Acta neurobiologiae experimentalis最新文献

Over the past decade glymphatic concept has gained more and more interest. Despite some lacking data regarding structural and functional aspects, glymphatic system is widely considered the main mechanism of water and solutes transport in brain parenchyma, as well as waste clearance from the brain. Glymphatic system modulates the extracellular space volume and is involved in spatial K+ buffering (via influencing Kir4.1 channel functioning), two factors crucial for neuronal excitability and seizure susceptibility, and is itself strongly stimulated during sleep. This review summarizes information regarding the potential role of the glymphatic system in the development and progression of epilepsy, especially the role of the glial water channel aquaporin‑4 in modulation of brain excitability and in epilepsy. Data from animal models and human studies are presented.

In the area of electrophysiology, the availability of comprehensive and user‑friendly tools for single-neuron data processing, statistical analysis, and fast, intuitive data visualization is limited. To address this gap, we introduce pylabianca, a Python library tailored for robust single and multi‑unit data processing. Pylabianca leverages the power of standard Python packages and adopts the application programming interface of MNE‑Python, one of the most widely used electrophysiology packages. One of pylabianca's primary objectives is to provide a low entry threshold for scientists, requiring only basic Python programming skills. Pylabianca was designed to streamline most common analyses of single neuron data, and provide convenient data structures to serve as a foundation for building custom analysis pipelines. We believe that pylabianca will contribute to enhancing researchers' capabilities and efficiency in the field of single-neuron electrophysiology.

Methamphetamine (METH) is a highly addictive psychostimulant known for its profound impact on the nervous system. Chronic METH use leads to neurotoxicity characterized by various molecular and structural alterations in the brain. This review article primarily aims to elucidate the mechanisms underlying METH‑induced neurotoxicity. METH's mechanism of action involves the inhibition of dopamine, serotonin, and norepinephrine reuptake, resulting in altered synaptic function. Prolonged METH exposure triggers oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, impaired axonal transport, autophagy, and programmed cell death, ultimately contributing to neurotoxicity. These neurotoxic effects manifest as increased neuronal firing rate, disruptions in intracellular ion balance (Ca2+ and Na+), energy production imbalances, and excessive reactive oxygen species production. The blood‑brain barrier is compromised, leading to structural, functional, and neurochemical alterations, particularly in the fronto‑striatal circuit. While our comprehensive review addresses these intricate molecular and structural changes induced by METH, we also examined the latest therapeutic strategies designed to mitigate neurotoxicity. Our investigation sheds light on the critical need to comprehend the complex pathways underlying METH‑induced neurotoxicity and develop effective treatment approaches.

Tsc1 is a gene which expression results in hamartin, a protein involved in regulation of the mTOR1 pathway. Inactivation of Tsc1 gives rise to hyperactivation of the mTOR1 machinery, increased proliferation and growth of cells with subsequent cell degeneration and cell death. In humans, mutations of Tsc1 result in an inherited disorder ‑ tuberous sclerosis complex (TSC) with the concomitant multiorgan non‑malignant tumors (tubers), epileptic seizures and autistic‑like manifestations. General mouse knock‑outs, homozygous for the inactivated Tsc1 alleles do not survive and die at early embryonal stages. To circumvent this problem, we utilized the Cre/loxP system and removed Tsc1 specifically in Purkinje cells using the pcp2/L7Cre mouse strain and the Tsc1tmDjk/J strains. Because of the published results showing the autistic‑like symptoms after the same crossbred, we have decided to look closer at the early postnatal period of these mutants. Surprisingly no evidence of any behavioral alterations were found, including the ultrasonic vocalizations of newborns. We decided to focus more attention on the interpretation of data, including a more detailed statistical evaluation of our results.

Epilepsy, especially the medial temporal lobe epilepsy (TLE), can result in cognitive impairment. Low‑frequency repetitive magnetic stimulation (rTMS) has been verified to suppress neural excitability and reduce seizures. Given its potential in modifying cortical activity, we aimed to investigate its impact on cognitive function in the context of epilepsy, a condition where the use of rTMS has not been extensively explored. However, the influence on cognitive function has not yet been investigated. Therefore, this study aimed to investigate the effects of low‑frequency rTMS on cognitive improvement in epileptic rats. Rats used in this study were randomly divided into five groups: the sham group, the epilepsy group, and three epilepsy groups treated with rTMS at different frequencies. Each group underwent the Morris water maze test to investigate hippocampus‑dependent episodic memory, to evaluate their cognitive performance. Further assessments included patch clamp and western blot techniques to estimate the synaptic function in the hippocampus. Comparison between groups showed that low‑frequency rTMS significantly reduced spontaneous recurrent seizures and improved spatial learning and memory impairment in epileptic rats. Additionally, rTMS remodeled the synaptic plasticity affected by seizures and notably enhanced the expression of AMPAR and synaptophysin. Low‑frequency rTMS can antagonize the cognitive impairment caused by TLE, and promote synaptic connections.

Alzheimer's disease (AD) is a major neurodegenerative disease, affecting more than two third cases of dementia in the world. Non‑steroidal anti‑inflammatory drugs (NSAIDs) are widely used anti‑inflammatory analgesic agents representing 7.7% of worldwide prescriptions of which 90% are in patients over 65 years old. Based on mixed findings a systematic review and meta‑analysis were conducted to develop a better understanding of the protective role of NSAIDs in AD. We used three database PubMed, Web of Science, and Embase to identify the literatures. The studies following cohort and case‑control design were investigated separately to check the effect of NSAIDs on AD, by the using their fundamental indicators (relative risk and odds ratio). The fixed effect or random effects model were used to estimate the pooled relative risk and pooled odds ratio separately for both the study design, based on magnitude of heterogeneity. A total of 14 studies were selected for meta‑analysis. Eight studies were following cohort study design, whereas, six studies were following case‑control study design. In meta‑analysis of cohort studies, the pooled relative risk was 0.67 with 95% C.I 0.39 to 1.15, which was statistically insignificant. In meta‑analysis of case‑control studies, the pooled odds ratio was 0.71 with 95% C.I 0.46 to 1.10, which was statistically insignificant. NSAIDs do not act as a protective factor for Alzheimer's disease. Additionally, methodologically sound randomized controlled trials are required to produce a robust result.