Brain Research最新文献

{"title":"Comparison of actions of ketamine and telazol on cochlear function in a rodent model of noise-induced hearing loss","authors":"Kayla Minesinger ,&nbsp;Maria Fernanda Yepes ,&nbsp;Suhrud M. Rajguru","doi":"10.1016/j.brainres.2025.149496","DOIUrl":"10.1016/j.brainres.2025.149496","url":null,"abstract":"<div><div>Research has shown that anesthesia used in rodent models studying trauma-related changes in the peripheral auditory system can impact the results of standard functional tests like the auditory brainstem response (ABR). The anesthetic agents may also confound the effects of potential therapeutics under evaluation in the preclinical models. Ketamine, a N-methyl-D-aspartate (NMDA) receptor antagonist, is a commonly employed anesthetic in rodent models. Studies have shown that ketamine, unlike other anesthetics, exerts minimal effects on ABR measurements. Tiletamine, a compound chemically akin to ketamine, is also an NMDA antagonist. Tiletamine combined with zolazepam (Telazol) may be a substitute for ketamine given its less severe side-effects and long-acting capacity. In this study, we serially compare cochlear function in rats exposed to hazardous noise to induce noise-induced hearing loss (NIHL) under the effects of either ketamine or telazol. Awake male Brown Norway rats were exposed to octave band noise (4–8 kHz) at 110 dB SPL for 1 h. Cochlear function was assessed over multiple time points using either intramuscular injection of ketamine (44 mg/kg) and xylazine (5 mg/kg) or intraperitoneally injected telazol (20 mg/kg) and xylazine (5 mg/kg). Changes in ABR threshold, latency, and amplitude were compared to baseline<!--> <!-->(pre-NIHL) over 28 days. Functional results demonstrated that both ketamine- and telazol-anesthetized animals experience permanent changes in thresholds following noise. While both amplitude and latency were affected by noise, there were no significant differences in the changes between ketamine and telazol groups. Our findings suggest that telazol behaves similarly to ketamine and could be an alternative in rodent model experiments for the evaluations of hearing sensitivity following noise trauma.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149496"},"PeriodicalIF":2.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439817","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":"Rhythmic deep-brain magnetic stimulation promotes angiogenesis and inhibits apoptosis by regulating the JAK2/STAT3 pathway in rats with superior sagittal sinus thrombosis","authors":"Min Li ,&nbsp;Jiahao Chen ,&nbsp;Ran Meng ,&nbsp;Xunming Ji","doi":"10.1016/j.brainres.2025.149509","DOIUrl":"10.1016/j.brainres.2025.149509","url":null,"abstract":"<div><div>The purpose of this study is to investigate the therapeutic value of rhythmic deep-brain magnetic stimulation (rDMS) and its potential mechanisms in Sprague-Dawley rats with superior sagittal sinus thrombosis (SSST). Rats were randomly allocated into Sham, SSST, SSST + rDMS and SSST + rDMS + AG490 group (N = 27 each). After 2 weeks of rDMS treatment, the motor function of rats was assessed using the open field, rotarod, and beam balance tests. Triphenyltetrazolium chloride (TTC) staining was used to determine the infarct volume. Magnetic resonance venography (MRV) and hematoxylin and eosin (H&amp;E) staining were used to assess the recanalization of the superior sagittal sinus. The protein expression levels of JAK2, p-JAK2, STAT3, p-STAT3, VEGF-A, Bcl-2, Bax, and caspase-3 was analyzed by Western blotting. The mRNA expression of VEGF-A was determined by quantitative real-time polymerase chain reaction (qPCR). Immunofluorescence staining was used to evaluate the protein expression of the capillary marker CD31. Rats with SSST exhibited motor dysfunction compared to sham rats. rDMS therapy alleviated the motor dysfunction as indicated by increased move distance (p &lt; 0.001), move time (p = 0.046) and latency to fall (p = 0.042), and decreased balance latency (p = 0.024) in rats with SSST. Remarkably, rDMS treatment reduced the infarction volume (p = 0.010) in the parasagittal sinus cortex without promoting recanalization of the superior sagittal sinus. rDMS therapy increased the expression of p-JAK2 (p = 0.006) and p-STAT3 (p &lt; 0.001) in rats with SSST, but had no effect on the expression of JAK2 and STAT3. rDMS therapy also increased the mRNA and protein expression of VEGF-A (p = 0.002; p = 0.030) and the density of CD31-positive capillaries (p &lt; 0.001) in rats with SSST. In addition, rDMS treatment increased the expression of Bcl-2 (p &lt; 0.001) and decreased the expression of Caspase-3 (p &lt; 0.001) and Bax (p &lt; 0.001) in rats with SSST. AG490, an inhibitor of JAK2, eliminated the therapeutic effect of rDMS. In conclusion, rDMS therapy improves motor dysfunction, reduces parasagittal infarct, promotes angiogenesis, and suppresses apoptosis in rats with SSST by activating the JAK2/STAT3 signaling pathway.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149509"},"PeriodicalIF":2.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432619","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":"Impact of preconceptional intermittent fasting on reflex ontogenesis, physical and somatic development of the offspring of Wistar rats","authors":"Alana Natalícia Vasconcelos de Araújo ,&nbsp;Larissa Maria Gomes Dutra ,&nbsp;Bruno Silva Dantas ,&nbsp;Adriano Francisco Alves ,&nbsp;Stephenson Andriola Almeida Gonçalves ,&nbsp;Angela Maria Tribuzy de Magalhães Cordeiro ,&nbsp;Juliana Késsia Barbosa Soares ,&nbsp;Jailane de Souza Aquino","doi":"10.1016/j.brainres.2025.149510","DOIUrl":"10.1016/j.brainres.2025.149510","url":null,"abstract":"<div><h3>Background</h3><div>Intermittent fasting (IF) has health benefits; however, little is known about its effects on the offspring when practiced by dams in the preconception period. The aim of the study was to evaluate the impact of IF during the preconception period on physical and somatic parameters, as well as on the reflex ontogenesis of Wistar rat offspring.</div></div><div><h3>Methods</h3><div>The female rats were randomized into two groups: control (CG) and intermittent fasting group (IF) submitted to a feed restriction of 16 h for four weeks during the preconception period. Reproductive performance, body weight, and energy intake were evaluated in dams. Reflex ontogeny, physical and somatic development, brain fatty acids and the brain histology were evaluated in the offspring.</div></div><div><h3>Results</h3><div>IF did not change the reproductive performance or weight of dams during the preconception period. An acceleration of vibrissae placing and negative geotaxis parameters of reflex ontogenesis was observed, as well as anticipation of the following physical development indicators: ear unfolding, an eruption of upper incisor teeth, and inferior teeth in the IF offspring. Although the nervous tissue did not present histological changes, the content of some brain fatty acids was found in greater amounts in the IF offspring such as dihomo-γ-linolenic acid (0.66 ± 0.01 %) and eicotrienoic acid (0.58 ± 0.03 %).</div></div><div><h3>Conclusion</h3><div>IF during preconception did not change the body weight or reproductive performance of the dams, and promoted beneficial effects on the neurodevelopment of the offspring in the early life.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149510"},"PeriodicalIF":2.7,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432615","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":"Outlook of SNCA (α-synuclein) transgenic fly models in delineating the sequel of mitochondrial dysfunction in Parkinson’s disease","authors":"Jennifer Sally Samson ,&nbsp;Kalyanaraman Rajagopal ,&nbsp;Venkatachalam Deepa Parvathi","doi":"10.1016/j.brainres.2025.149505","DOIUrl":"10.1016/j.brainres.2025.149505","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with mechanisms that results in loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) region of the brain. Being a complex heterogeneous disorder, there is a requisite in discovering the underlying molecular signatures that could potentially help in resolving challenges associated with diagnosis as well as therapeutic management. <em>SNCA</em> gene that encodes for the protein α-synuclein is widely known for its indispensable role in aggravating the progression of sporadic and familial PD, upon mutations. Likewise, mitochondrial dysfunction is inferred to be playing a central role in both forms of PD. Observations from experimental models and human PD cases displayed strong evidence for disruption of mitochondrial dynamics, inhibition of mitochondrial complex I protein’s function and elevation in reactive oxygen species (ROS) by the toxic aggregation of α-synuclein. Further, recent studies have raised the possibility of an underlying relationship, where the α-synuclein toxicity is exacerbated by the mutant mitochondrial complex proteins and vice-versa. In this review, we provide an overview of mechanisms influencing α-synuclein-related neurodegeneration, particularly, emphasizing the role of <em>SNCA</em> (α-synuclein) gene in leading to altered mitochondrial biogenesis during PD. We have described how transgenic <em>Drosophila</em> models were reliable at recapitulating some of the essential characteristics of PD. In addition, we highlight the capability of utilizing transgenic fly models in deciphering the altered α-synuclein toxicity and mitochondrial dysfunction, as induced by defects in the mitochondrial DNA.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149505"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422347","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":"Corrigendum to “Neurogranin binds alpha-synuclein in the human superior temporal cortex and interaction is decreased in Parkinson’s disease” [Brain Res. 1591 (2014) 102–110]","authors":"Andrew O. Koob ,&nbsp;Gideon M. Shaked ,&nbsp;Andreas Bender ,&nbsp;Alejandro Bisquertt ,&nbsp;Edward Rockenstein ,&nbsp;Eliezer Masliah","doi":"10.1016/j.brainres.2025.149504","DOIUrl":"10.1016/j.brainres.2025.149504","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149504"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The α-MG exhibits neuroprotective potential by reducing amyloid beta peptide-induced inflammation, oxidative stress, and tau aggregation in human neural stem cells","authors":"Ming-Chang Chiang ,&nbsp;Christopher J.B. Nicol ,&nbsp;Yu-Ping Yang ,&nbsp;Tairui Chiang ,&nbsp;Chiahui Yen","doi":"10.1016/j.brainres.2025.149506","DOIUrl":"10.1016/j.brainres.2025.149506","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the primary cause of dementia in older adults. Amyloid-beta (Aβ) and tau protein neurofibrillary tangles accumulate in the brain, leading to a progressive decline in memory, thinking, and behavior. Neuroinflammation and oxidative stress play a significant role in the development and progression of AD. Research has suggested that α-mangostin (α-MG), a compound found in mangosteen peels, may have anti-inflammatory, antioxidant, and neuroprotective properties, which could be beneficial in the context of AD. Further research is required to fully comprehend the therapeutic mechanisms of α-MG on AD and determine its potential as a treatment option. α-MG treatment significantly improves the viability of hNSCs exposed to Aβ and reduces caspase activity. Furthermore, this treatment is associated with a notable decrease in the expression of TNF-α and IL-1β. The treatment effectively restores alterations in the expression of IKK and NF-κB (p65) induced by Aβ, which are critical factors in the inflammatory response. Moreover, α-MG effectively reduces iNOS and COX-2 levels in Aβ-treated hNSCs, showcasing its potential therapeutic benefits. Treatment with α-MG protects hNSCs against Aβ-induced oxidative stress and effectively prevents the decrease in Nrf2 levels caused by Aβ. The treatment significantly enhances the activity and mRNA expression of Nrf2 downstream antioxidant target genes, including SOD-1, SOD-2, Gpx1, GSH, catalase, and HO-1, compared to Aβ-treated controls. α-MG significantly reduces tau and ubiquitin (Ub) aggregates, enhances proteasome activity, and increases the mRNA expression of HSF1, HSP27, HSP70, and HSP90 in Tau-GFP-expressed hNSCs. This study significantly improves our comprehension of the anti-inflammatory, antioxidative stress, and anti-aggregated effects of α-MG. These findings have potential therapeutic implications for developing treatments that could delay AD progression and promote healthy aging.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149506"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424520","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":"Habituation to novel stimuli alters hippocampal plasticity associated with morphine tolerance in male Wistar rats","authors":"Ghazaleh Ghamkharinejad ,&nbsp;Francesca Mottarlini ,&nbsp;Zohreh Tavassoli ,&nbsp;Lucia Caffino ,&nbsp;Fabio Fumagalli ,&nbsp;Judith R. Homberg ,&nbsp;Yaghoub Fathollahi","doi":"10.1016/j.brainres.2025.149508","DOIUrl":"10.1016/j.brainres.2025.149508","url":null,"abstract":"<div><div>Chronic morphine exposure affects neuroplasticity in the hippocampus, a key area for learning and memory. Since, novelty exploration influence rodent hippocampal plasticity, the aim of this study was to investigate the effects of habituation to novel contexts and odors on hippocampal plasticity in morphine-tolerant rats. For this purpose, neurogenesis markers, dendritic spine density and mRNA levels for various genes encoding neurotrophic factors were evaluated in the hippocampus tissue (ventral, vH vs. dorsal, dH) of male rats. Habituation to the new environment was established using animal models of morphine tolerance. Following multiple exposures to a novel context (open field habituation, OFH) or a series of novel odors (odor habituation, OH), markers (Ki67 or DCX) associated with neurogenesis were found to be lower in the morphine-tolerant rats that underwent habituation than the non-habituated morphine-tolerant rats, with specific regions (dH, vH), being differently influenced by specific type of habituation (OFH, OH, respectively). Further results showed subregion and habituation specific effects on the number of dendritic spines per spine type or levels of neurotropic factors including BDNF and TrkB mRNA levels in the dH and vH in morphine-tolerant rats that underwent habituation as compared to the non-habituated morphine-tolerant rats. We provide new evidence that habituation to novel contexts and novel odors appears to affect hippocampal plasticity in morphine-tolerant rats and that pro-plasticity molecules appear to mediate habituation effects on morphine tolerance plasticity.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1853 ","pages":"Article 149508"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424588","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":"Olfactory deprivation promotes amyloid β deposition in a mouse model of Alzheimer’s disease","authors":"Xirun Zhao ,&nbsp;Qing Zhou ,&nbsp;Huan Zhang ,&nbsp;Munenori Ono ,&nbsp;Takafumi Furuyama ,&nbsp;Ryo Yamamoto ,&nbsp;Tomoko Ishikura ,&nbsp;Masami Kumai ,&nbsp;Yukari Nakamura ,&nbsp;Hideaki Shiga ,&nbsp;Takaki Miwa ,&nbsp;Nobuo Kato","doi":"10.1016/j.brainres.2025.149500","DOIUrl":"10.1016/j.brainres.2025.149500","url":null,"abstract":"<div><div>Olfactory dysfunction is regarded as an early marker for Alzheimer’s disease (AD). Slowly progressing AD pathology is interpreted to impair cognition and olfactory sensation independently, while olfactory deficits emerge earlier. The present experiments tested the possibility that olfactory impairment may worsen cognition or AD pathology using 3xTg AD model mice with olfactory bulbectomy (OBX). In open-field tests, OBX was shown to increase anxiety-like behavior in both wild-type (WT) and AD model mice, and hyperactivity was induced in WT mice only. Spatial memory, assessed by the Morris water maze (MWM) test, was impaired in WT but not AD mice. Object memory, assessed by the novel object recognition test, was not changed by OBX either in WT or AD mice. Densitometry of Aβ plaques stained with 6E10 and anti-Aβ42 antibodies was carried out in sections containing the hippocampal formation obtained from AD mice aged 12 and 18 months. The plaque area was larger in the OBX than in the sham group at 12 months. At 18 months, there was also difference in the plaque area. Given that Aβ plaques emerge in 3xTg mice relatively later (&gt;9 months of age) than in other models, OBX in 3xTg mice appears to exacerbate Aβ pathology at the early phase of Aβ emergence, implying a causative link of smell loss to AD pathogenesis. The accelerated Aβ plaque formation by OBX was accompanied by microglial activation. Early intervention to smell loss may be beneficial for AD control.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149500"},"PeriodicalIF":2.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373776","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":"Impaired 2.5-Hz auditory steady-state response in schizophrenia","authors":"Wenpeng Hou ,&nbsp;Xiangqin Qin ,&nbsp;Yanbing Xiong ,&nbsp;Yujie Wen ,&nbsp;Yuan Zhou ,&nbsp;Fuchun Zhou ,&nbsp;Xianbin Li ,&nbsp;Chuanyue Wang","doi":"10.1016/j.brainres.2025.149503","DOIUrl":"10.1016/j.brainres.2025.149503","url":null,"abstract":"<div><h3>Background</h3><div>Delta-band (1–4 Hz) oscillation contributes to speech recognition and may be impaired in schizophrenia. This study primarily aimed to investigate the impairment of the 2.5-Hz auditory steady-state response (ASSR) and its correlation with other auditory cognitive indicators, clinical symptoms, and multidomain cognition in individuals with schizophrenia.</div></div><div><h3>Methods</h3><div>In this cross-sectional study, 30 patients with schizophrenia and 30 healthy controls underwent 2.5- and 40-Hz ASSR and mismatch negativity (MMN) assessment. The Positive and Negative Syndrome Scale (PANSS) was utilized to assess the patients’ clinical symptoms, and the MATRICS consensus cognitive battery (MCCB) was used to evaluate cognitive function.</div></div><div><h3>Results</h3><div>The 2.5-Hz ASSR inter-trial coherence (ITC) was significantly lower among patients with schizophrenia than among healthy controls (<em>P</em> = 0.012, Cohen’s <em>d</em> = 0.66). The 2.5-Hz ASSR ITC alone distinguished these groups, with 53.3 % sensitivity, 70.0 % specificity, and 61.7 % accuracy. In the schizophrenia group, the 2.5-Hz ASSR ITC did not correlate significantly with the MMN amplitude or any clinical symptoms or cognitive measurement. In healthy controls, the 2.5-Hz ASSR ITC correlated positively with verbal learning (<em>r</em> = 0.381, <em>P</em> = 0.038), although this correlation was not significant after Bonferroni correction.</div></div><div><h3>Conclusion</h3><div>The evoked activity maintaining delta-band oscillation entrainment in the auditory system reveals a deficit in schizophrenia and is valuable for the objective diagnosis of this disorder.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149503"},"PeriodicalIF":2.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381478","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":"Muscimol injection in the thalamic reticular nucleus reverts the effect of dopaminergic lesion on short-term memory in the rat globus pallidus externus","authors":"Evangelista-Arzate Christian Alexis,&nbsp;Mora-Zenil Janeth,&nbsp;Reyes-Mendoza Julio Daniel,&nbsp;García-Ramirez Martha,&nbsp;Chuc-Meza Eliezer","doi":"10.1016/j.brainres.2025.149495","DOIUrl":"10.1016/j.brainres.2025.149495","url":null,"abstract":"<div><div>The thalamic reticular nucleus (TRN) is a GABAergic nucleus essential for regulating information flow between the thalamus and cortex. It is involved in various cognitive processes, such as memory and attention, and receives GABAergic input from the external globus pallidus (GPe). The GPe is part of the indirect pathway of the basal ganglia, which is involved in the modulation of motor, limbic, and cognitive functions. Dopaminergic denervation in the GPe (DDGPe) has been linked to a decrease in short-term memory, which reflects the cognitive deficits often observed in the early stages of Parkinson’s disease. We hypothesize that DDGPe might disrupt GABAergic modulation in the TRN, impacting memory. To test this, rats with DDGPe were injected with varying concentrations of muscimol into the TRN and underwent an object recognition test. Results showed that muscimol restored the discrimination index (DI) values reduced by DDGPe, with recovery blocked by bicuculline. These findings suggest that a reduction in the GABAergic influence from the GPe on the TRN compromises the TRN’s functionality during memory processing.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149495"},"PeriodicalIF":2.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381484","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}