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Abstract:
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Hypoxia in neonates can lead to biochemical
and molecular alterations mediated through changes in
neurotransmitters resulting in permanent damage to brain.
In this study, we evaluated the changes in the receptor
status of GABAA in the cerebral cortex and brainstem of
hypoxic neonatal rats and hypoxic rats supplemented with
glucose and oxygen using binding assays and gene
expression of GABAAa1 and GABAAc5. In the cerebral
cortex and brainstem of hypoxic neonatal rats, a significant
decrease in GABAA receptors was observed, which
accounts for the respiratory inhibition. Hypoxic rats sup-
plemented with glucose alone and with glucose and oxygen
showed, respectively, a reversal of the GABAA receptors,
andGABAAa1 and GABAAc5 gene expression to control.
Glucose acts as an immediate energy source thereby
reducing the ATP-depletion-induced increase in GABA
and oxygenation, which helps in encountering anoxia.
Resuscitation with oxygen alone was less effective in
reversing the receptor alterations. Thus, the results of this
study suggest that reduction in the GABAA receptors
functional regulation during hypoxia plays an important
role in mediating the brain damage. Glucose alone and
glucose and oxygen supplementation to hypoxic neonatal
rats helps in protecting the brain from severe hypoxic
damage. |