Neuroscience
-
The purpose of this study was to examine variations in gut microbes and their metabolites between patients with original and recurrent stroke, providing insights and justification for the diagnosis and prevention of ischemic stroke progression from the perspective of the gut microbiota-metabolite-brain axis. ⋯ Compared with the Os, Rs was mainly characterized by severe destruction of anaerobic bacteria and significant depletion of SCFAs-producing bacteria. In addition, the related compounds involved in arachidonic acid metabolism and linoleic acid metabolism pathway may be biomarkers related to ischemic stroke progression.
-
Endogenous cannabinoids (eCBs) and nitric oxide (NO) are classical retrograde transmitters that modulate synaptic function throughout the brain. Although much is known about how these signals individually control synaptic activity and behavior, accumulating evidence suggests that they can also interact in a multitude of ways in the brain and beyond. Here, we present evidence for interactions between endogenous cannabinoids and nitric oxide in the brain. ⋯ We also provide an overview on how these transmitters work together or in opposition at the same synapses. This information will further our understanding of how two important, ubiquitous signals interact in the brain to ultimately affect neural function and behavior. Because eCBs and NO are involved in many physiological and pathological phenomena, understanding how these transmitters interact in non-human animals could lead to important therapeutic interventions in humans that potentially target both systems.
-
Recent studies have shown that cognitive overload disrupted the affective processing of taste attributes in food-related tasks, which is difficult to explain using dual-system theories with their reflective and impulsive systems (involved in the cognitive and affective processing of stimuli, respectively). The tripartite neurocognitive model proposes an additional interoceptive system that regulates the activities of reflective and impulsive systems. Using this framework, we studied self-control over food choices and hypothesized inferior processing of both affective (taste) and cognitive (health) components of choice-relevant attributes under increased cognitive load. ⋯ We also revealed an expected trend towards a stronger negative connectivity between the right AI and DLPFC in HL compared to LL condition. Our findings suggest that cognitively demanding task concurrent to food self-control task overloads AI and reduces the reinforcement of VS by AI. This helps in explaining how and why the affective processing of taste attributes, together with the cognitive processing of health attributes, may be disrupted under cognitive overload.
-
Exposure to PM2.5 is associated with neurotoxicity and mitochondrial dysfunction. Resveratrol, a natural polyphenol, has demonstrated antioxidant and neuroprotective properties. Still, its efficacy in mitigating PM2.5-induced damage in human neural stem cells (hNSCs) and within a 3D scaffold system remains underexplored. ⋯ Resveratrol can effectively reduce neurotoxicity and mitochondrial dysfunction caused by PM2.5 in hNSCs. Its protective effects against PM2.5-induced toxicity in hNSCs within a 3D bioprinted model highlight this study's translational potential. These findings emphasize its potential as a therapeutic agent against environmental neurotoxins and the development of neuroprotective strategies.
-
Prediabetic neuropathic pain has been classified as peripheral neuropathic pain associated with polyneuropathy caused by impaired glucose tolerance or impaired fasting glucose, which is a preclinical stage and might develop type 2 diabetes mellitus. Our previous research highlighted that prediabetes is accompanied by dramatic bilateral mechanical hyperalgesia following high energy diet (HED) which results in myelin and axonal degenerations along somatosensory system. However, the pathogenic mechanisms underlying prediabetic neuropathic pain remain unclear. ⋯ Moreover, siRNA-SIRT6 treatment induced a significant reduction in bilateral paw withdrawal mechanical thresholds, indicating that SIRT6 down-regulation contributed to prediabetic neuropathic pain induced by HED. Furthermore, it was also found that SIRT6 reduction induced the activation of HMGB1 via disinhibition of NF-κB in both DRG and spinal dorsal horn of prediabetic rats. In conclusion, prediabetic neuropathic pain is caused by SIRT6 reduction through upregulating HMGB1-RAGE signaling at both peripheral and spinal levels.