Neuroscience Letters最新文献

{"title":"Prolonged exposure of cerebrocortical neurons to diazepam induces downregulation of surface α1-containing GABAA receptors and uncoupling of GABA/benzodiazepine site interactions through different mechanisms","authors":"Leydi Carolina González Gómez,&nbsp;María Clara Gravielle","doi":"10.1016/j.neulet.2025.138495","DOIUrl":"10.1016/j.neulet.2025.138495","url":null,"abstract":"<div><div>GABA_A receptors play a crucial role in mediating fast inhibitory neurotransmission in the central nervous system. These receptors are targets of numerous pharmacological agents used clinically to control neuronal excitability in different neurological disorders. Sustained stimulation of GABA_A receptors by endogenous or exogenous modulators leads to adaptive homeostatic alterations in the receptor function. In particular, chronic benzodiazepine administration results in tolerance to most of the behavioral effects, limiting the clinical use of these drugs for long-term treatments. In previous studies, we found that prolonged exposure of rat cerebrocortical neurons to diazepam produces uncoupling of GABA/benzodiazepine site interactions and decreased expression of the GABA_A receptor α1 subunit gene, mediated by a mechanism involving the activation of L-type voltage-gated calcium channels (L-VGCCs). This work aimed to further explore the molecular basis of GABA_A receptor regulation induced by prolonged benzodiazepine stimulation. Our findings indicate that diazepam increases intracellular calcium levels, confirming the dependence of benzodiazepine-induced GABA_A receptor regulation on calcium entry through L-VGCCs. Immunocytochemical analyses revealed that sustained diazepam treatment reduces the expression of α1-containing GABA_A receptors on the cell surface, which likely impacts functional receptors. By knocking-down α1 subunit expression, we demonstrated that α1 downregulation alone results in minor, non-significant uncoupling, suggesting that additional GABA_A receptor modifications contribute to the observed uncoupling. Altogether, our results suggest that persistent exposure of GABA_A receptors to benzodiazepines produces uncoupling and downregulation of functional α1-containing GABA_A receptors through two distinct mechanisms, both initiated by calcium influx through L-VGCCs.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"873 ","pages":"Article 138495"},"PeriodicalIF":2.0,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145834447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of 5-HT2 receptor signaling impairs normal eye development in zebrafish","authors":"Zulvikar Syambani Ulhaq ,&nbsp;Mitsuyo Kishida","doi":"10.1016/j.neulet.2025.138491","DOIUrl":"10.1016/j.neulet.2025.138491","url":null,"abstract":"<div><div>Serotonin (5-HT) signaling plays essential roles in vertebrate development beyond neurotransmission, including in ocular morphogenesis. Here, we investigated the effects of Ritanserin, a non-selective 5-HT₂ receptor antagonist, on zebrafish embryonic development with a focus on eye formation. While Ritanserin exposure (0.1–10  μM) did not affect mortality or hatching rates up to 96 h post-fertilization (hpf), higher concentrations (5–10  μM) induced developmental abnormalities, such as microphthalmia, pericardial edema, blood congestion, and craniofacial malformations by 5 days post-fertilization (dpf). Ritanserin significantly reduced the expression of <em>cyp19a1b</em>, encoding brain aromatase (AroB) involved in local estrogen synthesis within the eye, and <em>pax6a</em>, a key regulator of retinal neurogenesis, without altering <em>cyp19a1a</em> levels. Co-treatment with exogenous 5-HT or estradiol (E₂) partially rescued eye size, optic nerve morphology, <em>pax6a</em> expression, and reduced retinal apoptosis. Moreover, visual deficits induced by Ritanserin, as shown by impaired visual background adaptation (VBA) and optomotor responses (OMR), were similarly reversed by 5-HT or E₂. These findings demonstrate that 5-HT₂ signaling is critical for proper eye development in zebrafish, likely through regulation of estrogen synthesis and neuroretinal gene expression, and suggest that serotonergic disruption during early development can lead to structural and functional visual deficits.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"873 ","pages":"Article 138491"},"PeriodicalIF":2.0,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The anti-epileptic mechanism of a ketogenic diet regulating the gut microbiota via SIRT2 activation of the PI3K/AKT signaling pathway","authors":"Minghua Li,&nbsp;Haifeng Deng,&nbsp;Ling Ma,&nbsp;Manli Sun","doi":"10.1016/j.neulet.2025.138488","DOIUrl":"10.1016/j.neulet.2025.138488","url":null,"abstract":"<div><h3>Purpose</h3><div>Epilepsy (EP) is a disorder caused by sudden abnormal discharges of neurons in the brain. A ketogenic diet (KD) has significant anticonvulsant effects in some epileptic patients, but the signaling pathway remains unclear. This study aims to investigate the mechanisms underlying the anticonvulsant effects of a KD.</div></div><div><h3>Methods</h3><div>Acute epilepsy models were induced by kainic acid (KA) and pentylenetetrazol (PTZ), synaptic electrical activity in the hippocampus was measured. The effects of KD on the expression levels of postsynaptic proteins and SIRT2 was determined, as well as the phosphorylation of the PI3K and Akt-S-473 signaling pathways. Metabolomic analysis was used to investigate the effect of KD on the gut microbiota.</div></div><div><h3>Results</h3><div>The KD inhibited acute seizures and promoted the amplitude of induced inhibitory postsynaptic current (IPSC) transmission and the frequency of spontaneous IPSC transmission in cortical brain regions. KD upregulated the expression of PI3K, activated the phosphorylation of AKT-S-473, and increased SIRT2 expression. Metabolomic analysis indicated shifts in host metabolism, particularly involving Clostridiales(e.g., Blautia and Lachnospiraceae). Based on existing literature, we hypothesize tha KD may support gut barrier function and anti-inflammatory responses.</div></div><div><h3>Conclusion</h3><div>The anti-epileptic effect of KD in the prefrontal cortex is associated with the activation of the PI3K/Akt signaling pathway and an increase in SIRT2 expression. Additionally, our data are consistent with the emerging concept that the anti-seizure effects of KD may also involve modulation of the gut microbiota. This provides valuable insights for the development of new therapeutic interventions.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138488"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145743511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of lithium chloride in N-methyl-N-nitrosourea induced retinal damage in rats","authors":"Canan Akdeniz İncili ,&nbsp;Yesari Eröksüz ,&nbsp;Hatice Eröksüz ,&nbsp;Abdullah Aslan","doi":"10.1016/j.neulet.2025.138489","DOIUrl":"10.1016/j.neulet.2025.138489","url":null,"abstract":"<div><div>The aim of the current study was to assess the potential neuroprotective effects of lithium chloride (LiCl) against retinal degeneration (RD) induced by N-methyl-N-nitrosourea (MNU) in the rats. 108 rats were assigned to 6 groups: Control, MNU (80 mg/kg), MNU + 30 mg/kg LiCI, MNU + 60 mg/kg LiCI, 30 mg/kg LiCI, and 60 mg/kg LiCI. The experimental groups comprised 18 rats each and the animals were euthanised on the 2nd, 7th and 14th days following the administration of MNU. Compared with the MNU group, both doses of LiCl significantly reduced retinal cell apoptosis and increased retinal thickness (<em>P</em> &lt; 0.05). MNU group had a higher apoptotic index than the treatment groups, as evidenced by increased immunoreactivities of caspase-3, caspase-6, Bax, and 8-OHdG and decreased immunoreactivities of Bcl-2 at day 2. The outer nuclear layer (ONL) of the retina in rats treated with MNU exhibited a significant reduction in comparison the control group on both days 7 and 14 (<em>P</em> &lt; 0.05). In contrast to the MNU-treated figgroup, the LiCl-injected rats exhibited a notable elevation in the expression levels of BDNF and Bcl-2 (<em>P</em> &lt; 0.05). Conversely, the MNU-treated group exhibited markedly increased expression of GSK-3β, Bax, 8-OHdG, caspase-3, and caspase 6 (<em>P</em> &lt; 0.05). In conclusion, LiCl demonstrated dose-dependent neuroprotective effects against MNU-induced RD in rats. These effects included a reduction in retinal cell apoptosis, an improvement in retinal thickness, and the potential involvement of anti-apoptotic mechanisms, glial activation inhibition, and neurotrophic factor modulation.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138489"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of guanethidine-induced sympathectomy on satellite glial cell activation in a rat model of neuropathic pain","authors":"Xicun Han ,&nbsp;Xiaohua Jiang ,&nbsp;Yabin Liu ,&nbsp;Guowu Chen","doi":"10.1016/j.neulet.2025.138483","DOIUrl":"10.1016/j.neulet.2025.138483","url":null,"abstract":"<div><div>The involvement of satellite glial cells (SGCs) in neuropathic pain has been well-established; however, it remains unclear whether the sprouted sympathetic fibers within the dorsal root ganglion (DRG) after peripheral nerve injury affect the activation of SGCs. A rat model of neuropathic pain induced by spinal nerve ligation injury (SNL) was established. The mechanical withdrawal threshold (MWT) was evaluated using the von Frey test on postoperative days (POD) 1, 3, 7, and 14 to quantify mechanical allodynia. Immunofluorescence staining was performed to detect the expression of glial fibrillary acidic protein (GFAP, a marker for activated SGCs), tyrosine hydroxylase (TH, a marker for sympathetic nerve fibers), and α2-adrenergic receptor (α2-AR) in the ipsilateral DRG. Reversible sympathectomy was achieved by means of a single high-dose intraperitoneal injection of guanethidine (Gua). Western blotting(WB) was used to assess the effect of sympathectomy on GFAP expression in the DRG of SNL rats. After spinal nerve injury, the MWT of the ipsilateral hindlimb in rats decreased rapidly. Immunofluorescence results confirmed that the expression levels of GFAP and TH in the ipsilateral DRG of SNL rats gradually increased along with the development of mechanical allodynia. Notably, the co-expression of α2-AR and GFAP in the DRG gradually increased after SNL, suggesting that the newly formed noradrenergic-SGCs signaling within the DRG was involved in the initiation and maintenance of neuropathic pain. On 14 days post-SNL, Gua-induced sympathectomy significantly alleviated mechanical allodynia in rats and remarkably inhibited GFAP expression in the ipsilateral DRG. We concluded that in the rat model of neuropathic pain induced by SNL, the sprouted sympathetic fibers within the DRG may also participate in the maintenance of neuropathic pain by regulating the activation of SGCs.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138483"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145678349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NNT inhibits microglial activation via mitochondrial oxidative stress in spinal cord injury","authors":"Ming Li ,&nbsp;Qiuyue Gu ,&nbsp;Zhenyu Fan ,&nbsp;Chengwei Duan","doi":"10.1016/j.neulet.2025.138486","DOIUrl":"10.1016/j.neulet.2025.138486","url":null,"abstract":"<div><div>Spinal cord injury (SCI) is a major public health challenge, often leading to severe neurological and physical disabilities. Microglia, the primary immune cells in the spinal cord, play critical roles in both the physiology and pathology of SCI. A deeper understanding of microglial activation is thus crucial for developing new therapeutic strategies. In this study, we observed that nicotinamide nucleotide transhydrogenase (NNT), a mitochondrial protein in eukaryotic cells, was upregulated in the injured spinal cord of mice, coinciding with elevated inflammatory factors and microglial activation. <em>In vitro</em>, lipopolysaccharide (LPS) induced microglial activation and increased NNT expression in BV2 cells. NNT overexpression effectively mitigated LPS-induced inflammation, proliferation, and oxidative stress in BV2 microglia. Furthermore, treatment with the mitochondria-targeting peptide SS-31 reduced mitochondrial superoxide levels. SS-31 also suppressed the inflammatory, proliferative, and oxidative stress responses caused by NNT deficiency in BV2 cells. Critically, <em>in vivo</em> overexpression of NNT in the spinal cord attenuated microglial activation and promoted functional recovery after SCI. Our findings reveal that NNT suppresses microglial activation by modulating mitochondrial oxidative stress, offering a promising therapeutic avenue for SCI.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138486"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145701385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structure–function characterization of Olea dioica Roxb. PGK-1: Acetylcholinesterase inhibition, molecular docking, and amelioration of Aβ40-induced toxicity in SH-SY5Y neuronal cells and the UAS-Aβ42; ey-GAL4 drosophila model of Alzheimer’s disease","authors":"G.K. Pratap ,&nbsp;Pramod G Nagaraju ,&nbsp;Chandrashekhar G. Joshi ,&nbsp;Lokesh Koodlur Sannegowda ,&nbsp;Manjula Shantaram ,&nbsp;Poornima Priyadarshini","doi":"10.1016/j.neulet.2025.138467","DOIUrl":"10.1016/j.neulet.2025.138467","url":null,"abstract":"","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138467"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145636883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MEGF10 knockout promotes cortical and hippocampal amyloid deposition in AD mouse model","authors":"Yu Fujita ,&nbsp;Taichi Yabe ,&nbsp;Yoshikazu Yamada ,&nbsp;Ryo Kiuchi ,&nbsp;Motoi Nagase ,&nbsp;Ryosuke Nakamori ,&nbsp;Seisuke Ichikawa ,&nbsp;Takahide Obara ,&nbsp;Hibiki Yasuda ,&nbsp;Jyoichiro Kurano ,&nbsp;Tsubasa Honda ,&nbsp;Hiroto Komano ,&nbsp;Kun Zou ,&nbsp;Yoshiyuki Tanabe ,&nbsp;Tomoji Maeda","doi":"10.1016/j.neulet.2025.138487","DOIUrl":"10.1016/j.neulet.2025.138487","url":null,"abstract":"<div><div>Multiple epidermal growth factor (EGF)-like domains 10 (MEGF10) is a single-pass transmembrane protein expressed in neurons and astrocytes, functioning as a phagocytic receptor for apoptotic cells and mediating homotypic adhesion in the mammalian brain. We previously demonstrated that MEGF10 facilitates the uptake of toxic amyloid-β (Aβ) species Aβ42 and Aβ43 by neurons and astrocytes <em>in vitro</em>. However, whether MEGF10 also serves as a phagocytic receptor for Aβ in the brain <em>in vivo</em>, particularly under neurodegenerative conditions such as Alzheimer’s disease (AD), remains unclear. To address this question, we generated MEGF10 knockout mice on an AD model background and analyzed brain Aβ deposition and Aβ42 levels. We observed a significant increase in Aβ deposition and Aβ42 levels in the hippocampus and cortex of MEGF10-deficient AD mice compared with AD model controls. To assess cognitive function, we performed the Y-maze test. MEGF10 knockout AD mice exhibited impaired spatial memory relative to wild-type controls; however, no significant difference was found between MEGF10 knockout AD mice and AD model controls. These findings suggest that MEGF10 contributes to Aβ clearance in the brain and support its role as a phagocytic receptor for Aβ <em>in vivo</em>, potentially helping to maintain brain homeostasis in the context of Alzheimer’s pathology.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138487"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145708705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Facilitation of supplementary motor area activity modulates the sense of effort: a theta burst stimulation study","authors":"Taishi Okegawa ,&nbsp;Daiki Yamasaki ,&nbsp;Naotsugu Kaneko ,&nbsp;Kimitaka Nakazawa","doi":"10.1016/j.neulet.2025.138482","DOIUrl":"10.1016/j.neulet.2025.138482","url":null,"abstract":"<div><div>The sense of effort, defined as the phenomenological experience of invested physical resources in the task, is a critical component of motor control. The supplementary motor area (SMA) has been implicated in generating this sense, yet it remains unclear how modulating SMA activity affects unconscious motor output when individuals intend to exert the same level of effort. The present study aimed to investigate how inhibiting and facilitating SMA activity influences the subjective sense of effort and associated motor output.</div><div>Twelve healthy volunteers received both facilitatory and inhibitory theta burst transcranial magnetic stimulation (TBS) applied to the SMA. We assessed corticospinal excitability, submaximal effort force production in an index finger abduction task (at a subjective effort level of 35% without visual feedback), and force-matching performance before and after the TBS protocols.</div><div>Results showed that facilitatory TBS led to a significant reduction in the submaximal index finger abduction force, which was accompanied by decreased EMG activity. In contrast, inhibitory TBS did not produce significant changes in submaximal force. Importantly, TBS applied to the SMA did not significantly alter motor-evoked potentials, indicating that corticospinal excitability remained unchanged. These findings suggest that enhanced SMA activity increases the effort required to produce a given force. The underlying mechanism likely involves changes in efference copy signals, as the effect occurred without altering the corticospinal excitability. In addition, force-matching performance was improved at 30 min after facilitatory TBS applied to the SMA. This delayed behavioral improvement may suggest a time-dependent modulation of sensorimotor processing, possibly involving the SMA and posterior parietal cortex, although network-level mechanisms remain speculative.</div><div>This study provides causal evidence for the SMA’s role in processing effort-related signals and contributes to a growing understanding of the cortical mechanisms underlying the sense of effort.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138482"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bovine lactoferrin-induced antinociception through 5-HT1A/1D receptors in formalin-induced tonic pain","authors":"Sergio Ernesto Ávila-Morales,&nbsp;Maria Elisa Drago-Serrano,&nbsp;Beatriz Godínez-Chaparro","doi":"10.1016/j.neulet.2025.138490","DOIUrl":"10.1016/j.neulet.2025.138490","url":null,"abstract":"<div><div>Bovine lactoferrin (bLF) is a multifunctional glycoprotein that displays modulatory effects on pain through pathways not fully known. Therefore, we determined the role of the serotonergic system as a potential mechanism underlying the antinociceptive effect of bLF on formalin-induced tonic nociception. The formalin test was used to assess the antinociceptive effect—pain-like behaviour (flinching) at 1 h. The bLF-induced antinociceptive effect was prevented by the intrathecal (3 µg/rat), but not the intraplantar (30 µg/rat) administration of methiothepin, a non-selective 5-hydroxytryptamine (5-HT) antagonist. Moreover, intrathecal administration of WAY-100635 (6 µg/rat; selective 5-HT_1A receptor antagonist) and BRL1555724 (4 µg/rat; selective 5-HT_1D receptor antagonist) prevented the bLF-induced antinociceptive effect. However, intrathecal administration of SB-224289 (5 µg/rat; selective 5-TH_1B receptor antagonist) and SB-699551 µg/rat; selective 5-TH_5A receptor antagonist) did not prevent the bLF-induced antinociceptive effect. The above finding suggests that bLF reduces acute nociception induced by formalin, and this antinociceptive effect is mediated, at least in part, by the serotonergic system, acting only at the spinal level and not at the peripheral level, via activation of central 5-HT_1A/1D serotonergic receptors.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"872 ","pages":"Article 138490"},"PeriodicalIF":2.0,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145735169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}