Journal of Neuroscience Research最新文献

{"title":"Non-Mammalian Models in Ischemic Stroke Research: Advances, Applications, and Translational Potential","authors":"Takamasa Mizoguchi,&nbsp;Ayako Tonoki,&nbsp;Atsushi Yamaguchi,&nbsp;Motoyuki Itoh","doi":"10.1002/jnr.70112","DOIUrl":"10.1002/jnr.70112","url":null,"abstract":"<div>\u0000 \u0000 <p>Ischemic stroke remains a major global health burden, consistently ranking among the leading causes of mortality and long-term disability. Although rodent models are widely utilized for ischemic stroke research, their limited translational success has driven the pursuit of alternative experimental systems. This review underscores the growing significance of non-mammalian models, particularly <i>zebrafish</i> and <i>Drosophila melanogaster</i>, in advancing ischemic stroke research. Zebrafish offer notable advantages, including high genetic homology with humans, optical transparency, a pronounced capacity for neural regeneration, in vivo live real-time imaging, and behavioral analyses. Photothrombotic and systemic hypoxia paradigms in zebrafish enable detailed investigation of neurovascular injury and recovery processes. <i>Drosophila</i>, characterized by a rapid life cycle and sophisticated genetic toolkit, serves as a valuable model for elucidating hypoxia-induced neuronal damage and stroke-related comorbidities such as sleep disturbances. These models are cost-efficient, ethically advantageous, and well-suited for high-throughput applications. Despite inherent anatomical and physiological disparities, non-mammalian systems provide critical complementary insights into stroke pathogenesis and therapeutic innovation, reinforcing their integration into multi-model research frameworks.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G Protein-Coupled Receptor Kinase 5 (GRK5) Modulates Nociceptin/Orphanin FQ Opioid (NOP) Receptor Desensitization in Rat Sympathetic Neurons","authors":"Mohamed Farrag,&nbsp;Marwa Soliman,&nbsp;Saifeldin Mahmoud,&nbsp;Lauren Miller,&nbsp;Paul B. Herold,&nbsp;Kristen Brandt,&nbsp;Victor Ruiz-Velasco","doi":"10.1002/jnr.70110","DOIUrl":"10.1002/jnr.70110","url":null,"abstract":"<p>Stimulation of nociceptin/orphanin FQ peptide (NOP) opioid receptors by the endogenous ligand nociceptin (Noc) leads to voltage-gated Ca²⁺ channel inhibition or G protein inwardly rectifying K⁺ channel activation. One mechanism of G protein-coupled receptor (GPCR) desensitization occurs when G protein-coupled receptor kinases (GRK) phosphorylate the agonist-bound receptors. In the continued presence of an agonist, Gβγ recruits GRK to the plasma membrane where GPCR are then phosphorylated by GRK. The purpose of this study was to identify the GRK subtype responsible for desensitization of the Noc-mediated Ca²⁺ current inhibition in rat stellate ganglion (SG) neurons. We observed that GRK2 and GRK5 are expressed in SG neurons. Further, silencing either GRK subtype alone or together employing siRNA did not overtly alter their Noc pharmacological profile. We assessed NOP receptor desensitization employing a protocol where the peak Ca²⁺ current inhibition was measured during intermittent application of high Noc concentrations in the continued presence of the IC₅₀ Noc concentration. With this approach, we observed complete Ca²⁺ current desensitization in neurons transfected with either scrambled or GRK2 siRNA following exposure to high Noc concentrations. On the other hand, full desensitization of the Ca²⁺ currents was not observed in neurons in which GRK5 was silenced alone or with GRK2. That is, coupling of NOP receptors with Ca²⁺ channels was still observed following application of high Noc concentration. These results suggest that GRK5 plays a key role in the mechanism that mediates NOP receptor desensitization in SG neurons.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12800729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Subcellular Localization of the Cystic Fibrosis Transmembrane Conductance Regulator in the Chicken Retina Suggests Multiple Roles in Retinal Function","authors":"Brandon Leviskas,&nbsp;Evanna Gleason","doi":"10.1002/jnr.70109","DOIUrl":"10.1002/jnr.70109","url":null,"abstract":"<div>\u0000 \u0000 <p>Protein function is influenced by multiple factors including cell type and subcellular localization. The cystic fibrosis transmembrane conductance regulator (CFTR) is well investigated in epithelial tissues, where life threatening symptoms stem from its dysfunction. A postsynaptic neuronal role was previously established by the Gleason lab where CFTR regulation of cytosolic Cl^– in retinal amacrine cells was shown. Other work from our lab showed that disruption of the synaptic vesicle cycle reduced action of CFTR, suggesting CFTR associates with synaptic vesicles. Here, we evaluate the hypothesis that CFTR localizes to the synapse with possible presynaptic function. To address this, the cellular and subcellular CFTR localization in mature chicken retina was examined using fluorescence light microscopy and immunogold-labeled transmission electron microscopy. CFTR labeling was detected throughout the retina, including photoreceptor outer segments and in the mitochondria rich region of the photoreceptor inner segment termed the ellipsoid. Synaptic labeling was found in both synaptic plexiform layers, pre-and post-synaptically. A subset of amacrine cells were strongly labeled and labeling was also found in Müller cells and in axons of the nerve fiber layer. Addressing whether the activity of CFTR plays a role in presynaptic function, amacrine cells were recorded using the whole cell voltage clamp method. Spontaneous postsynaptic quantal currents were recorded and found to increase in frequency upon pharmacological inhibition of CFTR suggesting that under normal circumstances, CFTR serves to limit the rate of spontaneous synaptic vesicle fusion. This work provides evidence CFTR might have multiple functions in the retina including synaptic transmission regulation.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145944547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tryptophan Hydroxylase: A Target for the Correction of Affective and Neurodegenerative Disorders","authors":"Valentina Mikhailovna Sviridova,&nbsp;Margarita Timurovna Absalyamova,&nbsp;Marina Nikolaevna Karpenko,&nbsp;Irina Sergeevna Ivleva","doi":"10.1002/jnr.70106","DOIUrl":"10.1002/jnr.70106","url":null,"abstract":"<div>\u0000 \u0000 <p>Tryptophan hydroxylase (TPH) is a key enzyme in the biosynthesis of serotonin, a neurotransmitter involved in the regulation of mood, emotional state, sleep, appetite, digestion, and cognitive functions. It plays a key role in the creation of a sense of well-being, reduction of anxiety and control of the response to stress. Imbalances in its levels are associated with many disorders, notably depression, anxiety disorders and migraines. This review examines the structural and functional aspects of the regulation of TPH activity with an emphasis on its isoforms, TPH1 and TPH2, which are responsible for serotonin synthesis in peripheral tissues and in neurons, respectively. Approaches to TPH regulation at the gene, protein, and enzymatic activity levels are discussed. The role of TPH in the pathogenesis of affective disorders such as depression, anxiety, attention deficit hyperactivity disorder and posttraumatic stress disorder is also discussed. Approaches to modulating TPH activity are proposed, including, for example, using calpain inhibitors.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Magic Mushroom (Psilocybe azurescens) on Social Interaction, Anxiety- and Depressive-Like Behaviors in Male Rats; the Role of Neuroinflammation, Oxidative Stress, and Neurotrophic Factors","authors":"Hediye Moghadam,&nbsp;Parisa Akbari,&nbsp;Elmira Beirami,&nbsp;Samaneh Nabavifard,&nbsp;Akram Ameli,&nbsp;Neda Valian","doi":"10.1002/jnr.70107","DOIUrl":"10.1002/jnr.70107","url":null,"abstract":"<div>\u0000 \u0000 <p>Psilocybin-containing mushrooms, commonly known as magic mushrooms, strongly affect mood, cognition, and behavior. <i>Psilocybe azurescens</i> is a species of psilocybin mushrooms that contains the main active compounds psilocybin and psilocin. Psilocybin mushrooms have been used since ancient times to improve the quality of life. However, their adverse effects have been less studied. This study aimed to investigate, for the first time, the effect of oral consumption of <i>P. azurescens</i> on social behavior, anxiety- and depressive-like behaviors in rats. The underlying mechanisms of these behaviors were also studied. Male Wistar rats received three doses of <i>P. azurescens</i> (10, 100, and 250 mg/kg) by gavage every other day for 14 days. Social interaction, anxiety- and depressive-like behaviors were assessed using the three-chamber, elevated plus maze, and forced swimming tests, respectively. Protein levels of neurotrophic (BDNF and GDNF), neuroinflammatory (IL-6 and TNFα), and oxidative stress (ROS and SOD) factors were measured in the hippocampus, prefrontal cortex (PFC), and amygdala by ELISA technique. The results showed that <i>P. azurescens</i> significantly increased anxiety- and depressive-like behaviors and disrupted social interaction behavior in rats. These effects were accompanied by increased neuroinflammation and oxidative stress and decreased neurotrophic factors in the hippocampus, PFC, and amygdala. This study suggests that the high doses of <i>P. azurescens</i> can cause mood disorders by increasing inflammatory responses and oxidative stress and decreasing the expression of neurotrophic factors.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of Magnetic Resonance Spectroscopy Levels of Glutamate and GABA by Ketamine in Treatment-Resistant Depression","authors":"Stephanie Njau,&nbsp;Artemis Zavaliangos-Petropulu,&nbsp;Shantanu Joshi,&nbsp;John Brooks,&nbsp;Joseph O'Neill,&nbsp;Woods P. Roger,&nbsp;Viviane Norris,&nbsp;Randall T. Espinoza,&nbsp;Katherine L. Narr","doi":"10.1002/jnr.70102","DOIUrl":"10.1002/jnr.70102","url":null,"abstract":"<div>\u0000 \u0000 <p>Ketamine has emerged as a highly effective intervention for treatment-resistant depression (TRD). Though it acts as a non-competitive antagonist of excitatory N-methyl-D-aspartate receptors (NMDAR), widely expressed in the brain, including on inhibitory γ-aminobutyric acid (GABA)-ergic cells, the mechanisms of its antidepressant action are less clear. To investigate the links between glutamate and GABA neurotransmission and the clinical benefits of ketamine, we used proton magnetic resonance spectroscopy (¹H-MRS) to measure both glutamate and GABA levels in the dorsal anterior cingulate cortex (dACC) in 60 participants with TRD before (~within 1 week), and 24 h after a 40-min intravenous infusion with 0.5 mg/kg of racemic (<i>R,S</i>)-ketamine. The 17-item Hamilton Depression Rating Scale (HDRS₁₇) was used as the primary measure of clinical improvement, and a 50% or greater improvement in HDRS₁₇ ratings was used to define treatment responders. Ketamine increased mean dACC glutamate levels in responders only 24 h after treatment (<i>n</i> = 25, <i>p</i> = 0.01). Further, lower glutamate levels at baseline predicted greater improvements in HDRS₁₇ scores at 24 h post treatment (<i>p</i> &lt; 0.0001). However, GABA levels remained stable after treatment irrespective of response status (<i>p</i> = 0.90). Metabolites associated with neuronal integrity (tNAA), metabolic function (tCr), and membrane turnover (tCho), which may serve as complementary biological evidence of ketamine-induced plasticity, also increased with treatment (all <i>p</i> &lt; 0.01). Results provide evidence of sustained enhancements of neurotransmission or other glutamate-related metabolic effects following subanesthetic ketamine in responders and a potential role of ACC glutamate levels as a biomarker of responsivity to ketamine.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145863177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortical Hierarchy Collapse in Alzheimer's Disease: Connectome Gradient Compression as a Potential Biomarker","authors":"Mei-Ting Zhao,&nbsp;Qi Gong,&nbsp;Ran Chen,&nbsp;Yun Jiao,&nbsp;Alzheimer's Disease Neuroimaging Initiative","doi":"10.1002/jnr.70099","DOIUrl":"10.1002/jnr.70099","url":null,"abstract":"<div>\u0000 \u0000 <p>This investigation centered on Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory impairment and cognitive decline. Functional connectome gradient analysis was utilized to investigate alterations in the hierarchical architecture of brain networks in AD. The study cohort consisted of 222 subjects, encompassing 111 AD patients and 111 normal controls (NC). Connectome gradients were computed via a dimensionality reduction technique based on diffusion map embedding and analyzed at both the region of interest (ROI) and network levels. Additional connectome gradient metrics, including network median distance and gradient eccentricity, were calculated, and the relationship between connectome gradients and rich-club organization was assessed. These connectome gradient values were subsequently correlated with clinical cognitive scores. The results demonstrated a significant reduction in the principal gradient range in AD patients. At the network level, gradient values exhibited an increase in the somatomotor (SMN) and visual networks (VIS), while decreasing in the default mode (DMN) and frontoparietal networks (FPN) relative to controls. Analyzes of network mean distance and gradient eccentricity further revealed compression of the brain cortical hierarchy in AD patients. Furthermore, rich-club analyzes indicated a reduction in the gradient value difference between hub and peripheral nodes in AD patients. Finally, clinical correlation analysis revealed a positive correlation between the degree of cognitive impairment and the degree of compression of the brain cortical hierarchy. These findings provide a novel perspective on the study of brain network organization in AD patients, contributing to a more comprehensive understanding of the neural mechanisms underlying Alzheimer's disease.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145804890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repetitive Blast Exposure Drives Chronic Pain in Female Rats","authors":"Amirah Wright,&nbsp;Susan F. Murphy,&nbsp;Pamela J. VandeVord","doi":"10.1002/jnr.70103","DOIUrl":"10.1002/jnr.70103","url":null,"abstract":"<p>Clinical studies have established that repeated blast traumatic brain injury (rbTBI) can result in chronic pain conditions, with outcomes exhibiting notable sex-dependent differences. However, limited preclinical rbTBI models have systematically investigated the behavioral and neuropathological outcomes of female subjects. In the present study, adult female rats were subjected to repeated blast exposures, and the subsequent development of chronic pain–related behaviors and neuropathological changes was assessed. Repeated blast events induced robust mechanical and thermal hypersensitivity beginning 48 h post-injury and persisted through 12 weeks, accompanied by anxiety and depressive-like behaviors at the chronic time point. These behavioral alterations were associated with increased glial activity, as evidenced by Glial Fibrillary Acidic Protein (GFAP) and Ionized Calcium-Binding Adaptor Molecule 1 (IBA-1) in the frontal cortex and posterior nucleus regions at 12 weeks following injury. Notably, expression levels of neuropeptide markers, Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP), remained unchanged. Collectively, these findings suggest that chronic pain behaviors following rbTBI in females are mediated primarily by sustained glial activation rather than neuropeptide dysregulation.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12714028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frequency and Timing-Dependent Effects of Ultrasound on Neural Responses: Comparative Analysis With Whisker Stimulation in Rats","authors":"Ye Yuan,&nbsp;Tian Liu,&nbsp;Jue Wang","doi":"10.1002/jnr.70100","DOIUrl":"10.1002/jnr.70100","url":null,"abstract":"<div>\u0000 \u0000 <p>This study explores whether ultrasound can induce short-term synaptic plasticity (STP)-like effects at the systems level by modulating cortical excitability and sensory responsiveness. We designed a temporally shifted sensory paradigm to test how ultrasound frequency (1, 2, and 4 MHz), inter-stimulus interval (10, 25, and 100 ms), and stimulation order (ultrasound–whisker vs. whisker–ultrasound) affect cortical responses in the rat barrel cortex. Thirty Sprague–Dawley rats underwent an identical experimental protocol. Electrocorticography (ECoG) signals were recorded from the C2 barrel column, and neural responses were assessed by peak amplitude, latency, and power spectral density. Whisker stimulation alone evoked strong cortical responses, significantly greater than ultrasound stimulation. Notably, when ultrasound preceded whisker stimulation by 25 ms, subsequent whisker responses were significantly enhanced, suggesting the existence of a cortical “excitability window” for neuromodulation. This facilitation effect was absent with time intervals of 10 and 100 ms. Mechanistically, ultrasound may modulate membrane tension and activate mechanosensitive ion channels to transiently lower the activation threshold of cortical neurons. These findings reveal that ultrasound can temporally enhance cortical excitability and sensory responsiveness in a frequency- and timing-dependent manner. Our results provide systems-level evidence of STP-like neuromodulation and provide the potential of ultrasound as a noninvasive method for dynamic control of sensory processing.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145762942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabidiol as a Neuroprotective Agent in Acrylamide-Induced Neurotoxicity: Effects on Oxidative Stress, Inflammation, and Cholinergic Function in Male Mice","authors":"Korina Atsopardi,&nbsp;Konstantinos Mesiakaris,&nbsp;Ioannis Sotiropoulos,&nbsp;Marigoula Margarity,&nbsp;Konstantinos Poulas","doi":"10.1002/jnr.70098","DOIUrl":"10.1002/jnr.70098","url":null,"abstract":"<p>The neuroprotective potential of cannabidiol (CBD) was assessed in a mouse model of acrylamide-induced neurotoxicity. Acrylamide (AA), an environmental and dietary pollutant, is known to cross the blood–brain barrier and induce oxidative stress, inflammation and neurotoxic effects. Male C57BL/6 mice were randomly assigned to four groups: Control (Con), Acrylamide (AA), Cannabidiol (CBD), and a combination treatment (AA + CBD). The AA group received acrylamide (10 mg/kg, i.p.) daily for 5 days. CBD was administered (10 mg/kg, i.p.) for 10 days in the CBD and AA + CBD groups. In the AA + CBD group, acrylamide (10 mg/kg, i.p.) was co-administered during the last 5 days of CBD treatment. Behavioral outcomes were analyzed using the open field test, revealing that CBD mitigated anxiety-like behavior induced by acrylamide, enhancing movement and center exploration. Further, CBD treatment modulated oxidative stress responses, reducing MDA levels and partially restoring antioxidant markers (GSH, SOD, and CAT) in the hippocampus and striatum. Inflammatory markers were also assessed, revealing that acrylamide elevated pro-inflammatory cytokines TNF-α and IL-6. Notably, CBD co-treatment reduced TNF-α levels in the hippocampus and cortex and attenuated IL-6 levels in the cortex and striatum, suggesting an anti-inflammatory effect. Additionally, CBD modulated neuroplasticity by increasing BDNF levels in the hippocampus, counteracting the reduction caused by acrylamide. CBD also influenced cholinergic activity by restoring Ach levels and altering AChE activity across brain regions. Findings suggest that CBD exhibits neuroprotective properties by reducing oxidative stress, inflammation and cholinergic dysregulation, thereby offering a promising therapeutic approach for mitigating pollutant-induced neurotoxicity and potentially treating neurodegenerative disorders.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 12","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12704046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145756903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}