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        <title>Experimental Biology and Medicine | Neuroscience section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/neuroscience</link>
        <description>RSS Feed for Neuroscience section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-04-22T17:08:11.22+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10827</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10827</link>
        <title><![CDATA[Elevated ApoC3 levels in cerebrospinal fluid predict poor outcomes in patients with aneurysmal subarachnoid hemorrhage]]></title>
        <pubdate>2026-04-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Bin Tong</author><author>Junjie Wang</author><author>Jiarui Chen</author><author>Qia Zhang</author><author>Zhouhan Xu</author><author>Kaichuang Yang</author><author>Xiaomin Chen</author>
        <description><![CDATA[Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating condition associated with approximately 30% mortality and 20% severe disability among survivors. Delayed cerebral ischemia due to cerebral vasospasm and hydrocephalus significantly contribute to poor neurological outcomes. Currently, reliable biomarkers for early prediction of these complications remain lacking. In this study, 63 patients with a mean age of 59.7 ± 11.53 years were enrolled. Functional outcomes were assessed by the modified Rankin Scale (mRS). Cerebrospinal fluid (CSF) samples were obtained through lumbar drainage (LD) or external ventricular drainage (EVD) and analyzed by ELISA. The predictive value of biomarkers was evaluated using receiver operating characteristic (ROC) curve analysis. Elevated Apolipoprotein C-III (ApoC3) levels in CSF of aSAH patients were observed. Furthermore, increased ApoC3 concentrations were significantly associated with poor prognosis and an elevated risk of severe complications. At an optimal cutoff value of 4,463 ng/mL, patients with high ApoC3 levels exhibited significantly worse 3-month functional outcomes and a higher incidence of delayed cerebral ischemia and hydrocephalus. Monitoring ApoC3 levels in CSF may be beneficial for predicting complications such as delayed cerebral ischemia and hydrocephalus in patients with aSAH.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10933</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10933</link>
        <title><![CDATA[Genetics of epilepsy]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Kynen Piacentini</author><author>Athanasios Gaitatzis</author><author>Sulev Kõks</author>
        <description><![CDATA[Epilepsy is one of the most common neurological diseases in the world, but it is also complex and difficult to study. There is a significant genetic component to epilepsy and more information is being published frequently. It is difficult to group and summarise all of this information in a way that is beneficial for both researchers and clinicians. The aim of this paper is to create a summary of all currently known epilepsy associated genes in order to aid epilepsy research to better understand the aetiology of the disease. This was achieved through gathering genetic data from three databases: Online Mendelian Inheritance in Man (OMIM), Clincal Genome (ClinGen), and PubMed. Genes were filtered based on specific criteria and were summarised into three tables: Epilepsy genes, Epilepsy associated genes and Predicted epilepsy associated genes. A fourth table was produced to showcase all epilepsy genes that were identified in all three databases. A total of 2,536 genes were identified to have some level of association with epilepsy. A total of 238 genes were classified as Epilepsy genes, 1,317 genes were classified as Epilepsy associated genes and 981 genes were classified as Predicted epilepsy genes. Finally, 86 genes were identified to be epilepsy genes that were found in all three genetic databases and represent the highest confidence in association with epilepsy. The significance of this study involves the ability to give researchers an up-to-date list of genes that have an association to epilepsy and a summary of information about said genes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10834</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10834</link>
        <title><![CDATA[A novel de novo ATP2B1 variant causes autosomal dominant intellectual developmental disorder 66 by disrupting calcium homeostasis via impaired membrane trafficking]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Huanhuan Zang</author><author>Xiaoyun Yang</author><author>Yucai Liu</author><author>Caiyun Ma</author><author>Dawei Yang</author>
        <description><![CDATA[Heterozygous pathogenic variants in ATP2B1 (encoding PMCA1) cause autosomal dominant intellectual developmental disorder 66 (MRD66; OMIM #619910). To date, only 12 pathogenic de novo ATP2B1 variants have been reported in MRD66. This study aimed to identify the genetic etiology in a Chinese infant with a neurodevelopmental disorder characterized by early-onset seizures and global developmental delay (GDD) and functionally characterize a novel ATP2B1 missense variant. Trio-based whole-exome sequencing revealed a heterozygous de novo ATP2B1 variant (c.2140A>C, p.Thr714Pro) in the proband. The proband presented with infantile spasms, GDD (Gesell Developmental Quotient: 65–74), and severe growth restriction (height/weight <−2 SD). To investigate the variant’s pathogenicity, the wild-type (WT) and mutant ATP2B1 constructs, N-terminally tagged with mScarlet, were transfected into HEK293T cells. Confocal imaging demonstrated profound cytoplasmic mislocalization of the p.Thr714Pro mutant protein, contrasting sharply with the characteristic plasma membrane localization of WT ATP2B1. Measurement of intracellular Ca2+ levels using Fluo-4 AM showed a significant 2.07-fold increase in basal Ca2+ levels in cells expressing the mutant compared to WT. This finding expands the spectrum of ATP2B1 variants associated with MRD66 and confirms calcium dyshomeostasis as the core pathomechanism. This case of MRD66 demonstrates a very early onset of seizures, consistent with the recognized phenotypic variability and the critical role of PMCA1 in early neurodevelopment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10835</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10835</link>
        <title><![CDATA[Skeletal muscle reprogramming in peripheral nerve injury: mechanisms, therapeutic roles, and complication management]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fuqiang Long</author><author>Xiaoru Pan</author><author>Anxin He</author><author>Xinlu Wang</author><author>Zairong Wei</author><author>Shaoying Gao</author>
        <description><![CDATA[Peripheral nerve injury (PNI) presents a significant clinical challenge, frequently leading to long-term neuromuscular dysfunction, muscle atrophy, fibrosis, and chronic pain. Traditional repair strategies, including microsurgical reconnection and neurotrophic support, often yield limited functional recovery, especially in cases of delayed or incomplete reinnervation. In this context, skeletal muscle reprogramming—defined as the intentional modulation of cellular fate, function, or metabolic state in muscle-resident cells—has emerged as a promising strategy to enhance regenerative outcomes. This process involves transcriptional, epigenetic, and metabolic interventions targeting myogenic progenitors, fibro-adipogenic progenitors (FAPs), satellite cells (MuSCs), and the broader muscle microenvironment. Recent studies demonstrate that reprogramming strategies can mitigate denervation-induced muscle atrophy, delay fibrotic remodeling, promote neuromuscular junction (NMJ) reconstruction, and even stimulate endogenous nerve regrowth via retrograde signaling. Mechanistic insights have uncovered pivotal roles for signaling pathways such as Wnt/β-catenin, TGF-β, Notch, and HDAC-regulated chromatin dynamics. Furthermore, innovations in small molecule cocktails, CRISPR-based transcriptional reactivation, and metabolic rewiring have expanded the therapeutic toolkit for muscle preservation and regeneration. This review comprehensively examines the molecular mechanisms, therapeutic roles, and translational challenges of skeletal muscle reprogramming in the context of PNI. We explore how muscle-targeted interventions can address complications of denervation, improve the efficacy of nerve repair, and offer a synergistic axis of regeneration when integrated with nerve-centric strategies. Finally, we identify key knowledge gaps and outline future research directions required to translate reprogramming-based therapies into clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10712</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10712</link>
        <title><![CDATA[Electrotherapy in the management of neuropathic corneal pain: narrative review]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>A. V. Shanmathi</author><author>Mingyi Yu</author><author>Chang Liu</author><author>Isabelle Xin Yu Lee</author><author>Louis Tong</author><author>Yu-Chi Liu</author>
        <description><![CDATA[Neuropathic corneal pain (NCP) is a debilitating condition resulting from corneal nerve damage or dysfunction, leading to persistent ocular pain, discomfort and hypersensitivity. Conventional therapy with eye drops often provides inadequate relief, necessitating the need for alternative therapeutic approaches. This review explores the role of electrotherapy in managing NCP, including its mechanisms, clinical efficacy, and potential integration into multimodal treatment strategies. We examine current evidence on various electrotherapy modalities such as transcutaneous electrical nerve stimulation, neurostimulation, and microcurrent stimulation. These electrotherapies have the potential to modulate pain pathways, promote nerve regeneration, and restore corneal homeostasis. Emerging studies suggest electrotherapy may alleviate NCP by altering neural signaling and reducing hyperalgesia. Integrating electrotherapy into existing pain management strategies may enhance the outcomes for patients with refractory NCP. However, its clinical application remains limited by a lack of standardized protocols and robust clinical trials. Although electrotherapy presents a promising and non-invasive option for NCP management, further research is needed to optimize the treatment parameters and optimal duration, assess the long-term efficacy, and establish guidelines for clinical use.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10805</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10805</link>
        <title><![CDATA[Characterisation of the function of a lncRNA containing SINE-VNTR-Alu 67 to regulate the genes at the MAPT locus]]></title>
        <pubdate>2025-11-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kynen Piacentini</author><author>Alexander Fröhlich</author><author>Abigail Pfaff</author><author>Sulev Kõks</author>
        <description><![CDATA[Parkinson’s disease (PD) is a complex neurodegenerative disease that involves many interlinking pathways and genetic elements that remain to be fully understood and characterised. Non-coding genetic elements have long been overlooked, however recent advancements in the field have highlighted their importance with an area of interest being transposable elements. SINE-VNTR-Alu (SVA) elements are the youngest and smallest subset of retrotransposons that are only found within hominid species. SVAs have been shown to have strong regulatory impacts within our genome and can affect progression of neurodegenerative disease such as PD. Previous studies identified an SVA, polymorphic for its presence/absence, that was associated with changes in gene expression at the MAPT locus. This particular SVA is located within a long non-coding RNA (lncRNA) and is known as SVA_67. Here, we evaluated the SVA67-lncRNA effects on gene expression within the MAPT locus, a region associated with several neurodegenerative diseases in the SH-SY5Y cell line. The expression of SVA67-lncRNA in the SH-SY5Y cell line was associated with differential expression of several genes at the MAPT locus including MAPT, KANSL1, ARL17A/B, LRRC37A/2, and NSF. This study provides the first analysis of this SVA67-lncRNA and potential evidence for its involvement in complex diseases, such as PD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10491</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10491</link>
        <title><![CDATA[Impact of aging and body mass index on upper extremity motor unit number index and size]]></title>
        <pubdate>2025-07-24T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Lauren I. Gulley Cox</author><author>Nicholas Dias</author><author>Chuan Zhang</author><author>Yingchun Zhang</author><author>Stacey L. Gorniak</author>
        <description><![CDATA[The focus of this study was to evaluate motor unit number and size across the upper extremity in older adults (aged 60+ years) versus young healthy adults (aged 20–30 years). We hypothesized that older adults would have: fewer motor units and increased motor unit size as compared to young healthy adults (H1), that motor unit size would differ across the upper extremity muscles as compared to young healthy adults (H2), and higher body mass index (BMI) would be associated with lower motor unit numbers (H3). Compound muscle action potential (CMAP), motor unit number index (MUNIX), and motor unit size index (MUSIX) were evaluated in five muscles of the upper extremity. Group differences in CMAP due to aging were accounted for by increased body mass index (BMI); group differences in MUSIX were not impacted by BMI. No difference in MUNIX was found; however, an influence of BMI was found across groups. While this data provides supporting evidence of age-related motor unit changes, body composition changes with age may confound these conclusions when surface electromyography is utilized as the measurement modality. Adiposity estimation should be considered in future EMG studies, particularly in populations with higher BMI values.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10567</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10567</link>
        <title><![CDATA[Mechanisms for reducing/eliminating chronic neuropathic pain with a focus on platelet-rich plasma]]></title>
        <pubdate>2025-06-30T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Damien P. Kuffler</author><author>Christian A. Foy</author>
        <description><![CDATA[Peripheral nerve trauma commonly results in chronic neuropathic pain by up-regulating the synthesis and release of pro-inflammatory mediators from local and invading cells and inducing hyperexcitability of nociceptive neurons and spontaneous electrical activity. The pain decreases when these cells down-regulate genes supporting the pro-inflammatory state, up-regulate genes for expressing anti-inflammatory factors, and modulate genes that reduce nociceptive neuron spontaneous electrical activity. Pharmacological agents, the primary technique for reducing pain, do not eliminate pain, and <50% of patients achieve benefits because they do not address the underlying causes of pain. Alternative techniques providing longer lasting, but not complete or long-term pain relief include surgical interventions, electrical stimulation, and antibody treatment. Anti-inflammatory mediators can reduce pain, but the effect is not complete or long-lasting. Platelet-rich plasma (PRP) contains a readably available evolutionarily developed cocktail of factors that induce longer-lasting and more significant, but not complete, pain relief than other techniques. However, a novel study shows that unique formulations of PRP can induce long-term pain elimination. This review examines (1) the efficacy of drugs, regenerative peripheral nerve interface (RPNI), targeted muscle reinnervation (TMR), and PRP in reducing chronic neuropathic pain, (2) recent clinical data showing that a novel PRP application technique induces long-term chronic neuropathic pain reduction/elimination, and (3) discusses why the novel PRP may be more effective in reducing/eliminating chronic neuropathic pain.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10330</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10330</link>
        <title><![CDATA[Deep brain stimulation for dystonia treatment in cerebral palsy: efficacy exploration]]></title>
        <pubdate>2025-06-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Haoyang Zheng</author><author>Duo Zhang</author><author>Wei Xiang</author><author>Yong Gan</author><author>Zesheng Peng</author><author>Yuyi Wu</author><author>Peng Fu</author>
        <description><![CDATA[Dystonia, a challenging movement disorder, poses significant therapeutic challenges due to its resistance to treatment, resulting in both physical impairment and substantial mental distress, ultimately impacting overall quality of life. Cerebral palsy (CP) is a major non-genetic cause of secondary dystonia, characterized by diverse clinical presentations. This study aims to comprehensively evaluate the effectiveness of deep brain stimulation (DBS) as a therapeutic intervention for individuals with dystonic CP. We conducted a systematic analysis of studies assessing the safety and effectiveness of DBS, with a focus on its long-term outcomes [PROSPERO (Unique identifier: CRD42023399285)]. We examined factors that influence treatment response and proposed strategies to enhance patient quality of life. DBS, especially when targeting the basal ganglia or innovative targets, shows promise as a therapeutic approach for dystonic CP. While existing controlled studies confirm its safety and effectiveness, a thorough evaluation of long-term efficacy remains crucial. This research highlights the potential of DBS in improving the lives of individuals with dystonic CP, providing hope for further refinement, innovation, and broader clinical application of this therapeutic approach.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10566</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10566</link>
        <title><![CDATA[Limitations to clinically restoring meaningful peripheral nerve function across gaps and overcoming them]]></title>
        <pubdate>2025-05-27T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Christian A. Foy</author><author>Damien P. Kuffler</author>
        <description><![CDATA[Clinically, reliably restoring meaningful peripheral sensory and motor nerve function across peripheral nerve gaps is limited. Thus, although autografts are the clinical “gold standard” repair technique for bridging nerve gaps, even under relatively good conditions, <50% of patients recover meaningful function. Due to this low recovery rate, many patients are not even provided repair surgery and, consequently, suffer permanent loss of function. This paper examines intrinsic and extrinsic changes associated with injured neurons and Schwann cells that reduce the extent of axon regeneration and recovery. It also examines how these changes can be reversed, leading to enhanced regeneration and recovery. It next examines the efficacy of platelet-rich plasma (PRP) in promoting axon regeneration and two novel techniques involving bridging nerve gaps with an autograft within a platelet-rich (PRP) collagen tube or only a PRP-filled collagen tube, which induce meaningful recovery under conditions where autografts alone are not effective. Finally, it looks at potential mechanisms by which platelet-released factors may enhance axon regeneration and recovery. This review shows that although there are many limitations to restoring meaningful function following peripheral nerve trauma, there are a number of ways these can be overcome. Presently, the most promising techniques involve using PRP.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10553</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10553</link>
        <title><![CDATA[In vivo silencing of the thalamic CaV3.1 voltage-gated calcium channels demonstrates their region-specific role in anesthetic mediated hypnosis]]></title>
        <pubdate>2025-05-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tamara Timic Stamenic</author><author>Simon Feseha</author><author>Brier Fine-Raquet</author><author>Vasilije P. Tadic</author><author>Slobodan M. Todorovic</author>
        <description><![CDATA[Although substantial progress has been made in the last three decades towards our understanding of how general anesthetics (GAs) act at the molecular level, much less is known about how GAs cause loss of consciousness at the level of neuronal networks. The role of thalamus as an important brain region in anesthetic-induced hypnosis is relatively well established, but the specific roles of voltage-gated ion channels in different functional regions of the thalamus in anesthetic mechanisms are not well studied. To address this gap in knowledge, we selectively silenced the Cacna1g gene that encodes the low-threshold-activated CaV3.1 T-type voltage-gated calcium channel subunit by injecting short-hairpin RNA (shRNA) into midline and intralaminar - nonspecific thalamus (MIT) and sensory - specific ventrobasal (VB) thalamic nuclei in wild-type (WT) mice. Control animals were injected with scrambled shRNA. To validate our silencing approach, we performed patch-clamp experiments in acute thalamic slices ex vivo. In injected animals we determined anesthetic endpoints such as hypnosis measured with loss of righting reflex (LORR) and immobilization measured with loss of withdrawal reflex (LOWR) in vivo after administration of a traditional volatile GA isoflurane. Effective CaV3.1 channel knock-down was documented by greatly diminished amplitudes of T-currents and absence of rebound burst firing in our patch-clamp recordings from thalamic slices. We found that knocking down CaV3.1 channels in MIT significantly decreased inhaled isoflurane concentration that is required to induce LORR, but it did not affect speed of anesthetic induction and the immobilizing effect of isoflurane. In contrast, knocking down the CaV3.1 channel in the VB thalamus did not affect any of the measured anesthetic endpoints. Hence, we concluded that CaV3.1 channels in nonspecific MIT thalamus have a preferential role in anesthetic hypnosis when compared to the sensory VB thalamus.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10549</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10549</link>
        <title><![CDATA[Anesthesia-induced developmental neurotoxicity in the setting of systemic inflammation: the role of microglia]]></title>
        <pubdate>2025-05-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nemanja Useinovic</author><author>Adre Newson</author><author>Michelle Near</author><author>Stefan Maksimovic</author><author>Benjamin Volvovitz</author><author>Nidia Quillinan</author><author>Vesna Jevtovic-Todorovic</author>
        <description><![CDATA[Although it is well documented in animal research that an early exposure to general anesthetics during critical stages of synaptogenesis disturbs normal brain development ultimately leading to cognitive and affective impairments, it is less clear whether and how surgical interventions and/or underlying systemic inflammation impact the detrimental effects of general anesthetics. Some emerging evidence suggests that aseptic systemic inflammation preceding exposure to the commonly used general anesthetics worsens anesthesia-induced neuroapoptosis and activates inflammasome pathways while resulting in impaired cognitive-affective behaviors. To improve our understanding of the underlying mechanisms, here we focused on multicellular interactions between damaged neurons and microglia since microglia is the resident macrophages within the brain that respond to stress. Using infant rats (post-natal day 7) and most commonly used inhaled anesthetic, sevoflurane, we examine microglia role in sevoflurane-induced inflammation-propagated developmental neurotoxicity. We show that sevoflurane exposure leads to a significant neuroapoptosis in young rat pup hippocampal subiculum, a neuroapoptosis that is worsened in the setting of systemic inflammation caused by either lipopolysaccharide (LPS) injection or trauma (tibial fracture). The worsening is not only shown in terms of the intensity of neuroapoptosis but in its duration and onset. We further report that sevoflurane-induced neuroapoptosis triggers activation of microglia, which in turn releases proinflammatory cytokine MCP-1 and upregulates endothelial cell adhesion molecule, ICAM-1. This leads to T-lymphocyte infiltration in the hippocampal subiculum, an event that further perpetuates microglia activation in an attempt to control neuroapoptosis which is suggested by the fact that microglia depletion leads to a significant worsening of sevoflurane-induced developmental neuroapoptosis. Our work gets us a step closer to making our animal work more relevant to the clinical setting and hence more translational. This is vitally important considering that exposure to anesthesia is exceedingly rare in the absence of any kind of a pathological process.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10545</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10545</link>
        <title><![CDATA[α-linolenic acid-induced facilitation of GABAergic synaptic transmission is mediated via acid-sensing ion channel (ASIC1a) activity in the basolateral amygdala]]></title>
        <pubdate>2025-05-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Volodymyr I. Pidoplichko</author><author>Taiza H. Figueiredo</author><author>Maria F. M. Braga</author><author>Ann M. Marini</author>
        <description><![CDATA[Epilepsy affects more than 70 million people worldwide. A seizure focus that develops in different cortical brain regions can present as either focal or generalized seizures. Temporal lobe epilepsy is a highly pharmacoresistant form of epilepsy that involves the amygdala, hippocampus with or without hippocampal sclerosis as well as other limbic structures. Loss and/or dysfunction of GABAergic inhibitory neurons play a critical role in tipping the balance toward excitation. Synchronous burst firing is a feature of inhibitory neurons that is thought to regulate and rectify large excitatory neuronal networks in the BLA and is thought to underlie higher cognitive function. Acid sensing ion channels (ASIC) activated by decreases in pH, the presence of ammonium ion or a slight lowering of temperature are present on excitatory and inhibitory neurons and can alter excitability. The net effect of the activation of ASIC1a channels in the BLA is inhibition. ASIC1a channels are active in the basal state, enhancing primarily GABAergic inhibition by direct depolarization of interneurons but also by indirect excitation of interneurons via ASIC1a-mediated depolarization of pyramidal neurons. In this study, we examine the contribution of ASIC1a channel activation on alpha-linolenic acid (ALA)-induced GABAergic inhibitory synchronous burst firing in the BLA. Our results show that ALA initiates inhibitory bursts that are dependent, in part, on the activation of ASIC1a channels that may in turn be mediated by mature brain-derived neurotrophic factor.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10171</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10171</link>
        <title><![CDATA[Subunit-specific mechanisms of isoflurane-induced acute tonic inhibition in dentate gyrus granule neuron]]></title>
        <pubdate>2024-10-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zhiqiang Yu</author><author>Xiaodan Chen</author><author>Zheng Liu</author><author>Ran Ding</author><author>Jin Xu</author>
        <description><![CDATA[Prolonged exposure to volatile anesthetics may raise the risk of developing cognitive impairment by acting on gamma-a Aminobutyric acid A receptors (GABAAR). The dentate gyrus plays an important role in the hippocampus and has a high potential for neural plasticity. However, it is unknown whether prolonged anesthesia induces a change in acute phasic or tonic inhibition in dentate gyrus granule cells (DGGCs) by acting on GABAAR. In order to verify the effects of volatile anesthetics on the current in DGGCs, a whole-cell patch was applied to record acute brain slices, and this study indicated that 4 h but not 2 h of isoflurane (ISO) exposure induced significantly larger tonic currents in DGGCs other than hippocampal CA1 pyramidal and thalamic relay neurons. Furthermore, this study demonstrated that the increased tonic current in DGGCs was dependent on the δ subunit-containing GABAARs by using transgenic δ subunit knockout mice. In conclusion, the δ subunit specific GABAAR is the key element that increased acute tonic inhibition in DGGCs of mice after prolonged ISO exposure, which may be one of the mechanisms of ISO neurotoxicity to the developing brain.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10120</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10120</link>
        <title><![CDATA[Non-coding RNAs and neuroinflammation: implications for neurological disorders]]></title>
        <pubdate>2024-02-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yvonne Chen</author><author>Julia Mateski</author><author>Linda Gerace</author><author>Jonathan Wheeler</author><author>Jan Burl</author><author>Bhavna Prakash</author><author>Cherie Svedin</author><author>Rebecca Amrick</author><author>Brian D. Adams</author>
        <description><![CDATA[Neuroinflammation is considered a balanced inflammatory response important in the intrinsic repair process after injury or infection. Under chronic states of disease, injury, or infection, persistent neuroinflammation results in a heightened presence of cytokines, chemokines, and reactive oxygen species that result in tissue damage. In the CNS, the surrounding microglia normally contain macrophages and other innate immune cells that perform active immune surveillance. The resulting cytokines produced by these macrophages affect the growth, development, and responsiveness of the microglia present in both white and gray matter regions of the CNS. Controlling the levels of these cytokines ultimately improves neurocognitive function and results in the repair of lesions associated with neurologic disease. MicroRNAs (miRNAs) are master regulators of the genome and subsequently control the activity of inflammatory responses crucial in sustaining a robust and acute immunological response towards an acute infection while dampening pathways that result in heightened levels of cytokines and chemokines associated with chronic neuroinflammation. Numerous reports have directly implicated miRNAs in controlling the abundance and activity of interleukins, TGF-B, NF-kB, and toll-like receptor-signaling intrinsically linked with the development of neurological disorders such as Parkinson’s, ALS, epilepsy, Alzheimer’s, and neuromuscular degeneration. This review is focused on discussing the role miRNAs play in regulating or initiating these chronic neurological states, many of which maintain the level and/or activity of neuron-specific secondary messengers. Dysregulated miRNAs present in the microglia, astrocytes, oligodendrocytes, and epididymal cells, contribute to an overall glial-specific inflammatory niche that impacts the activity of neuronal conductivity, signaling action potentials, neurotransmitter robustness, neuron-neuron specific communication, and neuron-muscular connections. Understanding which miRNAs regulate microglial activation is a crucial step forward in developing non-coding RNA-based therapeutics to treat and potentially correct the behavioral and cognitive deficits typically found in patients suffering from chronic neuroinflammation.]]></description>
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