Early postnatal development of reciprocal Ia inhibition in the murine spinal cord.
Early postnatal development of reciprocal Ia inhibition in the murine spinal cord.
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小鼠脊髓中 Ia 相互抑制的产后早期发育。
DOI：
10.1152/jn.90354.2008
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发表时间：
2008
影响因子：
2.5
通讯作者：
Frank,Eric
中科院分区：
文献类型：
--
作者：
Wang,Zhi;Li,LingYing;Goulding,Martyn;Frank,Eric
在成年猫中，从肌梭传入（Ia轴突）到运动神经元（MN）供应拮抗肌的相互抑制的介导通路已经得到了很好的研究，但对这种双突触通路的发展知之甚少。作为研究其发展的基础，我们在出生后第一周的小鼠中表征了这一通路，重点关注四头肌（Q）Ia轴突通过Ia抑制性中间神经元向后二头肌半腱（PBSt）MN的投射。Q神经刺激诱发的PBSt MNs的突触电位是双突触介导的，并被士的宁阻断，这意味着甘氨酸是成年猫的主要抑制性递质。在这个反射通路中的神经元连接的特异性在出生时就已经很高了; Q传入引起PBSt MN中的抑制性突触电位，但供应内收肌的传入则没有。类似于猫中的这种双突触通路，Renshaw细胞抑制插入的Ia中间神经元，因为它们减少来自Q轴突的双突触输入，但不直接抑制PBSt MN。交互抑制功能抑制单突触兴奋性反射在PBSt MN的P3，但这种功能抑制是弱的P1。最后，V1衍生的Renshaw细胞发育所需的转录因子Pax 6的缺失不会阻断该途径的发育。这表明Pax 6不是所有V1衍生的脊髓中间神经元的表型发育所必需的，或者这些抑制性中间神经元不是来自V1前体。
The pathway mediating reciprocal inhibition from muscle spindle afferents (Ia axons) to motoneurons (MNs) supplying antagonist muscles has been well studied in adult cats, but little is known about how this disynaptic pathway develops. As a basis for studying its development, we characterized this pathway in mice during the first postnatal week, focusing on the projection of quadriceps (Q) Ia axons to posterior biceps-semitendinosis (PBSt) MNs via Ia inhibitory interneurons. Synaptic potentials in PBSt MNs evoked by Q nerve stimulation are mediated disynaptically and are blocked by strychnine, implying that glycine is the major inhibitory transmitter as in adult cats. The specificity of neuronal connections in this reflex pathway is already high at birth; Q afferents evoke inhibitory synaptic potentials in PBSt MNs, but afferents supplying the adductor muscle do not. Similar to this disynaptic pathway in cats, Renshaw cells inhibit the interposed Ia interneurons, as they reduce the disynaptic input from Q axons but do not inhibit PBSt MNs directly. Reciprocal inhibition functionally inhibits the monosynaptic excitatory reflex in PBSt MNs by P3, but this functional inhibition is weak at P1. Finally, deletion of the transcription factor Pax6, which is required for the development of V1-derived Renshaw cells, does not block development of this pathway. This suggests either that Pax6 is not required for the phenotypic development of all V1-derived spinal interneurons or that these inhibitory interneurons are not derived from V1 precursors.