Neuroscience letters
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Neuroscience letters · May 1998
Sevoflurane suppresses behavioral response in the rat formalin test: combination with intrathecal lidocaine produced profound suppression of the response.
We investigated the effects of intrathecal (i.t.) lidocaine, inhalation sevoflurane, and a combination of i.t. lidocaine and sevoflurane on the formalin test in rats. Group 1 (control) received i.t. saline 10 microl. Groups 2 and 3 received i.t. lidocaine 200 microg and 400 microg, respectively. ⋯ Group 7 received i.t. lidocaine 200 microg and 1.2% sevoflurane. The biphasic behavioral activity of the hindpaw of rats was observed. This study showed that i.t. lidocaine or inhalation sevoflurane before formalin injection, significantly suppressed the behavioral activity of the hindpaw of rats, and that this suppression was significantly potentiated by the co-administration of i.t. lidocaine and inhalation sevoflurane.
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Neuroscience letters · May 1998
Effect of spinal cord stimulation on tactile hypersensitivity in mononeuropathic rats is potentiated by simultaneous GABA(B) and adenosine receptor activation.
In rats with abnormally low withdrawal thresholds ('allodynia') in one hindpaw induced by a photochemical sciatic lesion, an intrathecal catheter was inserted to the lumber enlargement and an epidural electrode was implanted at T11. I.t. administration of GABA(B) or adenosine A1 receptor agonists (baclofen, R(-)-N6-(2-phenylisopropyl)adenosine (R-PIA)) suppressed allodynia in a dose-dependent fashion. ⋯ In SCS responding rats, combination of a selective GABA(B) and an adenosine A1 receptor antagonist (CGP 55845, CPT) in low, ineffective doses abolished the SCS-induced threshold normalization. These results indicate that GABAergic and adenosine-dependent mechanisms are involved in the SCS effect and further suggest a strategy for enhancing the therapeutic efficacy of SCS.
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Neuroscience letters · May 1998
Motor denervation induces altered muscle fibre type densities and atrophy in a rat model of neuropathic pain.
Loose ligation of a sciatic nerve in rats (chronic constriction injury; CCI) provokes sensory, autonomic, and motor disturbances like those observed in humans with partial peripheral nerve injury. So far, it is unknown whether these motor disturbances result from (mechanical) allodynia or from damage to the motor neuron. These considerations prompted us to assess, in CCI rats, the density of motor axons in both the ligated sciatic nerve and the ipsilateral femoral nerve. ⋯ In line with these findings, we observed altered fibre type densities in muscle tissue innervated by the ligated sciatic nerve as well as the non-ligated femoral nerve indicative of motor denervation rather than hypokinesia. The findings of this study suggest that the motor disorder induced by partial nerve injury involves degeneration of motor nerve fibres not only within the primarily affected nerve but also within adjacent large peripheral nerves. This spread outside the territory of the primarily affected nerve suggests degeneration of motor neurons at the level of the central nervous system.