Neuroscience
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Placebo analgesia has great potential to overcome the inadequacies of current drug therapies to treat conditions of chronic pain. The rostral ventromedial medulla (RVM) has been implicated as a critical relay in the antinociceptive pathway underpinning placebo analgesia in humans. We developed a model of opiate-conditioned placebo analgesia in rats with neuropathic injury to identify medullary nuclei active during placebo analgesia. ⋯ We detected injury-specific c-Fos expression in the gracile nucleus and morphine-specific c-Fos expression in the serotonergic midline raphe nuclei and the caudal nuclei of the solitary tract. However, c-Fos expression did not differ between placebo reactors and non-reactors in either serotonergic or non-serotonergic neurons of the RVM. Despite a subpopulation of rats demonstrating placebo reactions, we found no evidence for enhanced activity in the nuclei from which the classical RVM → spinal cord descending analgesic pathways emerge.
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Developmental cortical malformations (DCM) are one of the main causes of refractory epilepsy. Many are the mechanisms underlying the hyperexcitability in DCM, including the important contribution of N-methyl-D-aspartate receptors (NMDAR). NMDAR blockers are shown to abolish seizures and epileptiform activity. ⋯ The video-EEG analyses revealed that the number of seizures and the total duration of stage IV-V seizures developed during the 1 h-period increased after memantine application in all groups. The EEG power spectral density (PSD) analysis showed an increased PSD of pre-ictal delta in Sham-M animals and increased PSD of slow, middle and fast gamma oscillations after memantine injection that persists during the pre-ictal period in all groups. Our findings suggested that memantine was unable to control the PTZ-induced seizures and that the associated enhancement of PSD of gamma oscillations may contribute to the increased probability of seizure development in these animals.
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Retracted Publication
Sustained hypoxia reduces GABAergic modulation on NTS neurons sending projections to ventral medulla of rats.
Peripheral chemoreflex is activated during short-term sustained hypoxia (SH), and the first synapse of these afferents is located in Nucleus Tractus Solitarius(NTS). NTS neurons projecting to the ventral lateral medulla (NTS-VLM) are part of the respiratory pathways of the chemoreflex. SH increases the magnitude of basal respiratory parameters in rats from Wistar-Hannover strain. ⋯ The data are showing that: (a) the amplitude of evoked inhibitory currents in NTS-VLM neurons of SH rats was reduced and not accompanied by any change in rise-time and decay-time; (b) the 1/CV2 and the number of failures in response to evoked currents were also affected by SH; (c) the frequency of spontaneous inhibitory currents was reduced by SH without changes in amplitude and half-width. These effects of SH were observed in NTS-VLM neurons located in caudal and intermediate NTS, but not in NTS-VLM neurons located in the rostral NTS. We conclude that SH causes a reduction in inhibitory modulation onto NTS-VLM neurons by pre-synaptic mechanisms, which may contribute to the observed changes in the respiratory pattern of Wistar-Hannover rats submitted to SH.