The pharmacological properties of tonic currents mediated by GABAA-Rs in BLA neurons

突触释放的GABA作用于突触后GABAA受体，不仅产生阶段性抑制，而且通过持续激活突触外受体而产生紧张性抑制。本研究旨在使用已知GABA能传递下调的野生型和PRIP-1 KO小鼠来检查性别差异的BLA神经元中由GABAA-Rs介导的紧张电流的药理学性质。应用GABAA-R拮抗剂荷包牡丹碱可阻断紧张性GABA能电流，其电流明显大于KO组。地西泮和唑吡坦的沐浴应用导致WT的强直性电导增加。相比之下，PRIP-1 KO小鼠对这些化合物的敏感性较低。这些数据表明，紧张性GABA能抑制存在于WT小鼠的基底外侧杏仁核的主要神经元，但PRIP-1 KO小鼠有这种抑制系统的不完善。

Synaptically released GABA acting on postsynaptic GABAA receptor produce not only phasic inhibition, but also tonic inhibition by persistent activation of extrasynaptic receptors. This study aimed at examining pharmacological properties of tonic currents mediated by GABAA-Rs in BLA neurons of sex differences using the wild type and PRIP-1 KO mice which is known of downregulation of GABAergic transmission. The application of GABAA-R antagonist bicuculline blocked tonic GABAergic current which was significantly larger than those in KO. Bath application of diazepam and zolpidem causes increase tonic conductance in WT. In contrast, PRIP-1 KO mice showed lower sensitivity to these compounds. These data indicate that tonic GABAergic inhibition exist in principal neurons of the basolateral amygdala in WT mice but PRIP-1 KO mice have imperfection of this inhibitory system.