Experimental neurology
-
Experimental neurology · Jul 2006
Comparative StudyMembrane-bound CSPG mediates growth cone outgrowth and substrate specificity by Schwann cell contact with the DRG neuron cell body and not via growth cone contact.
The central nervous system and peripheral nervous system (CNS/PNS) contain factors that inhibit axon regeneration, including myelin-associated glycoprotein (MAG), the Nogo protein, and chondroitin sulfate proteoglycan (CSPG). They also contain factors that promote axon regeneration, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). Axon regeneration into and within the CNS fails because the balance of factor favors inhibiting regeneration, while in the PNS, the balance of factor favors promoting regeneration. ⋯ Further, there was no apparent influence of diffusible or substrate-bound CSPG on neurite outgrowth. These results show that eliminating the CSPG of Schwann cells in contact with the cell body of DRG neurons eliminates the sensitivity of their growth cones to the CSPG-induced outgrowth inhibition. This may in turn allow the axons of these neurons to regenerate through the dorsal roots and into the spinal cord.
-
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.
-
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.
-
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.
-
Experimental neurology · Apr 2006
Comparative StudyDisruption of glial function enhances electroacupuncture analgesia in arthritic rats.
Activated glia play a major role in mediating behavioral hypersensitive state following peripheral inflammation. Electroacupuncture is well known to relieve persistent inflammatory pain. The present study was undertaken to examine whether fluorocitrate, a glial metabolic inhibitor, could synergize electroacupuncture antagonizing thermal hyperalgesia and mechanical allodynia evoked by ankle joint inflammation. ⋯ Unilateral electroacupuncture stimulation of "Huantiao" (GB30) and "Yanglingquan" (GB34) acupuncture points (100/2 Hz alternation, 1-2-3 mA) significantly elevated the PWLs and PWTs for 45 min after cessation of electroacupuncture in monoarthritic rats. Co-application of 0.1 or 1 nmol fluorocitrate with electroacupuncture significantly potentiated electroacupuncture analgesia, although 0.1 nmol fluorocitrate alone had no effect on PWLs and PWTs in monoarthritic rats. These results suggested that electroacupuncture and disrupting glial function could synergistically antagonize inflammatory pain, which might provide a potential strategy for the treatment of arthritic pain.