Neuroscience
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Neuropathic pain is a complication after a spinal nerve injury. The inflammasomes are now identified to be responsible for triggering inflammation in neuropathic pain. Autophagy participates in the process of neuropathic pain and can regulate the inflammasome activation in different diseases. ⋯ The absence of autophagy aggravated the inflammasome activity and hyperpathia. Hydrogen promoted autophagy related protein expression, inhibited the inflammasome NLRP3 pathway activation, and relieved the hyperpathia induced by neuropathic pain. Hydrogen treatment could alleviate hyperpathia by autophagy-mediated NLRP3 inactivation.
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Review
The Control of Neuronal Calcium Homeostasis by SNAP-25 and its Impact on Neurotransmitter Release.
The process of neurotransmitter release is central to the control of cell-to-cell communication in brain. SNAP-25 is a component of the SNARE complex, which, together with syntaxin-1 and synaptobrevin, mediates synaptic vesicle fusion with the plasma membrane. ⋯ Consistently, reduced levels of the protein affect presynaptic calcium homeostasis and result in pathologically enhanced glutamate exocytosis. The SNAP-25-dependent alterations of synaptic calcium dynamics may have direct impact on the development of neuropsychiatric disorders where the Snap-25 gene has been found to be involved.
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Training inhibitory control, the ability to suppress motor or cognitive processes, not only enhances inhibition processes, but also reduces the perceived value and behaviors toward the stimuli associated with the inhibition goals during the practice. While these findings suggest that inhibitory control training interacts with the aversive and reward systems, the underlying spatio-temporal brain mechanisms remain unclear. We used electrical neuroimaging analyses of event-related potentials to examine the plastic brain modulations induced by training healthy participants to inhibit their responses to rewarding (pleasant chocolate) versus aversive food pictures (unpleasant vegetables) with Go/NoGo tasks. ⋯ The electrophysiological results also revealed an interaction between reward responses and inhibitory control plasticity: we observed different effects of practice on the rewarding vs. aversive NoGo stimuli at 200 ms post-stimulus onset, when the conflicts between automatic response tendency and task demands for response inhibition are processed. Electrical source analyses revealed that this effect was driven by an increase in right orbito-cingulate and a decrease in temporo-parietal activity to the rewarding NoGo stimuli and the reverse pattern to the aversive stimuli. Our collective results provide direct neurophysiological evidence for interactions between stimulus reward value and executive control training, and suggest that changes in the assessment of stimuli with repeated motoric inhibition likely follow from associative learning and behavior-stimulus conflicts reduction mechanisms.
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Synaptosomal Associated Protein of 25 kD (SNAP-25) is an essential protein contributing 2 out of 4 α-helices in the formation of the core soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex which mediates regulated membrane fusion. Regulated exocytosis is a strictly controlled event in eukaryotic cells mediating important homeostatic processes and cellular communications. Altered release of neurotransmitters or hormones is usually considered as part of the progressing pathophysiology of central neurological or peripheral metabolic disorders. ⋯ SNAP-25b-deficient mice demonstrated alterations in synaptic transmission and increased insulin secretion which, with time, spontaneously progressed into a pronounced metabolic disease, including defects in glucose homeostasis, obesity, liver steatosis and perturbations in central homeostatic signaling. Thus, deregulated function of SNAP-25 and possibly other SNAREs or SNARE-interacting proteins, can, by itself, act as risk factors for the development of metabolic disease. Here, we provide an overview of the peripheral and central consequences of the deregulations in core SNARE complex with focus on SNAP-25.