Acta neurobiologiae experimentalis最新文献

Sevoflurane can produce toxicity to the hippocampal tissues of brain, leading to nerve damage, causing learning and cognitive dysfunction. CircRNAs have been indicated to act as a key mediator in anesthetic neurotoxicity. This study focused on the effect of circ_0016760 on sevoflurane‑induced neurological impairment. The GEO database (GSE147277) and RT‑qPCR were used to predict and  measure the circ_0016760 expression. The interaction of circ_0016760 and miR‑145 was verified by dual‑luciferase reporter assay. The CCK‑8 assay, flow cytometry, ELISA, ROS kit, MWM test were carried out to measure the cell viability, apoptosis, inflammation indicators, ROS level, and cognitive and memory function of the rats. Sevoflurane exacerbated neurotoxicity by restraining cell viability, inducing cell apoptosis, neuroinflammation, and ROS generation, and causing learning and cognitive dysfunction. Circ_0016760 expression was increased in POCD patients from the GEO database and upregulated after sevoflurane exposure. miR‑145 was a target miRNA of circ_0016760. Silencing of circ_0016760 weakened the effect of sevoflurane on cell viability, cell apoptosis, inflammation‑related factors, oxidative stress, which could be reversed by miR‑145 inhibitor. The animal experiments results showed that circ_0016760 played a protective effect on regulating the cognitive behavior of sevoflurane‑treated aged rats, expression of inflammation cytokine, and oxidative stress factors through targeting miR‑145 in sevoflurane‑treated aged rat's hippocampal neurons. Our results revealed that silencing of circ_0016760 attenuated sevoflurane‑induced hippocampal neuron injury by regulating miR‑145 expression, which may provide potential insights into the treatment of sevoflurane‑induced neurological impairment.

Speech understanding, watching a movie, listening to music etc., requires perception of the temporal order of at least two incoming events. A history of performing these tasks may be reflected in spontaneous brain activity. Here, we examined the relationship between the complexity (temporal dynamics) of resting‑state EEG (rsEEG) signal, assessed using the multivariate MultiScale Entropy (mMSE) algorithm, and the perception of event ordering, indexed by a visual temporal order threshold (TOT), i.e., the minimum duration necessary to correctly identify the before‑after relation between two stimuli. Healthy adolescents and young adults performed a psychophysical task measuring the TOT and underwent an eyes‑closed rsEEG study. The features of mMSE vectors, namely the area under curve (AUC) that represents total signal complexity, as well as the MaxSlope and the AvgEnt, corresponding to the entropy at fine‑ and coarse‑grained timescales, respectively, were obtained for the central (midline), anterior, middle and posterior channel sets. The greater the AUC and AvgEnt values in the central, left and right posterior areas, and the higher AUC in the right middle region, the higher the TOT. The most significant relationships were found for the midline electrodes (Fz, Cz, Pz, Oz). There were no significant correlations between the MaxSlope values and the TOT. To the best of our knowledge, this is the first study demonstrating that spontaneous EEG signal complexity is associated with the temporal order perception of two stimuli presented in rapid succession. Our findings may indicate that low total and coarse entropy levels of rsEEG signal are beneficial for visual temporal order judgments.

Dendritogenesis, a process of dendritic arbor development, is essential for the formation of functional neuronal networks, and in mammals, it begins in early life and continues into adulthood. It is a highly dynamic process in which dendritic branches form and regress until mature connectivity is achieved. Thereafter, dendritic branches are considered stable and do not undergo substantial rearrangements, although several exceptions have been described in the literature. After this long period of relative stability, significant changes in dendritic branching occur when the brain begins to age. Several neurological diseases, occurring both during development and in adulthood, have severe effects on the morphology of dendritic arbors, often associated with intellectual dysfunction. The molecular mechanisms of dendritogenesis are fairly well described. In contrast, knowledge of the molecular mechanisms of dendritic arbor stabilization and pathology‑induced instability is still quite incomplete, and several important questions remain unanswered. We describe the dynamic changes during development and adulthood and in different pathologies. Whenever possible, we also provide details on the molecular mechanisms behind dendritic dynamics and stability.

This paper was designed for delving into the mechanism adopted by interleukin‑4 (IL‑4) to relieve cerebral ischemia‑reperfusion injury (CIRI) in rats via suppressing autophagy. Herein, rats stochastically fell into sham operation (sham), model (RI), model + IL‑4 intervention (IL‑4), model + HIF‑1α inhibitor (2‑methoxyestradiol, 2ME2) and model + IL‑4 + 2ME2 (IL‑4 + 2ME2) groups. Next, western blotting was utilized to examine the protein expressions of microtubule‑associated protein 1 light chain 3 (LC3), p62, hypoxia‑inducible factor 1‑alpha (HIF‑1α) and Bcl‑2/adenovirus E1B 19 kDa‑interacting protein 3 (BNIP3). Relative to RI group, IL‑4 group had a significantly lower neurological impairment scale (NIS) score and an overtly lower apoptosis rate of neurons as well as a strikingly smaller cerebral infarction volume and number of autophagosomes (P<0.05). The LC3II/LC3I ratio and HIF‑1α and BNIP3 protein expressions dropped, but p62 protein expression rose pronouncedly in IL‑4 group (P<0.05). In contrast to those in RI group, the NIS score, neuronal apoptosis rate, cerebral infarction volume and autophagosome number were strikingly reduced (P<0.05). The NIS score, cerebral infarction volume, neuronal apoptosis rate, autophagosome number, LC3II/LC3I ratio and protein expressions of HIF‑1α and BNIP3 plummeted, while p62 protein expression sharply rose in IL‑4 + 2ME2 group relative to those in IL‑4 group (P<0.05). IL‑4 suppresses cell autophagy by inhibiting the HIF‑1α/BNIP3 pathway, thus relieving CIRI in rats.

The study aimed to compare the effect of a series of 20 sessions of whole‑body cryotherapy (WBC) on the level of CAT, GPx and SOD in women with multiple sclerosis and healthy women. The consent of the Bioethics Committee at the Regional Medical Chamber in Krakow was obtained, and the trial was registered in the Australian New Zealand Clinical Trials Registry. Thirty people took part in the study: the study group (MS) and the control group (CONT). All subjects participated in 20 cryotherapy sessions. Venous blood was collected for analysis before the WBC session and after 20 sessions. There were no changes in the examined parameters (CAT, GPx, SOD) after using WBC in the MS or control groups. There were also no differences between the groups in the first or the last study. There were no adverse changes in the parameters tested - WBC appeared to be a safe form of therapy, although the mechanisms of hypothermic protection are not fully understood.

Neuropeptides play an important role in the pathogenesis of epilepsy. In the present study, the effect of nesfatin‑1, a neuropeptide, was investigated on penicillin‑induced epilepsy model. Epileptiform activity was induced by an injection of penicillin into the somatomotor cortex at 56 albino Wistar rats. Nesfatin‑1 (i.c.v.) was administered at five different doses (12.5, 25, 50, 100, and 200 pmol) 30 min after a penicillin administration. Astressin 2B, a corticotropin‑releasing factor (CRF) receptor antagonist, was administered 10 minutes later the effective dose of nesfatin‑1 (50 pmol, i.c.v.). Superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and malondialdehyde (MDA) levels in cerebrum were analysed by ELISA method. Nesfatin‑1, at the doses of 25, 50 and 100 pmol, significantly reduced the frequency of epileptiform activity. However, none of the doses of nesfatin‑1 had any effect on the amplitude of epileptiform activity. Astressin 2B alone did not show any effect on epileptiform activity. In addition, astressin 2B had no effect on the anticonvulsant effect of nesfatin‑1. Nesfatin‑1 (at the doses of 25, 50, 100 pmol) did not alter SOD and GSH levels, but significantly increased the GPx and GR levels. Nesfatin‑1 (at a dose of 50 pmol) significantly decreased the MDA level in the cerebrum. Nesfatin‑1 shows anticonvulsant effect and astressin 2B did not affect the anticonvulsant effect of nesfatin‑1. We suggest that nesfatin‑1 has oxidative stress‑mediated anticonvulsant effect in the penicillin‑induced epileptic activity.

The function of microRNA (miRNA) in neuropathic pain (NP) has received widespread attention. The current research sought to address the contribution of miR‑488‑3p in NP and its downstream mechanisms. The NP rat model was constructed by chronic constriction injury (CCI) surgery in rats. Regulation of miR‑488‑3p or Rho‑associated coiled‑coil‑containing protein kinase 1 (ROCK1) in rats by intrathecal injection of lentivirus or plasmid. Real‑time quantitative reverse transcription polymerase chain reaction (RT‑qPCR) to examine the levels of miR‑488‑3p and ROCK1 in the dorsal root ganglion (DRG). Enzyme‑linked immunosorbent assay (ELISA) to monitor the secretion of pro‑inflammatory and anti‑inflammatory factors. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) for the evaluation of mechanosensitive and thermal nociceptive hypersensitivity of NP behaviors. Validation of molecular mechanism  between miR‑488‑3p and ROCK1 using RNA immunoprecipitation assay and dual‑luciferase reporter (DLR) assay. miR‑488‑3p was vigorously less expressed in the DRGs of CCI rats, while ROCK1 was upregulated. Elevated miR‑488‑3p alleviated the decrease of PWL and PWT in CCI rats, inhibited the secretion of pro‑inflammatory factors, and enhanced anti‑inflammatory factors levels. Mechanistically, ROCK1 was the target of miR‑488‑3p. Raised ROCK1 partially attenuated the mitigating effect of miR‑488‑3p on NP behavior and the suppression of inflammatory responses in rats. Current research demonstrated that miR‑488‑3p may be a novel therapeutic target for NP.

Many treatment initiatives, like herbal products and their active ingredients, aim to alleviate neurodegeneration to increase cognitive functions. Kaempferol may be a candidate molecule for treating neurodegeneration because of its antioxidant effects. In the present study, we examined the molecular changes associated with kaempferol's memory‑enhancing effects on streptozotocin (STZ)‑induced neurodegeneration. After intracerebroventricular STZ injection in Long‑Evans male rats, intraperitoneal kaempferol was administered for 12 days. The Morris water maze (MWM) was used to measure learning and memory performance in the rats, and proteins related to memory formation were investigated in the hippocampi with western blotting. Kaempferol improved learning performance and memory decline in STZ‑treated rats. At the molecular level, STZ‑induced neurodegeneration resulted in a decrease in the expression of GAD67, reelin, and phosphorylated‑NMDAR. However, kaempferol treatment ameliorated these changes by enhancing their levels similar to the controls. While neither STZ injection nor kaempferol treatment produced any significant change in phosphorylated‑CAMKII levels, they increased the expression of klotho and prealbumin. These results show that kaempferol has positive effects on memory loss, affecting synaptic plasticity by ameliorating both the levels and activity of memory‑relevant molecules through reelin signaling. In summary, this study provides a guide to future studies by examining in detail the healing effect of kaempferol as a candidate molecule in the treatment of neurodegeneration, such as that observed in Alzheimer's disease.

This study explored the protective effect and mechanism of hydrogen‑rich saline (HRS) on the neurological function of mice with cerebral ischemia. Effects of HRS on neurological function in mice with cerebral ischemia were evaluated by neurological function scores. Infarct volume and histological damage were evaluated by 2,3,5‑triphenyl tetrazolium chloride staining (TTC staining). Golgi‑Cox staining was conducted to measure the morphological changes of neuronal dendrites and dendritic spines. The expression of neuronal markers was detected by immunofluorescence. Western blot was used to detect protein expression. The infarct volume of mice in the HRS‑H group decreased significantly compared to that of the distal middle cerebral artery occlusion (dMCAO) group. Mice in the HRS‑H group had a lower neurological deficit score than that in the dMCAO group. Compared to the dMCAO group, the activity of superoxide dismutase (SOD) and the level of glutathione (GSH) significantly increased in the HRS‑H group. Compared with the dMCAO group, the number of apoptotic cells in the HRS‑H group decreased. Administration of HRS was shown to be able to decrease cavitation of the brain cortex after ischemia. The spine density in the HRS‑H group increased compared to that of the dMCAO group. In the in vitro experiment, compared with the oxygen‑glucose deprivation (OGD) group, the active oxygen content in the 75% HRM group decreased, and the mitochondrial membrane potential and adenosine triphosphate (ATP) content increased. Compared with the OGD group, the ratio of P‑AMPK and the levels of LC3II/LC3I in the hydrogen‑rich medium (HRM) group was upregulated, and P‑mTOR levels and P62 levels in the HRM group were down‑regulated. HRS can enhance neuroplasticity after ischemia and promote neurological recovery in mice with cerebral ischemia, which may involve the autophagy pathway mediated by the AMPK/mTOR signaling pathway.

Vitamin D (VD) is a vital liposoluble neurosteroid micronutrient, particularly crucial for women's health. International literature strongly correlates sufficient VD levels with comprehensive mental well‑being in women. This link is intricately related to neurobiological pathways and hormonal fluctuations, where low VD levels are notably associated with depression. This study comprehensively explores the neurobiological mechanisms that link VD and altered mood in women. Considering the increased susceptibility to hormonal shifts in women, our research investigates the intricate interplay between VD's neurobiology and mood regulation. Through the focused analysis of specific studies, we untangle the complex web of connections between VD and mood changes in women. Our approach takes into account the dynamic nature of hormonal changes, deepening our understanding of these mechanisms. Our study underscores VD's significant role as a neurosteroid micronutrient, especially in women's health. By examining the intricate relationships between VD's neurobiology and hormones, we propose strategies to improve mood regulation and psychological well‑being in women. In addition, we recommend targeted measures to achieve optimal VD levels, helping to manage challenges arising from hormonal fluctuations. The present review highlights the multifaceted contribution of VD to women's health, particularly in mood regulation. Through the analysis of the interplay of neurobiology, hormones and VD, our study provides avenues for enhancing women's mental and emotional well‑being through customized interventions.