Expression of neuronal plasticity markers in hypoglycemia induced brain injury.
The expression of neuroplasticity markers was analyzed in four brain regions, namely cerebral hemispheres (CH), cerebellum (CB), brain stem (BS) and diencephalon (DC) from insulin-induced hypoglycemic young adult rats. Significant decrease in neural cell adhesion molecule (NCAM) isoforms and growth-associated protein-43 (GAP-43) was observed following hypoglycemic injury from majority of brain regions studied. The glial fibrillary acidic protein (GFAP) level increased significantly in cerebral hemispheres and diencephalon regions, whereas, synaptophysin level increased in cerebellum, brain stem and diencephalon regions. The selective downregulation of the neuronal plasticity marker proteins (GAP-43 and NCAM), and enhanced expression of GFAP and synaptophysin suggests that in acute hypoglycemia, mechanisms other than energy failure may also contribute to neuronal cell damage in the brain.
Singh
Pawan
P
Neurochemistry and Neuroendocrinology Laboratory, Department of Biotechnology, Guru Nanak Dev University, Amritsar, India.
Heera
Pawan Kumar
PK
Kaur
Gurcharan
G
D000818:Animals; D015415:Biomarkers / Q000032:analysis*; D001921:Brain / Q000378:metabolism* / Q000473:pathology*; D019922:GAP-43 Protein / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007003:Hypoglycemia / Q000378:metabolism / Q000473:pathology*; D008297:Male; D019006:Neural Cell Adhesion Molecules / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D016708:Synaptophysin / Q000378:metabolism
D015415:Biomarkers; D019922:GAP-43 Protein; D005904:Glial Fibrillary Acidic Protein; D019006:Neural Cell Adhesion Molecules; D016708:Synaptophysin