Brain research
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We examined the effect of the peripheral application of glutamate and capsaicin to the temporomandibular joint (TMJ) in influencing the activation and central sensitization of TMJ-responsive nociceptive neurons in the trigeminal subnucleus caudalis/upper cervical cord (Vc/UCC). The activity of single neurons activated by noxious mechanical stimulation of the TMJ was recorded in the Vc/UCC of 49 halothane-anesthetized male rats. Cutaneous mechanoreceptive field (RF), cutaneous mechanical activation threshold (MAT), and TMJ MAT of each neuron were assessed before and after injection of 0.5 M glutamate (or vehicle) and 1% capsaicin (or vehicle) into the TMJ. ⋯ W., 2008a. Glutamate and capsaicin effects on trigeminal nociception I: activation and peripheral sensitization of deep craniofacial nociceptive afferents. Brain Res. doi:10.1016/j.brainres.2008.11.029], suggesting that peripheral and central sensitization may be differentially involved in the nociceptive effects of glutamate and capsaicin applied to deep craniofacial tissues.
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Threatening stimuli are thought to bias spatial attention toward the location from which the threat is presented. Although this effect is well-established in the visual domain, little is known regarding whether tactile attention is similarly affected by threatening pictures. We hypothesised that tactile attention might be more affected by cues implying physical threat to a person's bodily tissues than by cues implying general threat. ⋯ By contrast, the bias in auditory attention toward the side of the picture was significantly larger for general threat pictures than for physical threat pictures or neutral pictures. These findings therefore demonstrate a modality-specific effect of physically threatening cues on the processing of tactile stimuli, and of generally threatening cues on auditory information processing. These results demonstrate that the processing of tactile information from the body part closest to the threatening stimulus is prioritized over tactile information from elsewhere on the body.
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In tauopathies such as Alzheimer's disease (AD), the molecular mechanisms of tau protein aggregation into neurofibrillary tangles (NFTs) and their contribution to neurodegeneration remain not understood. It was recently demonstrated that tau, regardless of its aggregation, might represent a key mediator of neurodegeneration. Therefore, reduction of tau levels might represent a mechanism of neuroprotection. ⋯ These data indicate that GSK3beta might be selectively involved in the regulation of tau protein levels. Moreover, inhibition of PP2A by okadaic acid, but not that of PP2B (protein phosphatase-2B)/calcineurin by FK506, dose-dependently reversed lithium-induced tau decrease. These data indicate that GSK3beta regulates both tau phosphorylation and total tau levels through PP2A.