИ 341.45.21.83.17.35
Рубрики: ФИЗИОЛОГИЧЕСКИЕ АКТИВНЫЕ ВЕЩЕСТВА
ОКСИД АЗОТА
ЭНДОТЕЛИН-1
ДОФАМИН
ГЛУТАМАТ
ЦАМФ-РЕГУЛИРУЕМЫЙ ФОСФОПРОТЕИН M[T]32
ИШЕМИЯ МОЗГА
СТРИАТУМ
КРЫСЫ

Доп.точки доступа:
Kozlov, Andrey V.; Biagini, Giuseppe; Tomasi, Aldo; Zini, Isabella

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