{"title":"The expression of connexin 36 and 43 in animal models of trait and state anxiety","authors":"Mohammadreza Alizadeh , Sahel Motaghi , Mahya Moradi Sirchi , Mehdi Abbasnejad , Saeed Esmaili-Mahani","doi":"10.1016/j.neulet.2025.138269","DOIUrl":null,"url":null,"abstract":"<div><div>Few studies have investigated the role of gap junctions in anxiety. Gap junctions (GJs) are intercellular channels, and their subunit are connexins (CXs). The specific isoforms of connexins for neurons and astrocytes are CX36, and CX43 respectively. Neuronal CX36 and astrocytic CX43 are critical for brain synchrony and homeostasis. Elevated plus maze (EPM) was used for animal models of trait and state anxiety. The gene expression was assessed by Real-time PCR technique in the ventral hippocampus (v Hip), basolateral amygdala (BLA), and medial prefrontal cortex (m PC). The rats were grouped as follows (n = 6): control, trait anxiety, in which the rats were placed in the EPM apparatus, state anxiety, in which the animals were placed in the EPM apparatus after tolerating 120 min of isolation. The data showed that the anxiety of the animals in the state anxiety group was significantly greater than the trait anxiety group (<em>p < 0.05</em>). In the state anxiety animals, the gene expression of CX36 was lower in the m PC and BLA regions than the control and trait anxiety groups (<em>p < 0.01</em>). CX43 expression in the BLA, and v Hip structures was also lower than in the control and trait anxiety groups. These findings suggest that downregulation of CX36 and CX43 contributes to state anxiety pathophysiology, highlighting GJs as potential therapeutic targets.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"859 ","pages":"Article 138269"},"PeriodicalIF":2.0000,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Letters","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304394025001570","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Few studies have investigated the role of gap junctions in anxiety. Gap junctions (GJs) are intercellular channels, and their subunit are connexins (CXs). The specific isoforms of connexins for neurons and astrocytes are CX36, and CX43 respectively. Neuronal CX36 and astrocytic CX43 are critical for brain synchrony and homeostasis. Elevated plus maze (EPM) was used for animal models of trait and state anxiety. The gene expression was assessed by Real-time PCR technique in the ventral hippocampus (v Hip), basolateral amygdala (BLA), and medial prefrontal cortex (m PC). The rats were grouped as follows (n = 6): control, trait anxiety, in which the rats were placed in the EPM apparatus, state anxiety, in which the animals were placed in the EPM apparatus after tolerating 120 min of isolation. The data showed that the anxiety of the animals in the state anxiety group was significantly greater than the trait anxiety group (p < 0.05). In the state anxiety animals, the gene expression of CX36 was lower in the m PC and BLA regions than the control and trait anxiety groups (p < 0.01). CX43 expression in the BLA, and v Hip structures was also lower than in the control and trait anxiety groups. These findings suggest that downregulation of CX36 and CX43 contributes to state anxiety pathophysiology, highlighting GJs as potential therapeutic targets.
期刊介绍:
Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.