周边γ-氨基丁酸通过GABA_B受体调控骶髓后联合核神经元谷氨酸能突触

目的研究突触周边γ-氨基丁酸(ambient GABA)通过GABAB受体调控骶髓后联合核(SDCN)神经元谷氨酸能突触的机制。方法在急性切取的骶段脊髓薄片上,利用全细胞膜片钳法记录骶髓后联合核神经元谷氨酸能兴奋性突触后电流(EPSCs),将GABAB受体用其特异性受体拮抗剂CGP52432阻断,观察谷氨酸突触终末上的GABAB受体被周边GABA作用的影响。结果在突触后GABAB受体被从胞内阻断的条件下,再灌流CGP52432阻断谷氨酸能突触前GABAB受体,可增加刺激引发的EPSCs(eEPSCs)幅度;改变配对刺激的两个EPSC比率(paired-pulse ratio,PPR),并激发沉默突触(silent synapse)。但CGP52432对微小兴奋性突触后电流(mEPSCs)无影响。结论位于SDCN神经元谷氨酸能突触前的GABAB受体受周边GABA调控。这种影响参与调节谷氨酸释放并可能参与痛觉信息在脊髓水平的传递。

Ambient GABA modulates glutamatergic synapse in sacral dorsal commissural nucleus by presynaptic GABAB receptors

Aim To investigate the role of ambient γ-aminobutyric acid(GABA) on glutamatergic synapse via GABAB receptors in sacral dorsal commissural nucleus(SDCN).Method Using whole-cell voltage-clamp recordings on acute spinal cord slice,effect of blockade of GABAB receptors on glutamatergic synaptic transmission was studied.Results Blockade of GABAB receptors by a selective antagonist CGP52432 increased evoked excitatory postsynaptic currents(eEPSCs),decreased paired-pulse ration(PPR),switched "presynaptically" silent synapse to active one,indicating a presynaptic GABAB receptor-mediated modulation by ambient GABA.Conclusions Ambient GABA modulates glutamate release by GABAB receptors on presynaptic glutamatergic terminals to SDCN neurons;this action may contribute to nociception transmission at spinal cord level.