Dynamics of activity of postural asymmetry factor after unilateral injury to the motor cortex

Rogachii, M. G.; Klement'ev, B. I.; Vartanyan, G. A.

doi:10.1007/bf00804289

Cited by 6 publications

(4 citation statements)

References 2 publications

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“…The ipsilateral hindlimb flexion was induced by hemicerebellar lesion ( DiGiorgio, 1929 , 1942 ; Alella, 1948 ; Chamberlain et al , 1963 ; Patterson, 2001 ), or hemilabyrinthectomy ( Straka and Dieringer, 1995 ). In contrast, contralesional hindlimb flexion was developed after a focal injury of the hindlimb representation area of the sensorimotor cortex (although a small part of the hindlimb somatosensory cortex might have been aspirated in some rats as also was described elsewhere ( Tandon et al , 2007 )) or large injury of one hemisphere (( Varlinskaia et al , 1984 ; Vartanyan and Klementiev, 1991 ) and the present work). Search for neurotransmitter system involved in HL-PA formation demonstrated that opioid peptides and synthetic opioids ( Bakalkin et al , 1980 ; Chazov et al , 1981 ; Bakalkin et al , 1986 ; Bakalkin and Kobylyansky, 1989 ) along with Arg-vasopressin ( Klement’ev et al , 1986 ; Lukoyanov et al , 2018 ) may induce HL-PA in spinalized animals.…”

Section: Discussionsupporting

confidence: 56%

Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

Zhang

Watanabe

Sarkisyan

et al. 2020

Brain Communications

131

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Mechanisms of motor deficits (e.g. hemiparesis and hemiplegia) secondary to stroke and traumatic brain injury remain poorly understood. In early animal studies, a unilateral lesion to the cerebellum produced postural asymmetry with ipsilateral hindlimb flexion that was retained after complete spinal cord transection. Here we demonstrate that hindlimb postural asymmetry in rats is induced by a unilateral injury of the hindlimb sensorimotor cortex, and characterize this phenomenon as a model of spinal neuroplasticity underlying asymmetric motor deficits. After cortical lesion, the asymmetry was developed due to the contralesional hindlimb flexion and persisted after decerebration and complete spinal cord transection. The asymmetry induced by the left-side brain injury was eliminated by bilateral lumbar dorsal rhizotomy, but surprisingly, the asymmetry after the right-side brain lesion was resistant to deafferentation. Pancuronium, a curare-mimetic muscle relaxant, abolished the asymmetry after the right-side lesion suggesting its dependence on the efferent drive. The contra- and ipsilesional hindlimbs displayed different musculo-articular resistance to stretch after the left but not right-side injury. The nociceptive withdrawal reflexes evoked by electrical stimulation and recorded with EMG technique were different between the left and right hindlimbs in the spinalized decerebrate rats. On this asymmetric background, a brain injury resulted in greater reflex activation on the contra- versus ipsilesional side; the difference between the limbs was higher after the right-side brain lesion. The unilateral brain injury modified expression of neuroplasticity genes analysed as readout of plastic changes, as well as robustly impaired coordination of their expression within and between the ipsi- and contralesional halves of lumbar spinal cord; the effects were more pronounced after the left side compared to the right-side injury. Our data suggest that changes in the hindlimb posture, resistance to stretch and nociceptive withdrawal reflexes are encoded by neuroplastic processes in lumbar spinal circuits induced by a unilateral brain injury. Two mechanisms, one dependent on and one independent of afferent input may mediate asymmetric hindlimb motor responses. The latter, deafferentation resistant mechanism may be based on sustained muscle contractions which often occur in patients with central lesions and which are not evoked by afferent stimulation. The unusual feature of these mechanisms is their lateralization in the spinal cord.

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Section: Discussionsupporting

confidence: 56%

Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

Zhang

Watanabe

Sarkisyan

et al. 2020

Brain Communications

131

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“…Similarly, a spinal cord hemisection produced ipsilateral changes in spinal reflexes that were paralleled by asymmetry in locomotion ( Hultborn and Malmsten, 1983a , b ; Malmsten, 1983 ; Frigon et al , 2009 ; Rossignol and Frigon, 2011 ). Hindlimb postural asymmetry (HL-PA) manifested as differences in the position of the ipsi- and contralesional hindlimbs was also induced by localized lesion to the hindlimb area of the sensorimotor cortex ( Zhang et al , 2020 ) as well as by a large hemispheric injury ( Varlinskaia et al , 1984 ). In contrast to cerebellar or spinal cord injuries, the contralesional hindlimb was flexed after injury to the sensorimotor cortex.…”

Section: Introductionmentioning

confidence: 99%

Ipsilesionalversuscontralesional postural deficits induced by unilateral brain trauma: a side reversal by opioid mechanism

Watanabe

Nosova

Sarkisyan

et al. 2020

Brain Communications

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Unilateral traumatic brain injury and stroke result in asymmetric postural and motor deficits including contralateral hemiplegia and hemiparesis. In animals, a localized unilateral brain injury recapitulates the human upper motor neuron syndrome in formation of hindlimb postural asymmetry with contralesional limb flexion and the asymmetry of hindlimb nociceptive withdrawal reflexes. The current view is that these effects are developed due to aberrant activity of motor pathways that descend from the brain into the spinal cord. These pathways and their target spinal circuits may be regulated by local neurohormonal systems that may also mediate effects of brain injury. Here we evaluate if a unilateral traumatic brain injury induces hindlimb postural asymmetry, a model of postural deficits, and if this asymmetry is spinally encoded and mediated by the endogenous opioid system in rats. A unilateral right-sided controlled cortical impact, a model of clinical focal traumatic brain injury was centered over the sensorimotor cortex and was observed to induce hindlimb postural asymmetry with contralateral limb flexion. The asymmetry persisted after complete spinal cord transection, implicating local neurocircuitry in the development of the deficits. Administration of the general opioid antagonist naloxone and µ-antagonist β-funaltrexamine blocked formation of postural asymmetry. Surprisingly, κ-antagonists nor-binaltorphimine and LY2444296 did not affect the asymmetry magnitude but reversed the flexion side; instead of contralesional (left) hindlimb flexion the ipsilesional (right) limb was flexed. The postural effects of the right-side cortical injury were mimicked in animals with intact brain via intrathecal administration of the opioid κ-agonist U50,488 that induced hindlimb postural asymmetry with left limb flexion. The δ-antagonist naltrindole produced no effect on the contralesional (left) flexion but inhibited formation of the ipsilesional (right) limb flexion in brain-injured rats that were treated with κ-antagonist. The effects of the antagonists were evident before and after spinal cord transection. We concluded that the focal traumatic brain injury-induced postural asymmetry was encoded at the spinal level, and was blocked or its side was reversed by administration of opioid antagonists. The findings suggest that the balance in activity of the mirror symmetric spinal neural circuits regulating contraction of the left and right hindlimb muscles is controlled by receptors; and that this equilibrium is impaired after unilateral brain trauma through side-specific opioid mechanism.

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“…In 9 male cats, the cortical representation of the right hind limb (motor neocortex) was removed as previously described [1], after which CSF was collected from an occipital cistern (approximately 0.5 ml per kg body weight) and exposed for 2 rain to UV radiation predominantly of 254 nm in a quartz cuvette 10 cm-' in area, the radiation flux density being 2 mW/cm2; the CSF was then returned to the animal. The irradiation procedure was repeated on postoperative days 3, 5, and 8.…”

Section: Methodsmentioning

confidence: 99%

Ultraviolet irradiation of cerebrospinal fluid stimulates compensatory processes in cats with a unilaterally damaged central nervous system

et al. 1996

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Portions of cerebrospinal fluid (CSF) withdrawn from cats operated upon for unilateral removal of the motor neocortex were exposed to ultraviolet (UV) radiation and then returned to the cats to e~aluate the effects of irradiation on the recovery of voluntary movements by the affected limb and the activity of CSF peptide and protein neurohumoral factors durin~ tilt. i~o>toperative period. The exposure of CSF to UV radiation substantially acceleratcd ~,,rnpensatory processes (the recovery of motor functions) in the animals and activated t~',~, t~,,~y'nthesis of neurohumoral factors. Key Words: central m,r~,,,.~ ~vstem; ultraviolet radiation; cerebrospinal fluid; motor disordersAs demonstrated in numerous studies, p~'pttdc tactots displaying lateral tropism to moto: ct'v, tcrs of the spinal cord and activating their actl~zt~ appear in the central nervous system early in ttw c(v.~rsc of compensatory processes that develop attcr unilateral injuries to the motor analyzer [31 Sub~t.qtwntly these factors lose their activity by forming" cort:picxes with the emerging high-molecular protet:', factors (binding factors), some of which arc immtir:o~,lobulins [4]. Attempts to stimulate compensatt,~ processes by administering peptide factors or ~mmu-nomodulators during the acute posttraumatic period have produced encouraging results 15.71. Continuing the quest for agents capable of stimulatin~ compensatory processes should undoubtedly be on the list of research priorities.In this study, cerebrospinal fluid (CSF) withdrawn from cats operated upon for unilateral removal of the motor neocortex was exposed to ultraviolet (UV) radiation and then returned to the cats to evaluate the effects of CSF irradiation on the recovery of voluntary movements by the affect- MATERIALS AND METHODSIn 9 male cats, the cortical representation of the right hind limb (motor neocortex) was removed as previously described [1], after which CSF was collected from an occipital cistern (approximately 0.5 ml per kg body weight) and exposed for 2 rain to UV radiation predominantly of 254 nm in a quartz cuvette 10 cm-' in area, the radiation flux density being 2 mW/cm2; the CSF was then returned to the animal. The irradiation procedure was repeated on postoperative days 3, 5, and 8. The control group consisted of 6 male cats that differed from the test animals only in that their CSF was not irradiated after being placed in a cuvette for 2 min. In both groups, CSF samples were taken from the occipital cistern on days 3,5,8, 11, 14, 17, and 21 to determine the activity of peptide and protein factors. In view of the species nonspecificity of the neurohumoral factors under study [2], CSF from operated cats was tested for its ability to induce postural asymmetry in recipient rats before and after heat

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Dynamics of activity of postural asymmetry factor after unilateral injury to the motor cortex

Cited by 6 publications

References 2 publications

Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

Ipsilesionalversuscontralesional postural deficits induced by unilateral brain trauma: a side reversal by opioid mechanism

Ultraviolet irradiation of cerebrospinal fluid stimulates compensatory processes in cats with a unilaterally damaged central nervous system

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