Journal of Neuroscience Research最新文献

{"title":"Decreased Water Diffusivity Along the Perivascular Space in Older Adults With Poor Sleep Quality","authors":"Junko Kikuta,&nbsp;Koji Kamagata,&nbsp;Kaito Takabayashi,&nbsp;Yayoi Hayakawa,&nbsp;Toshiaki Taoka,&nbsp;Yuya Saito,&nbsp;Wataru Uchida,&nbsp;Sen Guo,&nbsp;Seina Yoshida,&nbsp;Keigo Yamazaki,&nbsp;Akihiko Wada,&nbsp;Hideyoshi Kaga,&nbsp;Yoshifumi Tamura,&nbsp;Ryuzo Kawamori,&nbsp;Hirotaka Watada,&nbsp;Shigeki Aoki","doi":"10.1002/jnr.70005","DOIUrl":"https://doi.org/10.1002/jnr.70005","url":null,"abstract":"<div>\u0000 \u0000 <p>This study included 52 Japanese older adults with Pittsburgh Sleep Quality Index (PSQI) scores &gt; 5 and 52 healthy controls (HCs) with PSQI score ≤ 5. Diffusion-weighted imaging (DWI) and 3D T1-weighted imaging were acquired using 3T magnetic resonance imaging. The diffusion tensor image analysis along the perivascular space (DTI-ALPS) index was calculated using preprocessed DWI. The choroid plexus volume (CPV) was calculated using FreeSurfer 6.0. The mean ALPS index and CPV were compared between the older adults with poor sleep quality (PSQ) and HCs using a general linear model, adjusted for covariates including age, sex, years of education, total intracranial volume, systolic blood pressure, hemoglobin A1c, and white matter lesion volume. We also conducted a partial correlation analysis between the mean ALPS index and CPV, Montreal Cognitive Assessment (MoCA), and PSQI scores, adjusting for all the mentioned covariates. The PSQ group had a significantly lower mean ALPS index than HCs. The mean ALPS index in the PSQ group was negatively correlated with CPV and positively correlated with the MoCA score. Therefore, older adults with PSQ may experience dysfunction in the excretory pathway of the perivascular space around the medullary veins. This impairment may be associated with an increase in CPV and cognitive dysfunction.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 12","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749361","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":"Efficacy of Low-Dose Ketamine and Propofol in the Treatment of Experimental Refractory Status Epilepticus on Male Rats","authors":"Gaye Boztepe Yılmaz,&nbsp;Kemal Tolga Saraçoğlu,&nbsp;Uğur Aykın,&nbsp;Metehan Akça,&nbsp;Cumaali Demirtaş,&nbsp;Ayten Saraçoğlu,&nbsp;Mehmet Yıldırım","doi":"10.1002/jnr.25393","DOIUrl":"https://doi.org/10.1002/jnr.25393","url":null,"abstract":"<p>Refractory status epilepticus (RSE) is a condition with serious mortality and morbidity rate, resistant to benzodiazepine and second-line antiepileptic drugs. This study aimed to electrophysiologically investigate the combination of NMDA receptor antagonist ketamine and GABAergic agent propofol in an RSE model induced by lithium-pilocarpine in male Sprague–Dawley rats. Seventy-two male Sprague–Dawley rats were divided into nine groups. The RSE model was induced by subcutaneous injection of lithium-CI (5 mEq/kg) and intraperitoneal injection of pilocarpine-HCl (320 mg/kg), after implanting tripolar EEG electrode. Ketamine (30, 60, and 90 mg/kg), propofol (20, 40, and 80 mg/kg), and combinations of both drugs (15 + 20 and 30 + 40 mg/kg) were administered intraperitoneally to animals with RSE. Video-EEG recordings were taken after inducing model and 48 h later. The efficacy of drugs was statistically evaluated based on spike frequencies (spikes/min) and amplitudes (mV). Compared to RSE group, it was determined that 30 and 60 mg/kg doses of ketamine provided effective seizure control and prevented mortality (<i>p</i> &lt; 0.001), while the 90 mg/kg showed toxic effects in all animals and caused mortality. The 80 mg/kg dose of propofol provided seizure control and reduced the mortality rate to 16.7% (<i>p</i> &lt; 0.001), whereas the 20 mg/kg resulted in a 100% mortality rate. The low-dose ketamine+propofol (15 + 20 mg/kg) combination provided early onset seizure control and were as effective as 80 mg/kg propofol (<i>p</i> &lt; 0.05). The study concluded that in the experimental RSE model, seizure control could be achieved with low-dose combination of ketamine and propofol without the need for high doses as in monotherapy, thus preventing dose-related adverse effects.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 11","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25393","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708342","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":"Deficits in or Preservation of Basic Number Processing in Parkinson's Disease? A Registered Report","authors":"Hannah D. Loenneker,&nbsp;Christina Artemenko,&nbsp;Klaus Willmes,&nbsp;Inga Liepelt-Scarfone,&nbsp;Hans-Christoph Nuerk","doi":"10.1002/jnr.25397","DOIUrl":"10.1002/jnr.25397","url":null,"abstract":"<p>Neurodegenerative diseases such as Parkinson's disease (PD) have a huge impact on patients, caregivers, and the health care system. Until now, diagnosis of mild cognitive impairments in PD has been established based on domain-general functions such as executive functions, attention, or working memory. However, specific numerical deficits observed in clinical practice have not yet been systematically investigated. PD-immanent deterioration of domain-general functions and domain-specific numerical areas suggests mechanisms of both primary and secondary dyscalculia. The current study systematically investigated basic number processing performance in PD patients for the first time, targeting domain-specific cognitive representations of numerosity and the influence of domain-general factors. The overall sample consisted of patients with a diagnosis of PD, according to consensus guidelines, and healthy controls. PD patients were stratified into patients with normal cognition (PD-NC) or mild cognitive impairment (level I-PD-MCI based on cognitive screening). Basic number processing was assessed using transcoding, number line estimation, and (non-) symbolic number magnitude comparison tasks. Discriminant analysis was employed to assess whether basic number processing tasks can differentiate between a healthy control group and both PD groups. All participants were subjected to a comprehensive numerical and a neuropsychological test battery, as well as sociodemographic and clinical measures. Results indicate a profile of preserved (verbal representation) and impaired (magnitude representation, place × value activation) function in PD-MCI, hinting at basal ganglia dysfunction affecting numerical cognition in PD. Numerical deficits could not be explained by domain-general cognitive impairments, so that future research needs to incorporate domain-specific tasks of sufficient difficulty.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 11","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25397","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644449","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-Specific Alternations in the Amplitude of Fluctuations in Tension-Type Headache: A Machine Learning Study","authors":"Xize Jia,&nbsp;Mengting Li,&nbsp;Shuxian Zhang,&nbsp;Collins Opoku Antwi,&nbsp;Linlin Zhan,&nbsp;Mengqi Zhao,&nbsp;Jianjie Wen,&nbsp;Su Hu,&nbsp;Zeqi Hao,&nbsp;Jun Ren","doi":"10.1002/jnr.25398","DOIUrl":"10.1002/jnr.25398","url":null,"abstract":"<div>\u0000 \u0000 <p>Brain neural signal at different frequency bands relates to different functions. However, the frequency-specific properties of spontaneous brain activity in tension-type headache (TTH)—the most rampant primary headache—remain largely unknown. We investigated the local neural activity of 33 TTH patients and 31 healthy controls (HCs) in the conventional frequency band and two sub-frequency bands (slow-4 and slow-5 frequency band), employing fractional amplitude of low-frequency fluctuations (fALFF), percent amplitude fluctuations (PerAF) and Wavelet-ALFF analytic methods. Using age as covariate, we performed two sample <i>t</i>-test to compare the between-group differences of each metrics in each frequency band. Support vector machine (SVM) was conducted to classify TTH patients and HCs on the basis of altered spontaneous brain activities. TTH patients showed lower fALFF values in the left cerebellar lobule X, left parahippocampal gyrus, and right supplementary motor area in slow-5 band. TTH patients showed lower PerAF in the left fusiform and cerebellar regions in three bands. Altered Wavelet-ALFF values in the right thalamus, left anterior cingulum gyrus, superior parietal gyrus and middle and parietal frontal regions in three frequency bands were detected. And the SVM classifier obtained an overall accuracy of 77.38%, 82.38%, and 95% based on fALFF, PerAF, and Wavelet ALFF values, respectively. TTH patients exhibited abnormal neural activity in various brain regions. The abnormal brain activities serve as powerful features for distinguishing TTH patients. This preliminary exploration provides a novel insight into the underlying mechanism of TTH.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 11","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622325","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 Hypothalamic Dopamine Neuron Activity by Interaction Between Caloric State and Amphetamine in Zebrafish Larvae","authors":"Pushkar Bansal,&nbsp;Mitchell F. Roitman,&nbsp;Erica E. Jung","doi":"10.1002/jnr.25396","DOIUrl":"10.1002/jnr.25396","url":null,"abstract":"<p>Dopamine (DA) signaling is evoked by both food and drugs that humans come to abuse. Moreover, physiological state (e.g., hunger versus satiety) can modulate the response. However, there is great heterogeneity among DA neurons. Limited studies have been performed that could resolve the interaction between physiological state and drug responsivity across groups of DA neurons. Here, we measured the activity of neurons in transgenic Tg (th2:GCaMP7s) zebrafish larva that expresses a calcium indicator (GCaMP7s) in A11 (posterior tuberculum) and a part of A14 (caudal hypothalamus and intermediate hypothalamus) DA populations located in the hypothalamus of the larval zebrafish. Fish were recorded in one of two physiological states: ad-libitum fed (AL) and food deprived (FD) and before and after acute exposure to different doses of the stimulant drug amphetamine (0, 0.7, and 1.5 μM). We quantified fluorescence change, activity duration, peak rise/fall time, and latency in the calcium spikes of the DA neurons. Our results show that baseline DA neuron activity amplitude, spike duration, and correlation between inter- and intra-DA neurons were higher in the FD than in the AL state. Dose-dependent AMPH treatment further increased the intensity of these parameters in the neuron spikes but only in the FD state. The DA activity correlation relatively increased in AL state post-AMPH treatment. Given that hunger increases drug reactivity and the probability of relapse to drug seeking, the results support populations of DA neurons as potential critical mediators of the interaction between physiological state and drug reinforcement.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 11","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25396","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604769","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":"Hypothalamus Connectivity in Adolescent Myalgic Encephalomyelitis/Chronic Fatigue Syndrome","authors":"Hollie Byrne,&nbsp;Sarah J. Knight,&nbsp;Elisha K. Josev,&nbsp;Adam Scheinberg,&nbsp;Richard Beare,&nbsp;Joseph Y. M. Yang,&nbsp;Stuart Oldham,&nbsp;Katherine Rowe,&nbsp;Marc L. Seal","doi":"10.1002/jnr.25392","DOIUrl":"10.1002/jnr.25392","url":null,"abstract":"<p>Adolescent Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a disabling illness of unknown etiology. Increasing evidence suggests hypothalamic involvement in ME/CFS pathophysiology, which has rarely been explored using magnetic resonance imaging (MRI) in the condition. This work aimed to use MRI to examine hypothalamus connectivity in adolescents with ME/CFS and explore how this relates to fatigue severity and illness duration. 25 adolescents with ME/CFS and 23 healthy controls completed a neuroimaging protocol consisting of structural and multishell diffusion-weighted imaging sequences, in addition to the PedsQL Multidimensional Fatigue Scale to assess fatigue severity. Information about illness duration was acquired at diagnosis. Preprocessing and streamlines tractography was performed using <i>QSIPrep</i> combined with a custom parcellation scheme to create structural networks. The number (degree) and weight (strength) of connections between lateralized hypothalamus regions and cortical and subcortical nodes were extracted, and relationships between connectivity measures, fatigue severity, and illness duration were performed using Bayesian regression models. We observed weak-to-moderate evidence of increased degree, but not strength, of connections from the bilateral anterior-inferior (left: <i>pd</i> [%] = 99.18, median [95% CI] = −22.68[−40.96 to 4.45]; right: <i>pd</i> [%] = 99.86, median [95% CI] = −23.35[−38.47 to 8.20]), left anterior-superior (<i>pd</i> [%] = 99.33, median [95% CI] = −18.83[−33.45 to 4.07]) and total left hypothalamus (<i>pd</i> [%] = 99.44, median [95% CI] = −47.18[−83.74 to 11.03]) in the ME/CFS group compared with controls. Conversely, bilateral posterior hypothalamus degree decreased with increasing ME/CFS illness duration (left: <i>pd</i> [%] = 98.13, median [95% CI]: −0.47[−0.89 to 0.03]; right: <i>pd</i> [%] = 98.50, median [95% CI]:-0.43[−0.82 to 0.05]). Finally, a weak relationship between right intermediate hypothalamus connectivity strength and fatigue severity was identified in the ME/CFS group (<i>pd</i> [%] = 99.35, median [95% CI] = −0.28[−0.51 to 0.06]), which was absent in controls. These findings suggest changes in hypothalamus connectivity may occur in adolescents with ME/CFS, warranting further investigation.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 10","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25392","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142467901","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 Role of Parvalbumin Interneurons in Autism Spectrum Disorder","authors":"Yiwei Yao,&nbsp;Qian Li","doi":"10.1002/jnr.25391","DOIUrl":"https://doi.org/10.1002/jnr.25391","url":null,"abstract":"<div>\u0000 \u0000 <p>As an important subtype of GABAergic interneurons, parvalbumin (PV) interneurons play a critical role in regulating cortical circuits and neural networks. Abnormalities in the development or function of PV interneurons have been linked to autism spectrum disorder (ASD), a neurodevelopmental disorder characterized by social and language deficits. In this review, we focus on the abnormalities of PV interneurons in ASD, including quantity and function and discuss the underlying mechanisms of impairments in PV interneurons in the pathology of ASD. Finally, we propose potential therapeutic approaches targeting PV interneurons, such as transplanting MGE progenitor cells and utilizing optogenetic stimulation in the treatment of ASD.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 10","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142435438","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":"Ascending Vagal Sensory and Central Noradrenergic Pathways Modulate Retrieval of Passive Avoidance Memory in Male Rats","authors":"Caitlyn M. Edwards,&nbsp;Inge Estefania Guerrero,&nbsp;Danielle Thompson,&nbsp;Tyla Dolezel,&nbsp;Linda Rinaman","doi":"10.1002/jnr.25390","DOIUrl":"10.1002/jnr.25390","url":null,"abstract":"<div>\u0000 \u0000 <p>Visceral feedback from the body is often subconscious, but plays an important role in guiding motivated behaviors. Vagal sensory neurons relay “gut feelings” to noradrenergic (NA) neurons in the caudal nucleus of the solitary tract (cNTS), which in turn project to the anterior ventrolateral bed nucleus of the stria terminalis (vlBNST) and other hypothalamic-limbic forebrain regions. Prior work supports a role for these circuits in modulating memory consolidation and extinction, but a potential role in retrieval of conditioned avoidance remains untested. To examine this, adult male rats underwent passive avoidance conditioning. We then lesioned gut-sensing vagal afferents by injecting cholecystokinin-conjugated saporin toxin (CSAP) into the vagal nodose ganglia (Experiment 1), or lesioned NA inputs to the vlBNST by injecting saporin toxin conjugated to an antibody against dopamine-beta hydroxylase (DSAP) into the vlBNST (Experiment 2). When avoidance behavior was later assessed, rats with vagal CSAP lesions or NA DSAP lesions displayed significantly increased conditioned passive avoidance. These new findings support the view that gut vagal afferents and the cNTS^NA-to-vlBNST circuit play a role in modulating the expression/retrieval of learned passive avoidance. Overall, our data suggest a dynamic modulatory role of vagal sensory feedback to the limbic forebrain in integrating interoceptive signals with contextual cues that elicit conditioned avoidance behavior.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 10","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381087","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":"Comparison of Nocifensive Behavior in NaV1.7–, NaV1.8–, and NaV1.9–Channelrhodopsin-2 Mice by Selective Optogenetic Activation of Targeted Sodium Channel Subtype-Expressing Afferents","authors":"Toyoaki Maruta,&nbsp;Satoshi Kouroki,&nbsp;Mio Kurogi,&nbsp;Kotaro Hidaka,&nbsp;Tomohiro Koshida,&nbsp;Ayako Miura,&nbsp;Hikaru Nakagawa,&nbsp;Toshihiko Yanagita,&nbsp;Ryu Takeya,&nbsp;Isao Tsuneyoshi","doi":"10.1002/jnr.25386","DOIUrl":"10.1002/jnr.25386","url":null,"abstract":"<p>Voltage-gated sodium channels, including Na_V1.7, Na_V1.8, and Na_V1.9, play important roles in pain transmission and chronic pain development. However, the specific mechanisms of their action remain unclear, highlighting the need for in vivo stimulation studies of these channels. Optogenetics, a novel technique for targeting the activation or inhibition of specific neural circuits using light, offers a promising solution. In our previous study, we used optogenetics to selectively excite Na_V1.7-expressing neurons in the dorsal root ganglion of mice to induce nocifensive behavior. Here, we further characterize the impact of nocifensive behavior by activation of Na_V1.7, Na_V1.8, or Na_V1.9-expressing neurons. Using CRISPR/Cas9-mediated homologous recombination, Na_V1.7–iCre, Na_V1.8–iCre, or Na_V1.9–iCre mice expressing iCre recombinase under the control of the endogenous Na_V1.7, Na_V1.8, or Na_V1.9 gene promoter were produced. These mice were then bred with channelrhodopsin-2 (ChR2) Cre–reporter Ai32 mice to obtain Na_V1.7–ChR2, Na_V1.8–ChR2, or Na_V1.9–ChR2 mice. Blue light exposure triggered paw withdrawal in all mice, with the strongest response in Na_V1.8–ChR2 mice. These light sensitivity differences observed across Na_V1.x–ChR2 mice may be dependent on ChR2 expression or reflect the inherent disparities in their pain transmission roles. In conclusion, we have generated noninvasive pain models, with optically activated peripheral nociceptors. We believe that studies using optogenetics will further elucidate the role of sodium channel subtypes in pain transmission.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 10","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25386","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372099","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":"Thalamocortical Dysconnectivity in Treatment-Resistant Depression","authors":"Pei-Chi Tu,&nbsp;Wei-Chen Lin,&nbsp;Wan-Chen Chang,&nbsp;Tung-Ping Su,&nbsp;Cheng-Ta Li,&nbsp;Ya-Mei Bai,&nbsp;Shih-Jen Tsai,&nbsp;Mu-Hong Chen","doi":"10.1002/jnr.25388","DOIUrl":"10.1002/jnr.25388","url":null,"abstract":"<p>Thalamocortical connectivity is associated with cognitive and affective processing. The role of thalamocortical connectivity in the pathomechanism of treatment-resistant depression (TRD) remains unclear. This study included 48 patients with TRD and 48 healthy individuals. We investigated thalamocortical connectivity by performing resting-state functional MRI with the bilateral thalamus as the seed. In addition, patients with TRD were evaluated using the Montgomery–Åsberg Depression Rating Scale (MADRS). Compared with the healthy individuals, the patients with TRD exhibited increased functional connectivity (FC) of the thalamus with the insula and superior temporal cortex and reduced the FC of the thalamus with the anterior paracingulate cortex and cerebellum crus II. Our study may support the crucial role of thalamocortical dysconnectivity in the TRD pathomechanism. However, the small sample size may limit the statistical power. A future study with a large sample size of patients with TRD would be required to validate our findings.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"102 10","pages":""},"PeriodicalIF":2.9,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.25388","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375581","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}