Neuroscience
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Focal injection of a minute quantity of tetanus toxin into the rat neocortex induces chronic epileptogenesis. Within a day, spontaneous and stimulus-evoked paroxysmal discharges appear in widespread regions of both hemispheres and this lasts for at least nine months. Tetanus toxin blocks transmitter release, apparently by catalysing the breakdown of synaptobrevin, a synaptic protein. ⋯ At earlier times (1.5 days) after the toxin injection, however, release was significantly depressed in both hemispheres. The results indicate that at first, the toxin induces focal neocortical epileptogenesis by directly impeding GABAergic synaptic transmission but that with time there is a recovery from this initial effect. We propose, as has also been suggested for other models, that the initial epileptogenesis leaves in its wake a long-lasting change in the local functional connectivity, such that the neocortex is rendered permanently epileptic.
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Thermal hyperalgesia was induced by UV irradiation of the glabrous skin of the hindpaw of adult female Sprague-Dawley rats. We have recorded single cell activity and studied excitability changes in wide dynamic range neurons in the lumbar spinal segments during the early phase (days 1-3) and late phase (days 5-7) of thermal hyperalgesia in animals under urethane anaesthesia. The proportion of spontaneously active wide dynamic range cells was increased following UV irradiation and the degree of spontaneous activity was enhanced during the course of hyperalgesia. ⋯ Cutting the dorsal roots (L2-5) evoked a significantly larger and more prolonged discharge in wide dynamic range cells in both UV-treated groups in comparison to control. Spontaneous activity in spinal wide dynamic range neurons was reduced after rhizotomy in each group. However, the decrease was only significant at days 1-3 (P < 0.05) but not at days 5-7.(ABSTRACT TRUNCATED AT 250 WORDS)
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Nerve terminals as well as glial cells are thought to possess high-affinity Na(+)-dependent transport sites for excitatory amino acids. However, recent immunocytochemical results with antibodies against such a transporter isolated from rat brain showed a selective labelling of glial cells [Danbolt et al. (1992) Neuroscience 51, 295-310]. Critical evaluation of the literature indicates that previous evidence for nerve terminal uptake of acidic amino acids might possibly be attributed to glia. ⋯ At the light-microscopic level the D-aspartate-like immunoreactivity showed a distinct laminar distribution, identical to that shown autoradiographically for D-[3H]aspartate and L-[3H]glutamate uptake sites [Taxt and Storm-Mathisen (1984) Neuroscience 11, 79-100], and corresponding to the terminal fields of the major excitatory fibre systems in the hippocampal formation. The novel approach described here establishes that glutamatergic nerve terminals as well as glia do sustain sodium-dependent high-affinity transport of excitatory amino acids, implying that more than one glutamate transporter must be present in the brain. Immunogold detection of D-aspartate gives a much higher anatomical resolution than electron microscopic autoradiography of D-[3H]aspartate or L-[3H]glutamate uptake, the only method that has been available previously for ultrastructural demonstration of uptake activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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It is now well established that the expression of peptides in rat primary sensory neurons is dramatically changed in response to peripheral nerve injury. Thus, as first shown by Jessell et al. peripheral axotomy causes a decrease in substance P levels in the dorsal horn of the corresponding spinal cord segments, and this is due to down-regulation of peptide synthesis in dorsal root ganglion neurons. In contrast, other peptides such as vasoactive intestinal polypeptide and peptide histidine isoleucine, galanin and neuropeptide Y are all markedly upregulated in the rat L4 and L5 dorsal root ganglia after sciatic nerve sectioning. ⋯ During the last few years a number of peptide receptors have been cloned, and they all belong to the family of G-protein coupled receptors with seven membrane spanning segments, among them the two cholecystokinin receptors cholecystokininA and cholecystokininB. Ghilardi et al. have recently described presence of cholecystokininB binding sites in rat dorsal root ganglia neurons. In the present study we report that the messenger RNA for the cholecystokininB receptor is present at very low levels in normal dorsal root ganglia of the rat, but axotomy causes a very marked increase in the number of sensory neurons of all sizes expressing cholecystokininB receptor messenger RNA, suggesting an increased sensitivity to cholecystokinin for many primary sensory neurons of different modalities after lesion.