Fernández de Sevilla David, Rodrigo-Angulo Margarita, Nuñez Angel, Buño Washington
Instituto Cajal, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain.
J Neurosci. 2006 Apr 12;26(15):4015-25. doi: 10.1523/JNEUROSCI.5489-05.2006.
Somatosensory information, conveyed through the gracilis nucleus (GN), is regulated by descending corticofugal (CF) glutamatergic fibers. In addition, the GN receives cholinergic inputs with still unclear source and functional significance. Using both the in vitro slice and intracellular recording with sharp and patch electrodes and in vivo extracellular single-unit recordings, we analyzed the effects of activation of cholinergic receptors on synaptic, intrinsic, and functional properties of rat GN neurons. The cholinergic agonist carbamilcholine-chloride [carbachol (CCh); 1-10 microM] in vitro (1) induced presynaptic inhibition of EPSPs evoked by both dorsal column and CF stimulation, (2) increased postsynaptic excitability, and (3) amplified the spike output of GN neurons. The inhibition by atropine (1 microM) and pirenzepine (10 microM) of all presynaptic and postsynaptic effects of CCh suggests actions through muscarinic M1 receptors. The above effects were insensitive to nicotinic antagonists. We searched the anatomical origin of the cholinergic projection to the GN throughout the hindbrain and forebrain, and we found that the cholinergic fibers originated mainly in the pontine reticular nucleus (PRN). Electrical stimulation of the PRN amplified sensory responses in the GN in vivo, an effect prevented by topical application of atropine. Our results demonstrate for the first time that cholinergic agonists induce both presynaptic and postsynaptic effects on GN neurons and suggest an important regulatory action of inputs from cholinergic neuronal groups in the pontine reticular formation in the functional control of somatosensory information flow in the GN.
通过薄束核（GN）传递的体感信息受下行皮质离心（CF）谷氨酸能纤维的调节。此外，GN还接受胆碱能输入，但其来源和功能意义尚不清楚。我们使用体外脑片、尖锐电极和膜片电极进行细胞内记录以及体内细胞外单单位记录，分析了胆碱能受体激活对大鼠GN神经元突触、内在和功能特性的影响。胆碱能激动剂氯化氨甲酰胆碱[卡巴胆碱（CCh）；1 - 10 μM]在体外（1）诱导对背柱和CF刺激诱发的兴奋性突触后电位（EPSP）的突触前抑制，（2）增加突触后兴奋性，以及（3）放大GN神经元的动作电位输出。阿托品（1 μM）和哌仑西平（10 μM）对CCh所有突触前和突触后效应的抑制表明其通过毒蕈碱M1受体起作用。上述效应对烟碱拮抗剂不敏感。我们在整个后脑和前脑寻找投射到GN的胆碱能纤维的解剖学起源，发现胆碱能纤维主要起源于脑桥网状核（PRN）。电刺激PRN可放大体内GN的感觉反应，局部应用阿托品可阻止这种效应。我们的结果首次证明胆碱能激动剂对GN神经元具有突触前和突触后效应，并表明脑桥网状结构中胆碱能神经元群的输入在GN体感信息流的功能控制中具有重要的调节作用。
