Experimental neurology
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Experimental neurology · Jul 2006
Comparative StudyLong-term facilitation of ipsilateral but not contralateral phrenic output after cervical spinal cord hemisection.
After chronic C2 spinal hemisection (C2HS), exposure to intermittent hypoxia (IH) evokes a persistent increase in phrenic output recorded ipsilateral to the injury (i.e., phrenic long-term facilitation, LTF; Golder and Mitchell, J. Neurosci. 25:2925-32, 2005). However, unilateral spinal cord injury induces compensatory increases in contralateral motoneuron activity that may reduce their capacity for further plasticity (i.e., a "ceiling effect"). ⋯ In contrast, LTF of ipsilateral phrenic amplitude occurred at both 4 (44 +/- 11% BL) and 8 weeks post-C2HS (129 +/- 30% BL, P < 0.05). A persistent increase in phrenic burst frequency after IH (i.e., "frequency LTF") was observed in control (+9 +/- 3 burst/min, P < 0.05), but not C2HS rats. We conclude that compensatory responses to unilateral cervical spinal cord injury prevent the expression of LTF in contralateral phrenic motoneurons.
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Experimental neurology · May 2006
Comparative StudyInfusion of human umbilical cord blood cells protect against cerebral ischemia and damage during heatstroke in the rat.
Intravenously delivered human umbilical cord blood cells (HUCBC) have been previously shown to improve both morphologic and functional recovery of heat-stroked rats. To extend these findings, we examined both the morphologic and functional alterations in the presence of HUCBC or human peripheral mononuclear cells (PBMC) 24 h before initiation of heatstroke. Anesthetized rats, 1 day before the initiation of heatstroke, were divided into three major groups and given the following: (a) serum-free lymphocyte medium (0.3 ml) intravenously; (b) PBMC (5 x 10(6) in 0.3 ml serum-free lymphocyte medium); or (c) HUCBC (5 x 10(6) in 0.3 ml serum-free lymphocyte medium). ⋯ The heatstroke-induced arterial hypotension, cerebral ischemia and hypoxia, and increased levels of iNOS-dependent NO in the striatum were all significantly reduced by pretreatment with HUCBC, but not with PBMC. Moreover, HUCBC were localized by immunohistochemistry and PCR analysis in the injured brain structures and spleen. These findings indicate that HUCBC transplantation, in addition to having therapeutic values, can be a good choice for preventing heatstroke occurrence.
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Experimental neurology · Apr 2006
Comparative StudyBDNF/TrkB signaling regulates HNK-1 carbohydrate expression in regenerating motor nerves and promotes functional recovery after peripheral nerve repair.
Functional recovery after peripheral nerve injury is often poor despite high regenerative capacity of peripheral neurons. In search for novel treatments, brief electrical stimulation of the acutely lesioned nerve has recently been identified as a clinically feasible approach increasing precision of axonal regrowth. The effects of this stimulation appear to be mediated by BDNF and its receptor, TrkB, but the down-stream effectors are unknown. ⋯ Accordingly, the degree of proper reinnervation of the quadriceps muscle, as indicated by retrograde labeling of motoneurons, was reduced in TrkB+/- mice compared to wild-type littermates. Also, recovery of quadriceps muscle function, evaluated by a novel single-frame motion analysis approach, and axonal regrowth into the distal nerve stump, assessed morphologically, were considerably delayed in TrkB+/- mice. These findings indicate that BDNF/TrkB signaling is important for functional recovery after nerve repair and suggest that up-regulation of the HNK-1 glycan is linked to this phenomenon.
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Experimental neurology · Apr 2006
Comparative StudyTraumatic axonal injury in the perisomatic domain triggers ultrarapid secondary axotomy and Wallerian degeneration.
Traumatic axonal injury (TAI) arising from diffuse brain injury (DBI) results in focally impaired axonal transport with progressive swelling and delayed disconnection over several hours within brainstem axons. Neocortical DBI-mediated perisomatic axotomy does not result in neuronal death, suggesting that a comparably delayed axotomy progression was responsible for this unanticipated response. To evaluate delayed perisomatic axotomy, the current study was initiated. ⋯ Distal axonal segment ultrastructure now revealed the initial stages of Wallerian degeneration. The site of perisomatic axotomy did not internalize dextran, suggesting that its pathogenesis occurred independent of altered axolemmal permeability. Collectively, this DBI-mediated ultrarapid perisomatic axotomy and its sequelae further illustrate the varied axonal responses to trauma.
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Experimental neurology · Apr 2006
Comparative StudyProgesterone administration modulates AQP4 expression and edema after traumatic brain injury in male rats.
This study investigates whether progesterone administration regulates AQP4 and GFAP expression in rats with bilateral contusion injuries of the medial frontal cortex. Male rats were given 0 or 16 mg/kg injections of progesterone at 1, 6, 24, and 48 h post-injury. Brains were extracted at 24 h or 72 h post-injury and assayed for cerebral edema and AQP4 and GFAP expression using Western blot analysis. ⋯ However, progesterone significantly reduced AQP4 expression at 72 h post-injury in the tissue bounded by the lateral ventricles and the peri-contusion areas compared to lesion+ vehicle rats, but increased AQP4 expression in the tissue surrounding the third ventricle. Also progesterone effects on GFAP expression varied according to brain region. Our results can be taken to show that the expression of AQP4 protein after TBI is time-dependent, region-specific, and possibly implicated in the formation and resolution of TBI-induced cerebral edema.