Abstract:
Primary auditory cortex is involved in the final processing of sound. Processing of frequency resolution is possible due to the combined activity of excitatory and inhibitory neurons of the auditory cortex. The auditory cortical excitation-inhibition balance is therefore crucial for proper frequency discrimination and learning acquisition in childhood. Extreme premature birth survivors who are likely to have hypoxic injury show language delays and worse frequency discrimination, thereby suggesting possible changes in the cortical inhibitory circuit. Therefore, the present study investigated the development of inhibitory circuit of the primary auditory cortex and the impacts of neonatal hypoxia on this development. Male Sprague-Dawley rats were exposed to humidified 1.5% O2, 5% CO2, and 93.5% N2 at 37oC, every 2h for a total of 12.5h.day-1 from P1 to P3. Auditory brainstem response (ABR) were recorded at P14, P20, and P98, while tissue was sacrificed at P20 and P98 for histological analyses. GABAa receptor subunit α expression in each layer of the primary auditory cortex was visualised using immunohistochemistry. Our results revealed increased GABAa receptor subunit α expression within the primary auditory cortex of hypoxic rats compared to normoxic rats, especially at layers V and VI. Furthermore the GABAa receptor subunit α expression was not observed to change between P20 and P98. These indicate that the inhibitory circuit within the primary auditory cortex in rats is well developed by the hearing onset and does not undergo further significant perinatal alterations. Since ABR revealed good hearing threshold and no difference between hypoxic and normoxic rats, effect of hearing ability could not be implicated in the present study. The findings from the present study suggests altered auditory cortical inhibitory circuitry in those with perinatal hypoxia.
