p38MAPK has been implicated in the regulation of proinflammatory cytokines and apoptosis in vitro. To understand its role in neurodegeneration, we determined the time course and localization of the dually phosphorylated active form of p38MAPK in hippocampus after global forebrain ischemia. Phosphorylated p38MAPK and mitogen-activated protein kinase-activated protein 2 activity increased over 4 days after ischemia.
View Article and Find Full Text PDFAlthough the interleukin-1beta converting enzyme (ICE)/CED-3 family of proteases has been implicated recently in neuronal cell death in vitro and in ovo, the role of specific genes belonging to this family in cell death in the nervous system remains unknown. To address this question, we examined the in vivo expression of one of these genes, Ice, after global forebrain ischemia in gerbils. Using RT-PCR and Western immunoblot techniques, we detected an increase in the mRNA and protein expression of ICE in hippocampus during a period of 4 d after ischemia.
View Article and Find Full Text PDFWe have investigated the possibility of using BATO complexes derivatized with the muscarinic acetylcholine receptor (mAChR) antagonist, quinuclidinyl benzilate (QNB), for mAChR imaging. The BATO complexes, TcCl(DMG)3B-QNB, were prepared using QNB derivatives containing a 4'-boronic acid substituent on one of the benzilic benzene rings (QNB-boronic acid). The QNB-boronic acid molecule has two chiral centers, and all four QNB-BATO stereoisomers were made and evaluated.
View Article and Find Full Text PDFTechnetium-99m-DMG-2MP (Chloro[bis[2,3-butanedionedioxime(1-)-0][2,3- butanedionedioximato (2-)-N,N',N'',N''',N'''',N'''''] (2-methylpropyl borato (2-))technetium]), also known as SQ 32097 is a member of a family of neutral lipophilic compounds generally known as boronic acid adducts of technetium dioxime complexes (BATOs). After i.v.
View Article and Find Full Text PDFIn order to determine the effect of inflammation on brain glycolysis in the absence of leukocyte infiltration, [14C]deoxyglucose autoradiography and hematoxylin-eosin (HE) counter-staining were applied to mice at various times after the induction of chemotoxic inflammatory brain lesions by the systemic administration of goldthioglucose. Glycolysis was intensely stimulated in affected circumventricular organs, without cellular infiltration. This result is consistent with the activation of anaerobic glycolysis by inflammatory sequelae that culminate in ischemic hypoxia in the lesion sites.
View Article and Find Full Text PDF