Department of Dental Anesthesiology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Neuroscience. 2010 Mar 31;166(3):1008-22. doi: 10.1016/j.neuroscience.2009.12.065. Epub 2010 Jan 6.
We previously reported that electrical stimulation of the reticular formation dorsal to the facial nucleus (RdVII) elicited excitatory masseter responses at short latencies and that RdVII neurons were antidromically activated by stimulation of the trigeminal motor nucleus (MoV), suggesting that excitatory premotor neurons targeting the MoV are likely located in the RdVII. We thus examined the properties of synaptic transmission from the RdVII to jaw-closing and jaw-opening motoneurons in horizontal brainstem preparations from developing rats using voltage-sensitive dye, patch-clamp recordings and laser photostimulation. Electrical stimulation of the RdVII evoked optical responses in the MoV. Combined bath application of the non-N-methyl-d-aspartate (non-NMDA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (APV) reduced these optical responses, and addition of the glycine receptor antagonist strychnine and the GABA(A) receptor antagonist bicuculline further reduced the remaining responses. Electrical stimulation of the RdVII evoked postsynaptic currents (PSCs) in all 19 masseter motoneurons tested in postnatal day (P)1-4 rats, and application of CNQX and the NMDA receptor antagonist (+/-)-3(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) reduced the PSC amplitudes by more than 50%. In the presence of CNQX and CPP, the GABA(A) receptor antagonist SR95531 further reduced PSC amplitude, and addition of strychnine abolished the remaining PSCs. Photostimulation of the RdVII with caged glutamate also evoked PSCs in masseter motoneurons of P3-4 rats. In P8-11 rats, electrical stimulation of the RdVII also evoked PSCs in all 14 masseter motoneurons tested, and the effects of the antagonists on the PSCs were similar to those in P1-4 rats. On the other hand, RdVII stimulation evoked PSCs in only three of 16 digastric motoneurons tested. These results suggest that both neonatal and juvenile jaw-closing motoneurons receive strong synaptic inputs from the RdVII through activation of glutamate, glycine and GABA(A) receptors, whereas inputs from the RdVII to jaw-opening motoneurons seem to be weak.
我们之前报道过,电刺激面神经核背侧的网状结构(RdVII)可在短潜伏期内引起咬肌兴奋反应,并且 RdVII 神经元可通过三叉运动核(MoV)的刺激产生逆行兴奋,这表明靶向 MoV 的兴奋性运动前神经元可能位于 RdVII 中。因此,我们使用电压敏感染料、膜片钳记录和激光光刺激,在发育中大鼠的水平脑干切片中检查了 RdVII 到闭合和张开下颌运动神经元的突触传递特性。RdVII 的电刺激诱发了 MoV 中的光反应。联合应用非 NMDA 受体拮抗剂 6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX)和 NMDA 受体拮抗剂 DL-2-氨基-5-磷酸戊酸(APV)可减少这些光反应,并且添加甘氨酸受体拮抗剂士的宁和 GABA(A)受体拮抗剂荷包牡丹碱进一步减少了剩余的反应。在出生后第 1-4 天的 19 个咬肌运动神经元中,电刺激 RdVII 可诱发突触后电流(PSC),并且应用 CNQX 和 NMDA 受体拮抗剂(+/-)-3(2-羧基哌嗪-4-基)丙基-1-膦酸(CPP)可使 PSC 幅度减少超过 50%。在 CNQX 和 CPP 的存在下,GABA(A)受体拮抗剂 SR95531 进一步降低了 PSC 幅度,并且添加士的宁可消除剩余的 PSCs。用笼状谷氨酸对 RdVII 进行光刺激也可诱发 P3-4 大鼠咬肌运动神经元的 PSCs。在 P8-11 天的大鼠中,电刺激 RdVII 也可诱发所有 14 个咬肌运动神经元的 PSCs,并且拮抗剂对 PSCs 的影响与 P1-4 天的大鼠相似。另一方面,RdVII 刺激仅在 16 个二腹肌运动神经元中的 3 个中诱发 PSCs。这些结果表明,新生和幼年的闭合下颌运动神经元通过激活谷氨酸、甘氨酸和 GABA(A)受体从 RdVII 接收强烈的突触输入,而 RdVII 到张开下颌运动神经元的输入似乎较弱。