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大脑皮层损毁、中脑横断和脊髓猫的虚构抓挠模式。

Fictive Scratching Patterns in Brain Cortex-Ablated, Midcollicular Decerebrate, and Spinal Cats.

机构信息

Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Guadalajara, Mexico.

Departamento de Fisiología, CUCS, Universidad de Guadalajara, Guadalajara, Mexico.

出版信息

Front Neural Circuits. 2020 Feb 27;14:1. doi: 10.3389/fncir.2020.00001. eCollection 2020.

DOI:10.3389/fncir.2020.00001
PMID:32174815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7056700/
Abstract

: The spinal cord's central pattern generators (CPGs) have been explained by the symmetrical half-center hypothesis, the bursts generator, computational models, and more recently by connectome circuits. Asymmetrical models, at odds with the half-center paradigm, are composed of extensor and flexor CPG modules. Other models include not only flexor and extensor motoneurons but also motoneuron pools controlling biarticular muscles. It is unknown whether a preferred model can explain some particularities that fictive scratching (FS) in the cat presents. The first aim of this study was to investigate FS patterns considering the aiming and the rhythmic periods, and second, to examine the effects of serotonin (5HT) on and segmental inputs to FS. : The experiments were carried out first in brain cortex-ablated cats (BCAC), then spinalized (SC), and for the midcollicular (MCC) preparation. Subjects were immobilized and the peripheral nerves were used to elicit the Monosynaptic reflex (MR), to modify the scratching patterns and for electroneurogram recordings. : In BCAC, FS was produced by pinna stimulation and, in some cases, by serotonin. The scratching aiming phase (AP) initiates with the activation of either flexor or extensor motoneurons. Serotonin application during the AP produced simultaneous extensor and flexor bursts. Furthermore, WAY 100635 (5HT1A antagonist) produced a brief burst in the tibialis anterior (TA) nerve, followed by a reduction in its electroneurogram (ENG), while the soleus ENG remained silent. In SC, rhythmic phase (RP) activity was recorded in the soleus motoneurons. Serotonin or WAY produced FS bouts. The electrical stimulation of Ia afferent fibers produced heteronymous MRes waxing and waning during the scratch cycle. In MCC, FS began with flexor activity. Electrical stimulation of either deep peroneus (DP) or superficial peroneus (SP) nerves increased the duration of the TA electroneurogram. Medial gastrocnemius (MG) stretching or MG nerve electrical stimulation produced a reduction in the TA electroneurogram and an initial MG extensor burst. MRes waxed and waned during the scratch cycle. : Descending pathways and segmental afferent fibers, as well as 5-HT and WAY, can change the FS pattern. To our understanding, the half-center hypothesis is the most suitable for explaining the AP in MCC.

摘要

脊髓的中央模式发生器 (CPGs) 已经通过对称半中心假说、爆发发生器、计算模型以及最近的连接体电路得到了解释。与半中心范式不一致的非对称模型由伸肌和屈肌 CPG 模块组成。其他模型不仅包括屈肌和伸肌运动神经元,还包括控制双关节肌肉的运动神经元池。目前尚不清楚是否有一种首选的模型可以解释猫的虚构抓挠 (FS) 所呈现的某些特殊性。本研究的第一个目的是研究 FS 模式,考虑到瞄准和节奏期,其次是检查 5-羟色胺 (5HT) 对 FS 的影响和节段性输入。实验首先在大脑皮层切除猫 (BCAC) 中进行,然后在脊髓化 (SC) 和中脑导水管 (MCC) 制剂中进行。实验对象被固定,外周神经用于引发单突触反射 (MR)、改变抓挠模式和记录电神经图。在 BCAC 中,FS 由耳廓刺激产生,在某些情况下由 5-羟色胺产生。抓挠瞄准阶段 (AP) 始于屈肌或伸肌运动神经元的激活。AP 期间应用 5-羟色胺会产生同时的伸肌和屈肌爆发。此外,WAY 100635(5-HT1A 拮抗剂)在前胫骨肌 (TA) 神经中产生短暂爆发,随后其电神经图 (ENG) 减少,而比目鱼肌 ENG 保持沉默。在 SC 中,在比目鱼肌运动神经元中记录到节奏阶段 (RP) 活动。5-羟色胺或 WAY 产生 FS 发作。Ia 传入纤维的电刺激在抓挠周期中产生异源 MRes 增减。在 MCC 中,FS 始于屈肌活动。深腓骨 (DP) 或浅腓骨 (SP) 神经的电刺激增加 TA 电神经图的持续时间。内侧腓肠肌 (MG) 拉伸或 MG 神经电刺激会导致 TA 电神经图减少和初始 MG 伸肌爆发。MRes 在抓挠周期中增减。下行通路和节段传入纤维以及 5-羟色胺和 WAY 都可以改变 FS 模式。据我们所知,半中心假说最适合解释 MCC 中的 AP。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/86b59d728b97/fncir-14-00001-g0013.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/3079b904f473/fncir-14-00001-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/18280734ab3c/fncir-14-00001-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/0d8e55b793c5/fncir-14-00001-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/98a2c4a44d3c/fncir-14-00001-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/f26f98d5db7b/fncir-14-00001-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/e1c651e48ee0/fncir-14-00001-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/138cd2a5e19b/fncir-14-00001-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/cb0e5c599496/fncir-14-00001-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/98469c385304/fncir-14-00001-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/0a406647f68a/fncir-14-00001-g0011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d704/7056700/96346fb7d503/fncir-14-00001-g0012.jpg
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