Neuroscience
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Whole-cell patch-clamp recordings were made from neurons in the substantia gelatinosa of adult rat spinal cord slices with attached dorsal root to study a slow synaptic current evoked by focal or dorsal root stimulation. Repetitive focal stimulation with a monopolar electrode positioned within substantia gelatinosa elicited a slow excitatory postsynaptic current preceded by a fast excitatory postsynaptic current in 73 of 83 neurons. A similar slow excitatory postsynaptic current was also elicited by stimulation of A delta afferent fibres. ⋯ These observations suggest that a transmitter released from interneurons or descending fibres which are activated in part by A delta afferents, mediates a slow excitatory postsynaptic currents in substantia gelatinosa neurons and that an excitatory amino acid is implicated in the generation of the slow excitatory postsynaptic current, although the receptor appears to differ from the known ligand-gated channels. C afferents are unlikely to contribute to the slow excitatory postsynaptic current. This slow synaptic response may participate in the pain pathway and play an important role in the processing of nociceptive information in the spinal dorsal horn.
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Abnormal pain-related behaviour that accompanies peripheral nerve injury may be the result of altered spinal neuronal function. The long-term loss of inhibitory function by GABA neurons in particular may be a mechanism by which abnormal neural hyperactivity occurs, leading to exaggerated sensory processing following nerve injury. In order to assess this, changes in spinal GABA immunoreactivity at several time points following constriction nerve injury were quantified in parallel with behavioural assessments of abnormal sensory responses to noxious and innocuous stimuli. ⋯ Parallel improvements in sensory responses to innocuous and noxious stimuli were also observed in these animals. The results of this study indicate that peripheral nerve injury can result in severe losses in spinal inhibitory mechanisms, possibly leading to exaggerated sensory processes in persistent pain states. In addition, adrenal medullary transplants may provide a neuroprotective function in promoting recovery and improving long-term survival of GABAergic neurons in the spinal dorsal horn which have been damaged by excitotoxic injury.
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The method of transneuronal retrograde transport of the Bartha strain of the swine alpha-herpes virus, pseudorabies virus, was used to identify putative interneurons presynaptic to motoneurons that supply a tail-flick muscle in the rat. We also investigated whether these interneurons also contribute to ascending somatosensory pathways. Two to five days after injection of pseudorabies virus into the left abductor caudae dorsalis muscle, and cholera toxin B into the right somatosensory thalamus and midbrain, rats were perfused and spinal cord sections processed immunohistochemically in a two-step procedure to stain cholera toxin B-immunoreactive cells black and pseudorabies virus-immunoreactive cells brown. ⋯ We also suggest that some lamina II cells are presynaptic to lamina I cells that project directly to abductor caudae dorsalis motoneurons. We observed cholera toxin B-immunoreactive cells (five to 20/section) in the expected locations (contralateral lamina I, deep dorsal horn and intermediate zone; lateral spinal nucleus bilaterally). Double-labeled (i.e. pseudorabies virus- and cholera toxin B-immunoreactive) neurons were only occasionally seen in the lateral spinal nucleus and were absent in the spinal gray matter, indicating that segmental interneurons do not collateralize in long ascending sensory pathways to the midbrain and somatosensory thalamus.