The Journal of physiology
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The Journal of physiology · May 2001
ReviewNeurotrophic factors, cellular bridges and gene therapy for spinal cord injury.
Injury to the adult mammalian spinal cord results in extensive axonal degeneration, variable amounts of neuronal loss, and often severe functional deficits. Restoration of controlled function depends on regeneration of these axons through an injury site and the formation of functional synaptic connections. ⋯ Further, more recent experiments have shown that neurotrophic factors can also promote axonal growth, and, when combined with Schwann cell grafts, can further amplify axonal extension after injury. Continued preclinical development of these approaches to neural repair may ultimately generate strategies that could be tested in human injury.
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The Journal of physiology · May 2001
Spino-bulbo-spinal pathway mediating vagal modulation of nociceptive-neuroendocrine control of inflammation in the rat.
Stimulation of nociceptors by intradermal capsaicin produces depression of bradykinin (BK)-induced synovial plasma extravasation (PE) that is markedly enhanced by subdiaphragmatic vagotomy. This depression is mediated by the adrenal medullae, a propriospinal pathway between the afferent nociceptive input and preganglionic neurones projecting to the adrenal medullae, and a spino-bulbo-spinal pathway. Here we investigated the role of spinal ascending and descending pathways in the interaction between noxious and vagal afferent inputs, leading to inhibition of BK-induced PE mediated by the adrenal medullae. ⋯ Contralateral and ipsilateral hemisection of the spinal cord (C5/C6) produced the same changes as the corresponding DLF lesions. Ipsi- or contralateral lesion of the dorsal funiculus at the spinal level T8/T9 had no effect on depression of BK-induced PE generated by cutaneous noxious stimulation of the forepaw. We suggest that noxious stimulation activates an ascending pathway of the spino-bulbo-spinal excitatory circuit which projects through the DLF contralateral to the nociceptive input, and that the inhibitory pathway which is activated by vagal afferent activity projects through the DLF ipsilateral to the nociceptive input.
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The Journal of physiology · May 2001
Evidence that nitric oxide- and opioid-containing interneurons innervate vessels in the dorsal horn of the spinal cord of rats.
In the dorsal horn of the spinal cord, activation of small fibre nociceptive afferents leads to the release of nitric oxide and enkephalins by interneurons. In this work we encountered unexpected relationships among local spinal cord dorsal horn blood flow, specific forms of afferent input, nitric oxide and intrinsic opioids. Selective rises in rat lumbar dorsal cord blood flow using laser Doppler flowmetry and microelectrode hydrogen clearance polarography were generated by ipsilateral, 'nociceptive' low (3 Hz) frequency stimulation of sciatic afferents. ⋯ Using immunohistochemistry, terminals apparently innervating dorsal spinal cord blood vessels were labelled with antibodies against neuronal NOS and met-enkephalin. We conclude that local nitric oxide and opioids, probably from interneurons, have competitive actions on dorsal horn microvessels once interneurons are activated during a nociceptive barrage. Collateral innervation of blood vessels may explain this property.