Activity-dependent changes in the electrophysiological properties of regular spiking neurons in the sensorimotor cortex of the rat in vitro

Canu, Marie‐Hélène; Picquet, Florence; Bastide, Bruno; Falempin, Maurice

doi:10.1016/j.bbr.2010.02.006

Cited by 8 publications

(4 citation statements)

References 38 publications

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“…Data performed by our team in the rat hindlimb unloading model (HU), a model of functional hypoactivity, have provided evidence for changes within the sensorimotor cortex. The excitability of pyramidal cells in the motor cortex is decreased [6], [7], and their dendritic spine density is increased [8]. Recent studies have suggested that alterations in corticospinal excitability should also be taken into account to explain the degradation of posture and locomotion in human following bed-rest [9], [10].…”

Section: Introductionmentioning

confidence: 99%

Hypoactivity Affects IGF-1 Level and PI3K/AKT Signaling Pathway in Cerebral Structures Implied in Motor Control

et al. 2014

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A chronic reduction in neuromuscular activity through prolonged body immobilization in human alters motor task performance through a combination of peripheral and central factors. Studies performed in a rat model of sensorimotor restriction have shown functional and biochemical changes in sensorimotor cortex. However, the underlying mechanisms are still unclear. Interest was turned towards a possible implication of Insulin-like Growth Factor 1 (IGF-1), a growth factor known to mediate neuronal excitability and synaptic plasticity by inducing phosphorylation cascades which include the PI3K–AKT pathway. In order to better understand the influence of IGF-1 in cortical plasticity in rats submitted to a sensorimotor restriction, we analyzed the effect of hindlimb unloading on IGF-1 and its main molecular pathway in structures implied in motor control (sensorimotor cortex, striatum, cerebellum). IGF-1 level was determined by ELISA, and phosphorylation of its receptor and proteins of the PI3K–AKT pathway by immunoblot. In the sensorimotor cortex, our results indicate that HU induces a decrease in IGF-1 level; this alteration is associated to a decrease in activation of PI3K-AKT pathway. The same effect was observed in the striatum, although to a lower extent. No variation was noticed in the cerebellum. These results suggest that IGF-1 might contribute to cortical and striatal plasticity induced by a chronic sensorimotor restriction.

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Section: Introductionmentioning

confidence: 99%

Hypoactivity Affects IGF-1 Level and PI3K/AKT Signaling Pathway in Cerebral Structures Implied in Motor Control

et al. 2014

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“…To observe the expression of growth-associated genes GAP-43, CAP-23, SPRR 1A, IL-6, JUN B and c-JUN after intratheral delivery of IL-6, total RNA was extracted from both sides of the sensorimotor cortex (around 2 mm posterior from the bregma, 2 mm lateral from the midline, with a depth of 1.5 mm from the dura matter of the brain) [ 10 , 17 ] with Trizol (Invitrogen) 7 days after delivery of IL-6, or IL-6 and AG 490, or saline (n = 3, respectively). Total RNA (100 ng) was reverse transcribed and amplified using TaqMan One-Step RT-PCR Master Mix (Applied Biosystems, Foster City, CA).…”

Section: Methodsmentioning

confidence: 99%

“…Seven days after spinal cord injury and intrathecal delivery of IL-6, IL-6 and AG490, or saline (n = 3 respectively), both sides of the sensorimotor cortex (around 2 mm posterior from the bregma, 2 mm lateral from the midline, with a depth of 1.5 mm from the dura matter of the brain) [ 10 , 17 ] were collected in cold PBS then homogenized in tissue lysis buffer containing 20 mM Tris-HCl, 150 mM NaCl, 2 mM EDTA, 0.1 mM EGTA, 1% Triton X-100, and 0.5% deoxyocholine with complete protease inhibitors (Roche). Samples were kept on ice for 30 min and then centrifuged at 13,000 g for 15 min to remove cell debris.…”

Section: Methodsmentioning

confidence: 99%

Intrathecal Delivery of IL-6 Reactivates the Intrinsic Growth Capacity of Pyramidal Cells in the Sensorimotor Cortex after Spinal Cord Injury

et al. 2015

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We have previously demonstrated the growth-promoting effect of intrathecal delivery of recombinant rat IL-6 immediately after corticospinal tract (CST) injury. Our present study aims to further clarify whether intrathecal delivery of IL-6 after CST injury could reactivate the intrinsic growth capacity of pyramidal cells in the sensorimotor cortex which project long axons to the spinal cord. We examined, by ELISA, levels of cyclic adenosine monophosphate (cAMP), adenylyl cyclase (AC, which synthesizes cAMP), phosphodiesterases (PDE, which degrades cAMP), and, by RT-PCR, the expression of regeneration-associated genes in the rat sensorimotor cortex after intrathecal delivery of IL-6 for 7 days, started immediately after CST injury. Furthermore, we injected retrograde neuronal tracer Fluorogold (FG) to the spinal cord to label pyramidal cells in the sensorimotor cortex, layers V and VI, combined with βIII-tubulin immunostaining, then we analyzed by immunohistochemisty and western blot the expression of the co-receptor gp-130 of IL-6 family, and pSTAT3 and mTOR, downstream IL-6/JAK/STAT3 and PI3K/AKT/mTOR signaling pathways respectively. We showed that intrathecal delivery of IL-6 elevated cAMP level and upregulated the expression of regeneration-associated genes including GAP-43, SPRR1A, CAP-23 and JUN-B, and the expression of pSTAT3 and mTOR in pyramidal cells of the sensorimotor cortex. In contrast, AG490, an inhibitor of JAK, partially blocked these effects of IL-6. All these results indicate that intrathecal delivery of IL-6 immediately after spinal cord injury can reactivate the intrinsic growth capacity of pyramidal cells in the sensorimotor cortex and these effects of IL-6 were partially JAK/STAT3-dependent.

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“…This cortical region is organized somatotopically: the different areas of the body are represented not in proportion to the actual size of the body parts, but rather to their functional importance (Feldman and Brecht 2005). Taking advantage of this organizational principle, previous studies have shown that periods of sensorimotor perturbation (SMP), and in particular of hindlimb unloading, induce a reduction in the cortical representation of the hindlimbs (Dupont et al 2001;Mysoet et al 2014;Mysoet et al 2015), and changes in cortical excitability (Canu et al 2010;Dupont et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Sensorimotor Perturbation Induces Late and Transient Molecular Synaptic Proteins Activation and Expression Changes

2021

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Plasticity of the cerebral cortex following a modification of the sensorimotor experience takes place in several steps that can last from few hours to several months. Among mechanisms involved in the dynamic modulation of the cerebral cortex in adults, it is commonly proposed that short-term plasticity reflects changes in synaptic connections. Here, we were interested in the time-course of synaptic plasticity taking place in the somatosensory primary cortex all along a 14-day period of sensorimotor perturbation (SMP), as well as during a recovery phase up to 24 hours. Activation and expression level of pre-(synapsin 1, synaptophysin, synaptotagmin 1) and postsynaptic (AMPA and NMDA receptors) proteins; postsynaptic density scaffold proteins (PSD-95 and Shank2); cytoskeletal proteins (neurofilaments-L and M, β3-tubulin, synaptopodin, N-cadherin) was determined in cortical tissue enriched in synaptic proteins. During the SMP period, most changes were observed as soon as D7 in the presynaptic compartment and were followed, at D14, by changes in the postsynaptic compartment. These changes persisted at least until 24h of recovery. Proteins involved in synapse structure (scaffolding, adhesion, cytoskeletal) were mildly affected and almost exclusively at D14. We concluded that experience-dependent reorganization of somatotopic cortical maps is accompanied by changes in synaptic transmission with a very close time-course.

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Activity-dependent changes in the electrophysiological properties of regular spiking neurons in the sensorimotor cortex of the rat in vitro

Cited by 8 publications

References 38 publications

Hypoactivity Affects IGF-1 Level and PI3K/AKT Signaling Pathway in Cerebral Structures Implied in Motor Control

Hypoactivity Affects IGF-1 Level and PI3K/AKT Signaling Pathway in Cerebral Structures Implied in Motor Control

Intrathecal Delivery of IL-6 Reactivates the Intrinsic Growth Capacity of Pyramidal Cells in the Sensorimotor Cortex after Spinal Cord Injury

Sensorimotor Perturbation Induces Late and Transient Molecular Synaptic Proteins Activation and Expression Changes

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