Neuroscience
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Neurons within the superficial dorsal horn (SDH) of the rodent spinal cord exhibit distinct firing properties during early life. While this may reflect a unique combination of voltage-gated Na(+) (Na(v)) and voltage-independent (i.e. "leak'') K(+) channels which strongly influence neuronal excitability across the CNS, surprisingly little is known about which genes encoding for Na(v) and leak K(+) channels are expressed within developing spinal pain circuits. The goal of the present study was therefore to characterize the transcriptional expression of these channels within the rat SDH at postnatal days (P) 3, 10, 21 or adulthood using quantitative real-time polymerase chain reaction. ⋯ In addition, a developmental shift occurred within the TREK subfamily due to decreased TREK-2 (KCNK10) mRNA within the mature SDH. Meanwhile, G-protein-coupled inward rectifying K(+) channels (K(ir)3.1 and K(ir)3.2) were expressed in the SDH at mature levels from birth. Overall, the results suggest that the transcription of ion channel genes occurs in a highly age-dependent manner within the SDH, raising the possibility that manipulating the expression or function of ion channels which are preferentially expressed within immature nociceptive networks could yield novel approaches to relieving pain in infants and children.
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We tested a hypothesis that the classical relation between movement time and index of difficulty (ID) in quick pointing action (Fitts' Law) reflects processes at the level of motor planning. Healthy subjects stood on a force platform and performed quick and accurate hand movements into targets of different size located at two distances. The movements were associated with early postural adjustments that are assumed to reflect motor planning processes. ⋯ The magnitude of postural adjustments prior to movement initiation scaled with ID for both short and long distances. Our results provide strong support for the hypothesis that Fitts' Law emerges at the level of motor planning, not at the level of corrections of ongoing movements. They show that, during natural movements, changes in movement distance may lead to changes in the relation between movement time and ID, for example when the contribution of different body segments to the movement varies and when the action of Coriolis force may require an additional correction of the movement trajectory.
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Biofeedback training is an efficient means to gain control over a physiological function typically considered involuntary. Accordingly, learning to self-regulate nociceptive physiological activity may improve pain control by activating endogenous modulatory processes. The aim of the present study was to assess whether trial-by-trial visual feedback of nociceptive flexion reflex (RIII-reflex) responses (an index of spinal nociception) evoked by brief painful shocks applied to the sural nerve could be beneficial to guide participants in adopting strategies aiming at modulating pain perception. ⋯ The biofeedback group was not significantly superior to the sham and the control groups in the modulation of RIII-reflex amplitude, pain intensity or unpleasantness. These results are consistent with the notion that RIII-reflex amplitude and pain perception can be modulated voluntarily by various cognitive strategies. However, immediate retrospective visual feedback of acute nociceptive responses presented iteratively in successive trials may not improve the efficacy of these self-regulation processes.
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The relationship between learning/memory performance and long-term potentiation (LTP) induction is ambiguous. Although a large body of data supports a strong correspondence between learning/memory performance and LTP, many studies have also provided evidence to the contrary. In this study, we found that 2-month-old senescence-accelerated mice/prone 8 (SAMP8 mice) displayed both impaired performance in a Morris Water Maze (MWM) and enhanced LTP compared to senescence-accelerated mice/resistance 1 (SAMR1). ⋯ Further analysis demonstrated that the increase in cytokine content was higher in the hippocampal tissues used for LTP recording in the SAMR1 and CFA-challenged animals compared to the SAMP8 and intact BALB/c mice. A correlation analysis demonstrated that pro-inflammatory cytokines (IL-6 and TNF-α) displayed a negative correlation with LTP, while an anti-inflammatory cytokine (IL-10) displayed a positive correlation with LTP. These results suggest that pro-inflammatory cytokines induced by LTP manipulation in experiments (e.g., via tissue injury caused by electrode insertion) may be one of the factors contributing to the observed lack of correspondence between memory/learning ability and LTP.
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There is accumulating evidence that glutamate and GABA release are key mechanisms of ischaemic events in the CNS. However, data on the expression of involved transporters for these mediators are inconsistent, potentially impeding further neuroprotective approaches. Here, we applied immunofluorescence labelling to characterise the expression pattern of vesicular glutamate (VGLUT) and GABA transporters (VGAT) after acute focal cerebral ischaemia and in two models of retinal ischaemia. ⋯ In contrast, retinae subjected to CRAO or HIOP displayed a rapid loss of VGLUT3-immunoreactivity. The expression of VGAT appears resistant to ischaemia as there was no significant alteration in all the regions analysed. In summary, these data indicate a region- and subtype-specific change of VGLUT expression in the ischaemia-affected CNS, whose consideration might help to generate specific neuroprotective strategies.