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Hypoglycemia induced brain injury poses a major setback to optimal blood glucose regulation during diabetes. It causes irreversible injury in several brain regions culminating in improper function. Neuregulin 1 and ErbB receptors are involved in regeneration in adulthood as well as in glucose homeostasis. We intended to understand the influence of extreme discrepancies in glycemic levels on Neuregulin 1, ErbB receptor subtypes and Ki67 expression in relation to motor deficits as a consequence of cellular dysfunction/degeneration in the cerebellum and brainstem during diabetes. Elevated oxidative stress and compromised antioxidant system havocs cerebellum and brainstem related function. Cellular alteration of Purkinje neurons in the cerebellum and presence of axonal spheroids in the brainstem are suggestive of impairment to neural circuits involved in motor function. Down regulation of Neuregulin 1, ErbB 2, ErbB 3, ErbB 4 and Ki67 expression observed during diabetes and hypoglycemia may critically cause regenerative deficiency in cerebellum. The coincident up regulation of Neuregulin 1, ErbB 2, ErbB 3 and ErbB 4 in brainstem during diabetes is an attempt to maintain regenerative homeostasis to ensure its function. However, hypoglycemic insults results in down regulation of Neuregulin 1, ErbB 4 expression that severely compromises their role in brainstem. Grid walking test confirmed motor impairment during diabetes that showed further deterioration due to hypoglycemic stress. Thus altered expression of Neuregulin 1, ErbB receptor subtypes and Ki67 during diabetes and hypoglycemia contributes to reduced cellular proliferation and deficits in motor function.
This article was published in the following journal.
Name: Behavioural brain research
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A peptide factor originally identified by its ability to stimulate the phosphorylation the erbB-2 receptor (RECEPTOR, ERBB-2). It is a ligand for the erbB-3 receptor (RECEPTOR, ERBB-3) and the erbB-4 receptor. Variant forms of NEUREGULIN-1 occur through alternative splicing of its mRNA.
Retrovirus-associated DNA sequences (erbB) originally isolated from, or related to, the avian erythroblastosis virus (AEV). These genes code for the epidermal growth factor receptor (EGFR) family of receptors which is important in the control of normal cell proliferation and in the pathogenesis of human cancer. The genes include erbB-1 (GENES, ERBB-1), erbB-2 (GENES, ERBB-2), and erbB-3, all of which show abnormalities of expression in various human neoplasms.
A cell surface protein-tyrosine kinase receptor that is found to be overexpressed in a significant number of adenocarcinomas. It has extensive homology to and can heterodimerize with the EGF receptor (RECEPTOR, EPIDERMAL GROWTH FACTOR), the erbB-3 receptor (RECEPTOR, ERBB-3) and the erbB-4 receptor. Activation of the erbB-2 receptor occurs during heterodimer formation with a ligand-bound erbB receptor family members.
The erbB-2 gene is a proto-oncogene that codes for the erbB-2 receptor (RECEPTOR, ERBB-2), a protein with structural features similar to the epidermal growth factor receptor. Its name originates from the viral oncogene homolog (v-erbB) which is a truncated form of the chicken erbB gene found in the avian erythroblastosis virus. Overexpression and amplification of the gene is associated with a significant number of adenocarcinomas. The human c-erbB-2 gene is located at 17q21.2.
The proto-oncogene c-erbB-1 codes for the epidermal growth factor receptor. Its name originates from the viral homolog v-erbB which was isolated from an avian erythroblastosis virus (AEV) where it was contained as a fragment of the chicken c-ErbB-1 gene lacking the amino-terminal ligand-binding domain. Overexpression of erbB-1 genes occurs in a wide range of tumors, commonly squamous carcinomas of various sites and less commonly adenocarcinomas. The human c-erbB-1 gene is located in the chromosomal region 7p14 and 7p12.
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