Sun W, Salvi R J
Hearing Research Lab, SUNY University at Buffalo, NY 14214, USA.
Neuroreport. 2001 Mar 26;12(4):803-7. doi: 10.1097/00001756-200103260-00037.
Lateral olivocochlear (LOC) efferent neurons, putatively dopaminergic, synapse on afferent dendrites of type I spiral ganglion neurons (SGNs) in the cochlea and depress their activity. To investigate the underlying mechanisms, whole-cell patch clamp recordings were obtained from mouse SGNs. Dopamine (DA), and D1-like (D1, D5) and D2-like (D2, D3 and D4) receptor agonists, reduced AP amplitude and induced a slow transient depolarization. Under voltage clamp, D1-like and D2-like agonists induced a dose-dependent inward current that was reversibly blocked by their receptor antagonists. The inward current was blocked by tetrodotoxin (TTX), implicating Na+ channels. The reduction of AP amplitude and voltage-gated Na+ current by DA and DA agonists provides a mechanism for suppressing spike activity in type I afferent neurons.
外侧橄榄耳蜗(LOC)传出神经元可能是多巴胺能神经元,它们与耳蜗中I型螺旋神经节神经元(SGNs)的传入树突形成突触,并抑制其活动。为了研究其潜在机制,我们从小鼠SGNs中获得了全细胞膜片钳记录。多巴胺(DA)以及D1样(D1、D5)和D2样(D2、D3和D4)受体激动剂降低了动作电位(AP)幅度,并诱导了缓慢的瞬时去极化。在电压钳制下,D1样和D2样激动剂诱导了剂量依赖性内向电流,该电流被其受体拮抗剂可逆性阻断。内向电流被河豚毒素(TTX)阻断,提示涉及钠离子通道。DA和DA激动剂对AP幅度和电压门控钠离子电流的降低为抑制I型传入神经元的放电活动提供了一种机制。