Neuroscience最新文献

Transient receptor vanillin 1 (TRPV1) is widely expressed in the neural axis and surrounding tissues, and is easily activated by harmful stimuli such as pain and inflammatory responses. Previous studies have shown that activated TRPV1 channels regulate all levels of nervous system activity by improving calcium influx and modulating nervous system excitability. Recent studies have suggested that TRPV1 activation in the peripheral nervous system may induce sleep disorders, while activation in the central nervous system may ameliorate sleep disorders and assist memory consolidation processes. Here, we summarize the risk factors for inducing sleep disorders, the alteration of these risk factors by TRPV1 receptor activation, and the driving effect of TRPV1 receptor activity on memory consolidation.

Loneliness is intricately connected to social cognition, yet the precise brain mechanisms that underscore their relationship need further exploration. The present study employed a theory of mind processing task that engaged participants in assessing the trajectories of geometric shapes while undergoing fMRI scans. The comprehensive data pool encompassed loneliness assessments and brain imaging data from a cohort of 157 participants. Utilizing a machine learning approach, task-induced functional connectivity data was used to forecast individuals' loneliness scores. The findings unveil that specific patterns of task-induced alterations in brain functional connectivity hold a remarkable capability to anticipate loneliness scores. Further dissection of the data disclosed pivotal nodes, including the prefrontal cortex, temporoparietal junction, and amygdala, among other cerebral regions. Furthermore, functional connectivity among the social network, the default mode network, and somatomotor networks emerged as crucial factors in prediction. Brain regions contributed strongly in prediction are involved in a variety of social cognitive processes, including intention inference, empathy, and information integration. The results illuminate the association between brain functional connectivity induced by social cognition and loneliness, which enhance the comprehensive understanding of this complex emotional state and may have implications for its diagnosis and intervention.

Postoperative neurocognitive disorder (PND) is a prevalent complication following surgery and anesthesia, characterized by progressive cognitive decline. The precise etiology of PND remains unknown, and effective targeted therapeutic strategies are lacking. Transcranial near-infrared light (tNIRL) has shown potential benefits for cognitive dysfunction diseases, but its effect on PND remains unclear. Our previous research indicated a close association between demyelination and PND. In other central nervous system (CNS) disorders, tNIRL has been demonstrated to facilitate remyelination in response to demyelination. In this study, we established the PND model in 18-month-old male C57BL/6 mice using isoflurane anesthesia combined with left common carotid artery exposure. Following surgery, PND-aged mice were subjected to daily 2.5-minute tNIRL treatment at 810 nm for three consecutive days. Subsequently, we observed that tNIRL significantly improved cognitive performance and reduced inflammatory cytokine levels in the hippocampus of PND mice. Furthermore, tNIRL increased the expression of oligodendrocyte transcription factor 2 (OLIG2) and myelin basic protein (MBP), promoting remyelination while enhancing synaptic function-associated proteins such as synaptophysin (SYP) and postsynaptic density protein 95 (PSD95). Further investigation revealed that tNIRL may activate the AKT1/mTOR pathway to facilitate remyelination in PND mice. These findings indicate that tNIRL is a novel non-invasive therapeutic approach for treating PND.

Motor variability is an intrinsic feature of human beings that has been associated with the ability for learning and adaptation to specific tasks. The purpose of this review is to examine whether there is a possible direct relationship between individuals' initial variability in their ability for learning and adaptation in motor tasks. Eighteen articles examined the relationship between initial motor variability and the ability for learning or adaptation. Twelve found a direct relationship. In reward-based tasks, greater initial variability was associated with greater learning and adaption improvement when assessed using linear measures of dispersion, however, this association was not observed with temporal structure variability. While in error-based task associations were reported with both greater amount variability and more complexity temporal structure. Nevertheless, bias in initial performance related to the amount of variability was found, so the temporal structure of initial variability seems to be a better indicator of improvement in this type of task. Further research is needed for further research to better understand the potential relationship between initial motor variability and the ability for learning or adaptation in motor tasks.

Similar to other brain regions, the neurons in the lateral septum (LS) are of heterogeneous populations. However, their resting membrane potential (RMP) on average is not too far apart. Cells were characterized based on biological markers by using brain slices, as under these in vitro conditions, neurons retain their morphologies. Since the LS neurons are not spontaneously excitable at RMP, the action potentials (APs) were evoked via injections of currents of moderate magnitude during the patch-clamp recordings. In coronal brain slices of rats, a smaller portion of neurons generated a train of APs of complex nature. In order to define the types of neurons with similar phenotypes, we subsequently used the four lines of td-Tomato transgenic mice. The brains of these mice express the promoter fluorophore td-Tomato and enhanced green fluorescent protein (eGFP). Therefore, recordings were conducted in a targeted manner in neurons expressing glutamic acid decarboxylase (GAD), parvalbumin (PV), somatostatin (SOM), or vasoactive intestinal polypeptide (VIP). Similar spike phenotypes that we refer to as type III, in order to distinguish from AP in principal cells - type I and those in interneurons - type II, also exist in mice, substantiating a similitude among rodents. The type III AP is selectively triggered by Ca²⁺ in GAD and SOM-positive neurons. Conclusions are supported by established pharmacologic tools, nimodipine, TTX, and ZD7288, a selective HCN channel antagonist.Collectively, these observations revitalize our knowledge from pioneering studies with regard to the brain of mammals in general and septal structures in particular.

We investigated proprioceptive acuity for location and motion of a never seen hand-held tool (30 cm long rod) and the accuracy of movements to place tool parts in the location of remembered visual targets. Ten blindfolded right-handed subjects (5 females) reached with the tool held in the right hand to touch the tip and midpoint to the stationary and moving left index-tip, to the right and left ear lobes and to remembered visual target locations. We also tested accuracy of left hand rod reaches to the ear lobes to determine if rod dimensions and control of tool movements experienced during right hand tool use could be used to accurately localize the rod parts when held in the left hand. Errors for right hand-held rod-tip movements to touch the stationary and moving left index-tip averaged only about 1 cm larger than observed previously for right hand movements to touch its index-tip to the left index-tip. The tool-tip was localized with lower mean distance errors (about 1 cm) than the tool-midpoint (5.5-6.5 cm) when reaching to touch the ear lobes with the rod in right and left hands. Right hand reaches to place the tool- tip and midpoint in remembered visual target locations were inaccurate with large overshoots of close targets and undershoots of far targets, similar to previous reports for reaching with the right hand to remembered visual targets. These results support the distalization hypothesis, that the tool endpoint becomes the effective upper limb endpoint when using the tool.

This article discusses the peculiarities of microglia behaviour and their interaction with other cells of the central nervous system (CNS) during neural tissue injury with a focus on spinal cord injury (SCI). Taking into account the plasticity of microglia, the influence of the microenvironment should be taken into account to establish the mechanisms determining the polarization pathways of these cells. Determination of the system of microglia interactions with other CNS cells during injury will reveal the patterns of post-traumatic microglia responses, in particular, determining both pro-inflammatory and anti-inflammatory responses. This review compiles information on changes in microglia activation, migration and phagocytosis, as well as their reciprocal effects on other CNS cells, such as neurons, astrocytes and oligodendrocytes, in the background of SCI. The information contained in this article may be of interest not only to scientists studying traumatic injuries of the central nervous system, but also to specialists in the field of studying and treating neurodegenerative diseases, since the mechanisms occurring in the injured spinal cord may also be characteristic of pathological events in degenerative processes.

Controversy persists regarding the representation of linguistically negated actions, specifically concerning activation and inhibitory mechanisms in the motor system, and whether negated action sentences evoke an initial motor simulation of the action to be negated. We conducted two experiments probing corticospinal excitability (CSE) and short-interval intracortical inhibition (SICI) in the primary motor cortex at different latencies while reading affirmative and negative action sentences. In experiment one, twenty-six participants read action and non-action sentences in affirmative or negative forms. Using transcranial magnetic stimulation, we probed CSE in hand muscles at rest and at several latencies after verb presentation. We observed a greater CSE for action sentences compared to non-action sentences, regardless of verb form. In experiment two, nineteen participants read affirmative and negative action sentences. We measured CSE and SICI at short and long latencies after verb presentation. CSE was greater for affirmative and negative action sentences at both latencies compared to rest. SICI did not change at the short latency but increased at longer latencies, regardless of verb form. Negated action sentences showed the same motor excitability as affirmed action sentences with no additional inhibition at early latencies. These results lend support for the idea that actions to be negated are initially simulated within the motor system. Neural differences between affirmative and negative action sentences may occur outside the primary motor cortex.

Thyroid hormones play an important morphogenetic role during the fetal and neonatal periods and regulate numerous metabolic processes. In the central nervous system, they control myelination and overall brain development, regional gene expression, and regulation of oxygen consumption. Their deficiency in the fetal and neonatal periods causes severe mental retardation, due to lack of thyroid function, or to iodine deficiency. At the same time, nitric oxide is an atypical neurotransmitter that also has special relevance in neuronal development and plasticity and functions as a vasodilator, regulating cerebral blood flow. Although under physiological conditions it functions as a neuroprotector, in excess it can be neurotoxic. We have studied, by immunocytochemical and Western blot techniques, the evolution of the expression of neuronal and inducible isoforms of the enzyme nitric oxide synthase, and of nitrotyrosine as a marker of protein nitration produced by the presence of nitric oxide, during the early stages of postnatal brain development. We induced hypothyroidism by administering mercaptomethylimidazole to pregnant mothers, from the seventh day of gestation until the sacrifice of the offspring. The results show a delay in the evolution of the expression of the two isoforms of the enzyme nitric oxide synthase in hypothyroid animals, followed by an anomalous overexpression in later stages. Finally, the expression of nitrotyrosine follows an evolution that is synchronized with that shown by both isoenzymes in control and hypothyroid animals.

Sevoflurane impairs learning and memory of the developing brain. However, strategies to mitigate these detrimental effects have been scarce. Herein, we investigated whether tetramethylpyrazine pretreatment could alleviate the impairment of learning and memory and its underlying mechanism in sevoflurane-exposed neonatal rats. Postnatal 7-day Sprague-Dawley (SD) rats or primary hippocampal neurons were pretreated with tetramethylpyrazine and then exposed to sevoflurane. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and lactate dehydrogenase (LDH) assays were used to detect neuronal injury. Learning and memory function were evaluated by novel object recognition and Morris water maze tests. Long-term potentiation (LTP) was recorded to evaluate synaptic plasticity electrophysiologically in the hippocampal slices. Golgi-Cox staining or PSD95 immunochemistry was used to detect the morphology of dendritic spines. Western blotting was employed to assess the expressions of cleaved Caspase-3, PSD95, N-methyl-D-aspartate receptor (NMDAR) subunits NMDAR1, NMDAR2A and NMDAR2B in the hippocampus or cultured neurons. It was found that neonatal exposure of sevoflurane impaired learning and memory, increased neuronal apoptosis, altered the morphology of dendritic spines, upregulated the expressions of NMDAR2A and PSD95, and induced LTP deficits. Pretreatment with tetramethylpyrazine not only alleviated impairment of learning and memory, but also improved sevoflurane-induced changes in neuronal damage, dendritic spine morphology, NMDAR2A and PSD95 expressions, as well as LTP. These findings indicated that pretreatment with tetramethylpyrazine alleviated the impairment of learning and memory induced by sevoflurane through improvement of hippocampal synaptic plasticity in neonatal rats.