Negative regulation of gamma-aminobutyric acid type A receptor on free calcium ion levels following facial nerve injury

Previous studies have demonstrated that muscarinic, and nicotinic receptors increase free Ca2＋ levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca2＋ overload can trigger either necrotic or apoptotic cell death. Gamma-aminobutyric acid （GABA）, an important inhibitory neurotransmitter in the central nervous system, exists in the facial nerve nucleus. It is assumed that GABA negatively regulates free Ca2＋ levels in the facial nerve nucleus. The present study investigated GABA type A （GABAA） receptor expression in the facial nerve nucleus in a rat model of facial nerve injury using immunohistochemistry and laser confocal microscopy, as well as the regulatory effects of GABAA receptor on nicotinic receptor response following facial nerve injury. Subunits α1, α3, α5, β1, β2, δ, and γ3 of GABAA receptors were expressed in the facial nerve nucleus following facial nerve injury. In addition, GABAA receptor expression significantly inhibited the increase in nicotinic receptor-mediated free Ca2＋ levels in the facial nerve nucleus following facial nerve injury in a concentration-dependent fashion. These results suggest that GABAA receptors exhibit negative effects on nicotinic receptor responses following facial nerve injury.