Neuroscience letters
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Neuroscience letters · Jul 1999
Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy.
We investigated whether interleukin-1 (IL-1), a mediator of inflammatory pain, also plays a role in pain induced by nerve injury. Female C57BL/6-mice with a chronic constrictive injury of one sciatic nerve, an established model of neurogenic hyperalgesia and allodynia, were treated with different doses (10-80 microg) of a neutralizing monoclonal rat antibody to IL-1 receptor I (anti-IL-1RI). ⋯ Degeneration of myelinated fibers was not altered by any of the treatment schedules. We conclude that IL-1 may be a mediator of hyperalgesia after nerve lesion.
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Neuroscience letters · Jul 1999
Is sympathetic sprouting in the dorsal root ganglia responsible for the production of neuropathic pain in a rat model?
Partial peripheral nerve injury often results in neuropathic pain that is aggravated by sympathetic excitation and induces sympathetic nerve sprouting in both the injured nerve and corresponding dorsal root ganglia (DRGs). Presently, the functional mechanisms of the interactions between the sprouting and injured somatic afferents remain uncertain. ⋯ Immuno-histochemical staining with tyrosine hydroxylase (TH) antibody of the injured S1 DRG taken from both groups of rats after behavioral tests revealed that the magnitude of penetration of TH-positive fibers into the S1 DRG was not significantly different between the two groups. These results suggest that sympathetic nerve sprouting in the injured DRG is not a key factor in the development of neuropathic pain.
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Neuroscience letters · Jul 1999
Lidocaine produces a shunt in rat [correction of rats] thalamocortical neurons, unaffected by GABA(A) receptor blockade.
Low concentrations of lidocaine reversibly decrease input resistance and shunt action potentials in neurons of the ventral posterolateral thalamic nucleus (VPL) in vitro. Using differential interference contrast infrared videomicroscopy and whole-cell patch-clamp techniques in rat brain slices, we studied the effects of bicuculline methobromide to test whether the lidocaine-induced shunt in VPL neurons is mediated by GABA(A) receptors. ⋯ Likewise, bicuculline did not affect the shunt-induced reductions of spike-afterhyperpolarizations produced by lidocaine. The results of this study imply that the effects of low lidocaine concentrations in thalamocortical neurons are not mediated by GABA(A) receptors.