Brain injuries can interrupt descending neural pathways that convey motor commands from the cortex to spinal motoneurons. Here, we demonstrate that a unilateral injury of the hindlimb sensorimotor cortex of rats with completely transected thoracic spinal cord produces hindlimb postural asymmetry with contralateral flexion and asymmetric hindlimb withdrawal reflexes within 3 hr, as well as asymmetry in gene expression patterns in the lumbar spinal cord. The injury-induced postural effects were abolished by hypophysectomy and were mimicked by transfusion of serum from animals with brain injury. Administration of the pituitary neurohormones β-endorphin or Arg-vasopressin-induced side-specific hindlimb responses in naive animals, while antagonists of the opioid and vasopressin receptors blocked hindlimb postural asymmetry in rats with brain injury. Thus, in addition to the well-established involvement of motor pathways descending from the brain to spinal circuits, the side-specific humoral signaling may also add to postural and reflex asymmetries seen after brain injury.

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Systemic administration of antihistamine drug dimebon improves active avoidance conditioning in rats with chronic partial deprivation of cerebral cholinergic functions caused by intracerebroventricular injections of AF64A. The effects of dimebon on learning are similar to those of tacrine used in the treatment of Alzheimer's disease.

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26A paradigm in neurology is that brain injury-induced motor deficits (e.g. hemiparesis and 27 hemiplegia) arise due to aberrant activity of descending neural pathways. We discovered that a 28 unilateral injury of the hindlimb sensorimotor cortex of rats with completely transected thoracic 29 spinal cord produces hindlimb postural asymmetry with contralateral flexion, and asymmetric 30 changes in nociceptive hindlimb withdrawal reflexes and gene expression patterns in lumbar spinal 31 cord. The injury-induced postural effects were abolished by prior hypophysectomy and were 32 mimicked by transfusion of serum from animals with unilateral brain injury. Antagonists of the 33 opioid and vasopressin receptors blocked formation of hindlimb postural asymmetry suggesting 34 that these neurohormones mediate effects of brain injury on lateralized motor responses. Our data 35 indicate that descending neural control of spinal circuits is complemented by a previously 36 unknown humoral signaling from injured brain to the contra-and ipsilesional hindlimbs, and 37 suggest the existence of a body side-specific neuroendocrine regulation in bilaterally symmetric 38 animals. 39 In this study we challenge the neurological paradigm by investigating whether a unilaterally 62 injured brain may signal to the lumbar spinal cord through non-spinal mechanism. We applied a 63 "reversed strategy" protocol in which brain injury was performed after complete transection of the 64 spinal cord at a superior thoracic level. 65 66 Results 67Brain injury induces postural asymmetry in rats with transected spinal cord 68 We first demonstrated that the unilateral injury of the hindlimb representation area of the 69 sensorimotor cortex in rats induces formation of HL-PA (Figure 1A,D,E; Figure 1-figure 70 supplement 1). The effect was evident under pentobarbital anesthesia within 5 min after the lesion 71 and lasted for 14 days. The HL-PA median values and probability to develop HL-PA greater than 72 the 1 mm threshold were markedly higher in rats with UBI (n = 8) compared to those with sham 73 surgery (sham; n = 7). The UBI rats displayed a contralesional hindlimb flexion which correlated 74 with motor deficits of the same limb in the beam-working and ladder rung tests (UBI, n = 11/12; 75 sham, n = 8) (Figure 1B,C). The UBI rats showed the high number of slips of the contralesional 76 hindlimb compared to the ipsilesional limb, and to both hindlimbs in rats with sham surgery. 77 Consistent with earlier studies (Chamberlain et al., 1963; DiGiorgio, 1929; Hultborn & Malmsten, 78 1983; Rossignol & Frigon, 2011;Wolpaw, 2012), the HL-PA was retained after complete 79 transection of the spinal cord performed at the T2-T3 level (Figure 1-figure supplement 1E-G). 80 We hypothesized that the HL-PA is maintained either due to neuroplastic changes in the lumbar 81 spinal cord induced through the descending neural tracts before spinalization, or due to non-spinal 82 cord mediated signaling from the injured brain to the lumbar neural circui...

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