Brain research
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Comparative Study
Sensory fibers containing vanilloid receptor-1 (VR-1) mediate spinal cord stimulation-induced vasodilation.
Spinal cord stimulation (SCS) is used to improve peripheral blood flow in selected populations of patients with ischemia of the extremities. Previous studies show that antidromic activation of sensory fibers is an important mechanism that contributes to SCS-induced vasodilation. However, the characteristics of sensory fibers involved in vasodilation are not fully known. This study investigated the contribution of vanilloid receptor type 1 (VR-1) containing fibers to SCS-induced vasodilation. ⋯ SCS-induced vasodilation is predominantly mediated via VR-1 containing sensory fibers.
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Blockage of the salivary duct can produce pain and inflammation from the build up of saliva in the parotid gland. The processing of parotid inflammation-induced pain, however, is poorly understood. The purpose of this study was to clarify the functional involvement of the trigeminal subnucleus interpolaris/caudalis transition region (Vi/Vc) and upper cervical spinal cord (C1/C2) in processing nociceptive input relevant to parotitis. ⋯ Receptive field sizes also increased in C1/C2 but not Vi/Vc neurons. At the Vi/Vc transition region, pinch-evoked activity increased in neurons receiving convergent inputs from the parotid gland and facial skin when compared to non-convergent neurons. The present data indicate that the hyperalgesia and referred pain associated with parotitis may result from sensitization of C1/C2, but not Vi/Vc nociceptive neurons.
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The proliferative activity of neural precursors from the subventricular zone (SVZ) was investigated after a unilateral lesion was formed in the nigrostriatal pathway in adult rats. The lesion was formed by unilateral injection of 6-hydroxydopamine (6-OHDA) into the nigrostriatal pathway, and then bromodeoxyuridine (BrdU) was injected (ip) for 4 days or 2 weeks 10 days after the lesion was formed. The rats were killed, and the brain sections were immunohistochemically stained to detect the expression of BrdU, polysialylated neural-cell-adhesion molecule (PSA-NCAM), glial fibrillary acidic protein (GFAP) and tyrosine hydroxylase (TH) in the SVZ and the striatum (STR). ⋯ The number of positive cells decreased at 4 weeks after the lesion was formed. The number of nigrostriatal projections with TH(+) decreased significantly in the STR on the lesion side, and the level of decrease was related to the quantity of BrdU-labeled cells at 2 weeks. These results indicate that the neural precursors in the SVZ of adult rats may increase after a lesion has been formed in the nigrostriatal pathway, and these cells might migrate into the STR on the same side.
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Comparative Study
The good, the bad and the neutral: electrophysiological responses to feedback stimuli.
The feedback error-related negativity (fERN) is a component of the event-related brain potential elicited in gambling and trial-and-error learning tasks by negative, but not positive, feedback stimuli. Here, we present the results of a series of five experiments that investigated the response of the fERN to the presentation of neutral feedback stimuli. ⋯ Across the five experiments, we found that neutral feedback stimuli elicited a fERN about as large as that elicited by negative feedback stimuli. This result is consistent with recent proposals that the evaluative system that produces the fERN classifies outcomes into two categories: those outcomes that indicate that a goal has been satisfied and those that do not.
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We wished to determine the ability of radiolabeled annexin V to concentrate at sites of ischemic injury in patients with acute cerebral stroke. Secondly, we sought to correlate annexin V imaging in these patients with the degree of blood-brain barrier (BBB) breakdown. ⋯ This study shows that it is possible to identify in vivo regions of ischemic neuronal injury using radiolabeled annexin V in patients with acute stroke. Annexin imaging can play a major role in the selection of therapy in the initial period following stroke in adults.