Activation of mitogen-activated protein kinases in gerbil hippocampus with ischemic tolerance induced by 3-nitropropionic acid
T Sugino, K Nozaki, N Hashimoto - Neuroscience letters, 2000 - Elsevier
T Sugino, K Nozaki, N Hashimoto
Neuroscience letters, 2000•ElsevierThe present study investigated the activation of c-Jun NH2-terminal kinases (JNK), p38
mitogen-activated protein kinases (p38) and extracellular signal-regulated kinases (ERK) in
the gerbil hippocampus by immunohistochemistry to clarify the role of these kinases in
ischemic tolerance induced by 3-NP. Intraperitoneal administration of 3-NP (3 or 10 mg/kg)
caused the activation of JNK in CA1 subfield, which induced tolerance to subsequent
ischemia and prevented delayed neuronal death (DND). As concerns p38 and ERK, no …
mitogen-activated protein kinases (p38) and extracellular signal-regulated kinases (ERK) in
the gerbil hippocampus by immunohistochemistry to clarify the role of these kinases in
ischemic tolerance induced by 3-NP. Intraperitoneal administration of 3-NP (3 or 10 mg/kg)
caused the activation of JNK in CA1 subfield, which induced tolerance to subsequent
ischemia and prevented delayed neuronal death (DND). As concerns p38 and ERK, no …
The present study investigated the activation of c-Jun NH2-terminal kinases (JNK), p38 mitogen-activated protein kinases (p38) and extracellular signal-regulated kinases (ERK) in the gerbil hippocampus by immunohistochemistry to clarify the role of these kinases in ischemic tolerance induced by 3-NP. Intraperitoneal administration of 3-NP (3 or 10 mg/kg) caused the activation of JNK in CA1 subfield, which induced tolerance to subsequent ischemia and prevented delayed neuronal death (DND). As concerns p38 and ERK, no activation was induced by intoxication of 3-NP. Our results show the activation of JNK following chemical preconditioning with low dose of 3-NP is closely related to the acquisition of resistance to DND.
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