The origins of the afferent fibers of the parafascicular nucleus were studied with the retrograde tracing method of HRP in eight rats by injecting HRP into the left thalamic parafascicular nucleus. The labeled cells were found mainly in the bilateral reticular formation, the ipsilateral central gray, intermediate and deep gray layers of the superior celliculus and some area of the cerebral cortex. A few labeled cells were found in the contralateral dorsal horn of spinal cord. The labeled cells were also found to varying degrees in some other nuclei of the brain.The modified injection method of concentric glass-micropipettes was discussed.The origins of afferent fibers of parafascicular nucleus and their functions concerned with pain were discussed.

AIM:To investigate the expression of GAP-43 mRNA and protein of the motor neurons in spinal cord following the brachial plexus avulsion injury.METHODS: In the present study,three kinds of models of brachial plexus avulsion injury were made: right C7 anterior root avulsion(group A),C7 anterior root avulsion with right C5-T1 posterior roots breaking(group B),right C7 anterior root avulsion with hemi-transect between C5 and C6 segment of spinal cord(group C).The expression of GAP-43 mRNA in anterior horn of spinal cord was detected at 14 days after operation by SYBR green quantification RT-PCR technique.The amounts of GAP-43 positive neurons in spinal cord were detected at 1,3,7 and 14 days after operation by immunohistochemistry technique.RESULTS: In control group,the expression of GAP-43 mRNA was very low in anterior horn.By 14 days after operation,the expression of GAP-43 mRNA was evidently up-regulated compared with control group.GAP-43 positive neuron was observed in control group at 1st day and 3rd day after operation.GAP-43 positive neurons appeared at 7th day and peaked at 14th day after operation.The expression of GAP-43 mRNA and protein were maximum in group C,group B was the lowest.CONCLUSION: The expression of GAP-43 mRNA and GAP-43 protein were up-regulated following brachial plexus injury.The expression of GAP-43 protein results from the recombination of proteins.GAP-43 is closely related to the axon regeneration and functional reconstruction.

AIM: To investigate the influence of Ginkgo biloba extract (EGb761) on c-jun expressions and motoneurons survival following root avulsion. METHODS: One hundred and eighty adult Sprague-Dawley female rats were randomly divided into control and EGb761 groups. Immediately after avulsion of C5-T1 nerve roots, the rats were injected ip with either 1 mL of EGb761 25 mg?kg~(-1)?d~(-1) or the same volume of normal saline, and the treatment repeated everyday. At 4 h to 6 weeks following avulsion, the C7 spinal segments of all rats were collected and prepared for c-jun immunocytochemistry and neutral red stain. The numbers of (c-jun) positive and survival motoneurons were counted and compared between two groups at each time point. RESULTS: In control rats following avulsion, c-jun positive motoneurons appeared at 4 h, reached its maximum at 1 d and declined to 2 weeks. Avulsion-induced motoneurons death started at 2 weeks, climbed to its maximum at 4 weeks-6 weeks. In EGb761 treated rats, both numbers of c-jun positive and survival motoneurons were more than that in control group at each time point. CONCLUSION: EGb761 attenuates avulsion-induced motoneurons death, and this effect may be related to up-regulation of c-jun gene in avulsed motoneurons. [

OBJECTIVETo quantitatively analyze the temporal and spatial pattern of RhoA expression in injured spinal cord of adult mice.

METHODSA spinal cord transection model was established in adult mice. At 1, 3, 7, 14, 28, 56 and 112 days after the surgery, the spinal cords were dissected and cryosectioned for RhoA/NF200, RhoA/GFAP, RhoA/CNPase or RhoA/IBA1 double fluorescent immunohistochemistry to visualize RhoA expressions in the neurons, astrocytes, oligodendrocytes and microglia. The percentages as well as the immunostaining intensities of RhoA-positive cells in the parenchymal cells were quantitatively analyzed.

RESULTSRhoA was weakly expressed in a few neurons and oligodendrocytes in normal spinal cord. After spinal cord injury, the percentage of RhoA-positive cells and RhoA expression intensity in the spinal cord increased and peaked at 7 days post injury (dpi) in neurons, oligodendrocytes and astrocytes, followed by a gradual decrease till reaching a low level at 112 dpi. In the microglia, both the RhoA-positive cells and RhoA expression intensity reached the maximum at 14 dpi and maintained a high level till 112 dpi.

CONCLUSIONTraumatic spinal cord injury can upregulate RhoA expression in the neurons as well as all the glial cells in the spinal cord. RhoA expression patterns vary with post-injury time, location and among different parenchymal cells in the injured spinal cord.

Animals ; Astrocytes ; metabolism ; Female ; Mice ; Mice, Inbred Strains ; Microglia ; metabolism ; Neuroglia ; metabolism ; Neurons ; metabolism ; Spinal Cord ; metabolism ; Spinal Cord Injuries ; metabolism ; rho GTP-Binding Proteins ; metabolism