DOI: 10.6084/m9.figshare.5924671.v1
title: Early movement restriction effects on sensorimotor cortex and movement disorders in rats

description: This dataset contains raw experimental results for sensorimotor restriction (SMR) and control (sham) group rats, along with graphics of primary somatosensory (S1) and motor (M1) cortices maps.<br>The dataset consists of a single<b> .xlsx</b> file that can be openly accessed via MS Excel and open office applications, an openly accessible .png file and a single .cvx graphic file accessible via ACD Systems Canvas software.<br>Sprague-Dawley rat pups of either sex from different litters were pseudo-randomly assigned to two groups: 1) a group subjected to transient hind limb immobilization from P1 to P28 for 16 hours per day, thus producing sensorimotor restriction (SMR); and 2) a control group (Cont).<b><br></b><b>alldatatot_cont_SMR_aug17.xlsx </b>- complete dataset for 19 sham group rats and 17 SMR group rats. The wide range of variables (105) include: rat identifier, gender, group and a wide range of biometric and motor measures (weight at birth, tibial length), Microdialysis and Western blot results (levels of extracellular glutamate, vesicular glutamate transporter, (VGLUT1) and vesicular GABA, transporter (VGAT)).<br><b>Fig_M1maps_cont_sev.cvx</b> - primary motor (M1) cortex map: SMR, n = 8; Cont, n = 9<br><b>Cont_S1.png </b>- primary somatosensory (S1) cortex map: SMR, n = 9; Cont, n= 10<br>All experiments and animal use were carried out in accordance with the guidelines laid down by NIH (NIH Publication #80-23) and EC Council Directive (2007/526/EEC). This research involving animals was approved by the Direction Départementale des Services Vétérinaires – Préfecture des Bouches du Rhône, France (permit # C13-055-18).<br><br><b>Background of related study</b>Motor control and body representations in the central nervous system are built, i.e., patterned, during development by sensorimotor experience and somatosensory feedback/reafference. Yet, early emergence of locomotor disorders remains a matter of debate, especially in the absence of brain damage. We showed recently that postnatal sensorimotor restriction (SMR), induced using daily casting to restrict hind limb movement from birth to one month, led to digitigrade locomotion related to ankle-knee overextension that persisted after cessation of the casting, degraded musculoskeletal tissues (e.g., gastrocnemius atrophy), and clear signs of spinal hyperreflexia, suggestive of spasticity; each individual disorder likely interplaying through a self-perpetuating cycle. We hypothesized that these degraded outcomes originated from developmental disorganization of the sensorimotor circuitry as a result of the atypical somatosensory reafference during the SMR. Here, we investigated the impact of postnatal SMR on the anatomical and functional organization of the primary somatosensory (S1) and motor (M1) cortices. We found that prolonged SMR for 30 days degraded the topographical organization of hind limb S1 maps, reduced the M1 map area and altered the neuronal response properties in the S1 and M1 cortices several months after the cessation of SMR. We found no neuroanatomical histopathology in the S1-M1 area, yet increased glutamatergic neurotransmission within the hind limb S1-M1 area that matched clear signs of spasticity and hyperexcitability in the adult lumbar spinal networks, previously observed after similarly prolonged SMR. Thus, even in the absence of a brain insult, movement disorders and brain dysfunction can emerge as a consequence of reduced and atypical patterns of motor outputs and somatosensory feedback that induce maladaptive neuroplasticity, especially in the S1 cortex. Our results may contribute to understand the inception and mechanisms underlying some neurodevelopmental disorders.<br>