Neuroscience bulletin最新文献

Sleep deprivation has been shown to exacerbate pain sensitivity and may contribute to the onset of chronic pain, yet the precise neural mechanisms underlying this association remain elusive. In our study, we explored the contribution of cholinergic neurons within the medial habenula (MHb) to hyperalgesia induced by sleep deprivation in rats. Our findings indicate that the activity of MHb cholinergic neurons diminishes during sleep deprivation and that chemogenetic stimulation of these neurons can mitigate the results. Interestingly, we did not find a direct response of MHb cholinergic neurons to pain stimulation. Further investigation identified the interpeduncular nucleus (IPN) and the paraventricular nucleus of the thalamus (PVT) as key players in the pro-nociceptive effect of sleep deprivation. Stimulating the pathways connecting the MHb to the IPN and PVT alleviated the hyperalgesia. These results underscore the important role of MHb cholinergic neurons in modulating pain sensitivity linked to sleep deprivation, highlighting potential neural targets for mitigating sleep deprivation-induced hyperalgesia.

In neurons and myocytes, selective ion channels in the plasma membrane play a pivotal role in transducing chemical or sensory stimuli into electrical signals, underpinning neural and cardiac functionality. Recent advancements in biomedical research have increasingly spotlighted the interaction between ion channels and electromagnetic fields, especially terahertz (THz) radiation. This review synthesizes current findings on the impact of THz radiation, known for its deep penetration and non-ionizing properties, on ion channel kinetics and membrane fluid dynamics. It is organized into three parts: the biophysical effects of THz exposure on cells, the specific modulation of ion channels by THz radiation, and the potential pathophysiological consequences of THz exposure. Understanding the biophysical mechanisms underlying these effects could lead to new therapeutic strategies for diseases.

Previous studies have proposed two cognitive mechanisms responsible for the Ebbinghaus illusion effect, i.e., contour interaction and size contrast. However, the neural underpinnings of these two mechanisms are largely unexplored. The present study introduced binocular depth to the Ebbinghaus illusion configuration and made the central target appear either in front of or behind the surrounding inducers in order to disturb size contrast instead of contour interaction. The results showed that the illusion effect, though persisted, was significantly reduced under the binocular depth conditions. Notably, the target with a larger perceived size reduced early alpha-band power (8-13 Hz, 0-100 ms after stimulus onset) at centroparietal sites irrespective of the relative depth of the target and the inducers, with the parietal alpha power negatively correlated with the illusion effect. Moreover, the target with a larger perceived size increased the occipito-parietal beta-band power (14-25 Hz, 200-300 ms after stimulus onset) under the no-depth condition, and the beta power was positively correlated with the illusion effect when the depth conditions were subtracted from the no-depth condition. The findings provided neurophysiological evidence in favor of the two cognitive mechanisms of the Ebbinghaus illusion by revealing that early alpha power is associated with low-level contour interaction and late beta power is linked to high-level size contrast, supporting the claim that neural oscillations at distinct frequency bands dynamically support different aspects of visual processing.

Nicotine addiction is a concern worldwide. Most mechanistic investigations are on nicotine substance dependence properties based on its pharmacological effects. However, no effective therapeutic treatment has been established. Nicotine addiction is reinforced by environments or habits. We demonstrate the neurobiological basis of the behavioural aspect of nicotine addiction. We utilized the conditioned place preference to establish nicotine-associated behavioural preferences (NABP) in rats. Brain-wide neuroimaging analysis revealed that the medial prefrontal cortex (mPFC) was activated and contributed to NABP. Chemogenetic manipulation of µ-opioid receptor positive (MOR⁺) neurons in the mPFC or the excitatory outflow to the nucleus accumbens shell (NAcShell) modulated the NABP. Electrophysiological recording confirmed that the MOR⁺ neurons directly regulate the mPFC-NAcShell circuit via GABA_A receptors. Thus, the MOR⁺ neurons in the mPFC modulate the formation of behavioural aspects of nicotine addiction via direct excitatory innervation to the NAcShell, which may provide new insight for the development of effective therapeutic strategies.