Experimental neurology
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Experimental neurology · Jan 2010
Clinical TrialBilateral symmetry and coherence of subthalamic nuclei beta band activity in Parkinson's disease.
Abnormal synchronization of neuronal activity in the basal ganglia has been associated with the dysfunction of sensorimotor circuits in Parkinson's disease (PD). In particular, oscillations at frequencies within the beta range (13-35 Hz) are specifically modulated by dopaminergic medication and are correlated with the clinical state of the subjects. ⋯ Here we demonstrate for the first time that the beta band oscillations recorded in the local field potential of the subthalamic nuclei (STN), while appearing different across subjects, are occurring at the same frequencies bilaterally (p<0.001) and are coherent between the two STNs of individual PD subjects (11/12 cases, p<0.05). These findings suggest the existence of a bilateral network controlling the beta band activity in the basal ganglia in PD.
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Experimental neurology · Jan 2010
Clinical TrialMechanical but not painful electrical stimuli trigger TNF alpha release in human skin.
Pro-inflammatory cytokines-in particular tumor necrosis factor (TNF)-alpha-play an important role in pain and hyperalgesia. The stimuli inducing TNF-alpha release in humans and the time course of this release are largely unknown. We performed dermal microdialysis in healthy subjects (n=36) during three experimental conditions: The first condition (control) was microdialysis without stimulation, the second condition was 30 min of electrical current stimulation (1 Hz, 20 mA, moderately painful), the third condition was 30 min of repetitive mechanical stimulation via an impact stimulator (bullet 0.5 g; velocity 11 m/s, minimally painful). ⋯ Flare intensity was highest in the electrical current stimulation condition and only marginally different from control in mechanical stimulation. Our results show that minimal mechanical trauma is sufficient to induce significant TNF-alpha release in the skin. These results may be relevant to the treatment of posttraumatic pain disorders.
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Experimental neurology · Jan 2010
Chronic treatment with agonists of beta(2)-adrenergic receptors in neuropathic pain.
Expression of beta(2)-adrenoceptors (beta(2)-ARs) within the nociceptive system suggested their potential implication in nociception and pain. Recently, we demonstrated that these receptors are essential for neuropathic pain treatment by antidepressant drugs. The aim of the present study was to investigate whether the stimulation of beta(2)-ARs could in fact be adequate to alleviate neuropathic allodynia. ⋯ This action of beta(2)-AR agonists might implicate the endogenous opioid system; indeed chronic clenbuterol effect can be acutely blocked by the delta-opioid receptor antagonist naltrindole. Present results show that beta(2)-ARs are not only essential for the antiallodynic action of antidepressant drugs on sustained neuropathic pain, but also that the stimulation of these receptors is sufficient to relieve neuropathic allodynia in a murine model. Our data suggest that beta(2)-AR agonists may potentially offer an alternative therapy to antidepressant drugs for the chronic treatment of neuropathic pain.
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Complex regional pain syndrome (CRPS) is a pain disorder involving the somatosensory, the somatomotor and the sympathetic nervous systems. Based on experiments conducted by Bove (2009), it is suggested that changes in impulse activity in small-diameter afferents and postganglionic axons generated by neuritis can contribute to signs of early CRPS. The potential mechanisms involved are discussed. These mechanisms include the possibility that CRPS, a disorder of the central nervous system, may be caused by a nerve inflammation.
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Experimental neurology · Dec 2009
Influence of the vanilloid receptor TRPV1 on the activation of spinal cord glia in mouse models of pain.
Although activation of spinal glia has been implicated in the development of pathological pain, the mechanisms underlying glial activation are not fully understood. One such mechanism may be triggered by reaction to neuroactive substances released from central axons of sensory afferents. ⋯ We found that (i) naïve KO mice had denser immunostaining for both Iba1 and GFAP than naive WT mice; (ii) the immunostaining for Iba1 increased significantly in treated mice, compared to naïve mice, 3 days after capsaicin and 7-14 days after AIA or PSNL, and was significantly greater in WT than in KO mice 3 days after capsaicin, 7-14 days after AIA, and 7 days after PSNL; and iii) the immunostaining for GFAP increased significantly in treated mice, compared to naïve mice, 3 days after capsaicin and 14-21 days after AIA or PSNL, and was significantly greater in WT than in KO mice 14 days after AIA or PSNL. Our results suggest that TRPV1 plays a role in the activation of spinal glia in mice with nociceptive, inflammatory, and neuropathic pain.