Synaptic inputs of feline rubrospinal neurons from the parietal association cortex, pretectum and medial lemniscus, and their lesion-induced sprouting.
Synaptic inputs of feline rubrospinal neurons from the parietal association cortex, pretectum and medial lemniscus, and their lesion-induced sprouting.
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来自顶叶联合皮层、前顶盖和内侧丘系的猫红核脊髓神经元的突触输入及其损伤诱导的出芽。
DOI：
10.2170/jjphysiol.33.197
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
N. Tsukahara
中科院分区：
文献类型：
--
作者：
Y. Fujito;J. Maeda;F. Murakami;N. Tsukahara
对猫大脑皮质、顶盖前区(PRT)和内侧丘脑(ML)红核(RN)神经元的突触传入进行了电生理学研究。刺激同侧顶叶联合皮质(PASC)和次级感觉区(SII)产生缓慢上升的约3毫秒上升时间的单突触EPSP，在某些情况下，随后出现超极化，类似于先前观察到的感觉运动皮质(SM)诱发的PSP。刺激对侧大脑皮层永远不会产生可检测到的PSP。发现PASC-Rub投射的地形排列。刺激PASC外侧部分主要在支配颈胸段脊髓节段的RN细胞产生EPSPS，而刺激PASC内侧部分主要在支配腰骶髓的RN细胞产生EPSPS。此外，PASC诱发的EPSP在RN的吻侧比在尾侧更频繁。刺激同侧PRT和ML可诱发单突触和多突触IPSP。PRT和ML诱导的EPSPS的峰值时间为1.0+/-0.4毫秒(平均+/-S.D.)和1.6+/-0.5毫秒，分别位于大脑脚(CP)和小脑核(IP)诱发的EPSPS的中间。此外，PRT诱导的EPSPS对膜超极化的敏感性介于CP-EPSPS和IP-EPSPS之间，而ML诱导的EPSPS幅度低于IP-EPSPS。因此，PRT和ML纤维的突触很可能是在远端树突和胞体之间形成的，这些树突是CP-红斑型突触的终止点，胞体是IP红斑型突触的终止点。在慢性IP和SM损毁后，PASC诱导的EPSP有一个新的快速上升成分，在IP和SM损毁的猫中，ML刺激诱导RN细胞单位峰的有效性明显增加。提示IP和SM破坏后，PASC纤维在RN细胞胞体-树突膜近端萌发并形成新的突触。在IP和ML损伤后，锥体束RN细胞的侧支纤维也可以长出新的突触。
Synaptic inputs of rubrospinal (RN) neurons from the cerebral cortex, pretectal area (PRT), and medial lemniscus (ML) were investigated electrophysiologically in the cat. Stimulation of the ipsilateral parietal association cortex (PASC) and secondary sensory area (SII) produced slow-rising about 3 msec rise time monosynaptic EPSPs which were, in some cases, followed by hyperpolarizations, similar to the sensorimotor cortex (SM)-induced PSPs previously observed. Stimulation of the contralateral cerebral cortex never produced detectable PSPs. Topographical arrangement of PASC-rubral projection was found. Stimulation of the lateral part of PASC induced EPSPs predominantly in RN cells innervating the cervicothoracic spinal segments, while stimulation of the medial part of PASC produced EPSPs predominantly in RN cells innervating the lumbosacral cord. Furthermore, PASC-induced EPSPs were more frequently recorded at the rostral half of RN than at the caudal half. Monosynaptic EPSPs and multisynaptic IPSPs were induced by stimulation of the ipsilateral PRT and ML. PRT- and ML-induced EPSPs had times-to-peak of 1.0 +/- 0.4 msec (mean +/- S.D.) and 1.6 +/- 0.5 msec, respectively, which were intermediate to those of the cerebral peduncle (CP)- and nucleus interpositus of the cerebellum (IP)-induced EPSPs. Furthermore, sensitivity of amplitudes of PRT-induced EPSPs to membrane hyperpolarization was intermediate to those of CP- and IP-EPSPs, and that of ML-induced EPSPs was lower than that of IP-EPSPs. Therefore, it is likely that synapses of PRT and ML fibers are formed between the distal dendrites where CP-rubral synapses terminate and soma where IP-rubral synapses terminate. PASC-induced EPSPs after chronic IP and SM lesions had a new fast-rising component and the effectiveness of ML stimulation to induce the unit spike of RN cells was clearly increased in IP and SM lesioned cats. It was suggested that PASC-rubral fibers sprouted and formed new synapses at the proximal portions of soma-dendritic membranes of RN cells after IP and SM destructions. Collateral fibers to RN cells of the pyramidal tract were also shown to sprout new synapses following IP and ML lesions.