Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P80404 (GABA transaminase)
 786 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postero-medial barrel-subfield (PMBSF) of the SI cortex of normal adult mice contains clusters of cells called "barrels". Each barrel histochemically shows increased activity of succinate, lactate, and glucose-6-phosphate dehydrogenase and also GABA-T activity. Some neuronal perikarya in the barrel walls show GABA-T activity. Mitochondrial alpha-GPDH and AChE show equal activities in the hollows and in the walls of the barrels. On this cortical vibrissa field, the contralateral and ipsilateral vibrissae project somatotopically in a way which coincides with the barrels. The mystacial vibrissae and the common fur of the muzzle project to different loci. The cortical surface area for the normal fur is 0.025 mm2, whereas the cortical vibrissal area is 1.0 mm2. In mice with lesioned whisker pads the succinate-dehydrogenase activity of the IVth layer in the vibrissal area becomes a continuous sheet similar to the adjacent IVth layer, the thickness of the cortex is relatively preserved, and the total enzyme activities, biochemically assayed, are unchanged. These features can be explained by a functional substitution. In mice with whisker pads lesioned since birth, the vibrissal area can still be identified by the projections from ipsilateral vibrissae (undamaged side). This vibrissal area, and this alone, is found to be invaded by projections from the contralateral common fur of the muzzle. Experimental data suggest that the compensatory process may result from an invasion of the vibrissal area by a new set of ascending fibers, and not merely from axonal sprouting either at the periphery or at the cortical level.
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PMID:Cortical organization of the postero-medial barrel-subfield in mice and its reorganization after destruction of vibrissal follicles after birth. 676 63

We have developed defective herpes simplex virus 1 (HSV-1) vectors, based on amplicon plasmids with a replication-deficient mutant, as helper for the transfer of the glutamic acid decarboxylase (GAD67) or beta-galactosidase (beta-gal) gene as control directed by HCMV promoter into neuronal-like cells (PC12) and primary neurons. GAD67 protein was detected immunochemically, while GAD67 activity in virus-producing and nonproducing cell lines was detected enzymatically or by GABA release. Infection with GAD67-expressing amplicon vectors enhanced the resistance of PC12 cells to H(2)O(2). This protection was related to increased energy metabolism, as shown by MTT reduction and ATP level, and involved the GABA shunt, as shown by the reduction in ATP level seen in the presence of gamma-vinyl GABA (GVG), a specific GABA transaminase inhibitor. Level of glutathione (GSH), which requires ATP for its synthesis, was increased by the GAD67 transgene. The activity of glucose-6-phosphate dehydrogenase involved in the maintenance of the NADPH that can be used for the regeneration of the GSH pool, was increased by infection with amplicon vectors. Thus, replication-deficient HSV-1 and the GAD67 transgene have complementary neuroprotective effects and infection with GAD67-expressing amplicon vectors was able to protect nondifferentiated cortical neurons from glutamate toxicity mediated by oxidative stress. Such defective GAD67-expressing HSV-1, as neurotropic vector, should be helpful in neurodegenerative diseases implicating alterations of energy metabolism and oxidative stress in neuronal cells expressing GABA transaminase.
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PMID:Enhancement of neuronal protection from oxidative stress by glutamic acid decarboxylase delivery with a defective herpes simplex virus vector. 1463 8