引用

基底前脑(BF)接收来自脑干上升通路的传入信号，Moruzzi和Magoun(1949)首先提出了诱发前脑激活和皮层觉醒/清醒行为的理论;然而，对脑干抑制输入如何影响胆碱能功能知之甚少。在本研究中，甘氨酸作为脑干神经元的主要抑制性神经递质和局部胶质细胞的胶质递质，在雄性小鼠中测试了其与BF胆碱能(BFC)神经元的潜在相互作用。在BF中，甘氨酸受体亚单位免疫反应(IR)位点定位于胆碱乙酰转移酶(ChAT)-IR神经元。甘氨酸对BFC神经元的影响是通过抗双甘蓝碱、士的宁敏感的自发IPSCs (sIPSCs;在全细胞条件下记录0.81 0.25 10(-1)Hz。在胆碱能神经元的细胞外空间，通过与ChAT-IR细胞相对应的甘氨酸转运蛋白1型(GLYT1)-和GLYT2-IR过程表明了潜在的甘氨酸神经元和胶质来源。超微结构分析发现，在ChAT-IR神经元上存在glyt2阳性轴突末端的突触，以及glyt1阳性星形胶质突起，它们位于ChAT-IR神经元突触附近。脑干大缝被确定为甘氨酸能轴突的主要来源，从BF逆行追踪。我们的研究结果表明甘氨酸对BFC神经元有直接影响。 Furthermore, the presence of high levels of plasma membrane glycine transporters in the vicinity of cholinergic neurons suggests a tight control of extracellular glycine in the BF.SIGNIFICANCE STATEMENT Basal forebrain cholinergic (BFC) neurons receive various activating inputs from specific brainstem areas and channel this information to the cortex via multiple projections. So far, very little is known about inhibitory brainstem afferents to the BF. The current study established glycine as a major regulator of BFC neurons by (1) identifying glycinergic neurons in the brainstem projecting to the BF, (2) showing glycine receptor subunit-immunoreactive (IR) sites in choline acetyltransferase (ChAT)-IR neurons, (3) demonstrating glycine transporter type 2 (GLYT2)-positive axon terminals synapsing on ChAT-IR neurons, and (4) localizing GLYT1-positive astroglial processes in the vicinity of synapses of ChAT-IR neurons. The effect of glycine on BFC neurons was demonstrated by bicuculline-resistant, strychnine-sensitive spontaneous IPSCs recorded in whole-cell conditions.