Neuroscience
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Patients sometimes complain that non-vital teeth after root canal treatment (RCT) are paresthesia compared with vital teeth, and previous psychological studies on the tactile sensibility of non-vital teeth remained controversial. In the present study, intrinsic signal optical imaging, which served as an objective tool, was employed to compare the cortex response characteristics following forces applied to the cat non-vital and vital canines. Based on the evoked cortical responses, the response threshold, signal strength, spatial pattern, temporal dynamics and the preference of force direction, they were not significantly different between vital and non-vital canines. It seemed that the tactile sensibility of vital and non-vital teeth was comparable at the cortical response level, and pulpal receptors were not concerned in tactile function.
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Obstructive sleep apnea (OSA) is accompanied by altered structure and function in cortical, limbic, brainstem, and cerebellar regions. The midbrain is relatively unexamined, but contains many integrative nuclei which mediate physiological functions that are disrupted in OSA. We therefore assessed the chemistry of the midbrain in OSA in this exploratory study. ⋯ Higher Asc levels may result from oxidative stress induced by intermittent hypoxia in OSA. Additionally, Asc and Glu are involved with glutamatergic processes, which are likely upregulated in the midbrain nuclei of OSA patients. The altered metabolite levels help explain dysfunction and structural deficits in the midbrain of OSA patients.
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Behavioral effects of transcranial magnetic stimulation (TMS) have been shown to depend on various factors, such as neural activation state, stimulation intensity, and timing of stimulation. Here we examined whether these factors interact, by applying TMS at either sub- or suprathreshold intensity (relative to phosphene threshold, PT) and at different time points during a state-dependent TMS paradigm. The state manipulation involved a behavioral task in which a visual prime (color grating) was followed by a target stimulus which could be either congruent, incongruent or partially congruent with the color and orientation of the prime. ⋯ Only TMS applied at suprathreshold intensity facilitated the detection of incongruent stimuli, with no effect with subthreshold stimulation. The need for higher stimulation intensity is likely to reflect reduced susceptibility to TMS of neurons responding to visual stimulation. Furthermore, the finding that in Experiment 2 only suprathreshold TMS induced a behavioral facilitation on incongruent targets (whereas facilitations in the absence of priming have been reported with subthreshold TMS) indicates that priming, by reducing neural excitability to incongruent targets, shifts the facilitatory/inhibitory range of TMS effects.
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Odors are typically bimodal in nature, interacting with the olfactory and trigeminal systems. The trigeminal component may be noticed (e.g. menthol) or perceptually ignored, leading to different neural substrates being recruited during odor encoding. Therefore, the current study was designed to explore the perceptual and central-nervous activations in response to pleasant bimodal odors using functional magnetic resonance imaging (fMRI). ⋯ This includes large bilateral activations within the OFC, insula, cerebellum and parts of the cingulate cortex. Additionally, activation of the thalamus was seen early in the stages of bimodal odor encoding suggesting its role of mediating attention toward the presence of two stimuli. Lastly, intensity encoding during bimodal processing shows overlap of previously demonstrated simple trigeminal encoding areas (medial cingulate cortex) and the more complex olfactory encoding areas (bilateral insula, superior temporal gyrus, OFC, and cerebellum), but not the amygdala.
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Neuroprotection is an unmet need in eye disorders characterized by retinal ganglion cell (RGC) death, such as prematurity-induced retinal degeneration, glaucoma, and age-related macular degeneration. In all these disorders excitotoxicity is a prominent component of neuronal damage, but clinical data discourage the development of NMDA receptor antagonists as neuroprotectants. Here, we show that activation of mGlu1 metabotropic glutamate receptors largely contributes to excitotoxic degeneration of RGCs. ⋯ We also injected MSG to crv4 mice, which lack mGlu1 receptors because of a recessive mutation of the gene encoding the mGlu1 receptor. MSG did not cause retinal degeneration in crv4 mice, whereas it retained its toxic activity in their wild-type littermates. These findings demonstrate that mGlu1 receptors play a key role in excitotoxic degeneration of RGCs, and encourage the study of mGlu1 receptor NAMs in models of retinal neurodegeneration.