Alberto Avila-Luna , Rodrigo Cruz-Castro , Antonio Verduzco-Mendoza , Adriana Olmos-Hernández , Arturo Gálvez-Rosas , Alfonso Alfaro-Rodríguez , José-Antonio Arias-Montaño , Antonio Bueno-Nava
{"title":"创伤性脑损伤,单独或纹状体出血样延伸,会短暂降低大鼠纹状体运动缺陷中的GABA和谷氨酸水平:一项体内研究。","authors":"Alberto Avila-Luna , Rodrigo Cruz-Castro , Antonio Verduzco-Mendoza , Adriana Olmos-Hernández , Arturo Gálvez-Rosas , Alfonso Alfaro-Rodríguez , José-Antonio Arias-Montaño , Antonio Bueno-Nava","doi":"10.1016/j.neulet.2024.138070","DOIUrl":null,"url":null,"abstract":"<div><div>The cerebral cortex is connected to the striatum via the axons of the pyramidal glutamatergic neurons, and this pathway is intimately involved in motor function. In the striatum, glutamatergic afferents initiate the activity of GABAergic medium spiny neurons. This study addressed whether traumatic brain injury (TBI) affects GABA and glutamate extracellular levels in the dorsal striatum as an indicator of effects on the cortico-striatal pathway, in rats with motor deficits and recovered animals. Animals were assigned to a sham group, a TBI-alone group, and a TBI + striatal injury group (local injection of a FeCl<sub>2</sub> solution to mimic hemorrhagic lesion). In the TBI-alone and TBI + striatal injury groups, motor deficits were accompanied by decreased extracellular GABA and glutamate levels in the striatum at 3 days post-injury. The TBI + striatal injury group showed higher motor deficits, which lasted 7 days longer, and GABA levels were significantly different compared to the TBI alone group. At 18 days post-injury, in recovered rats from the TBI-alone group GABA and glutamate levels returned to control levels. Alterations in extracellular GABA and glutamate levels indicate damage to the cortico-striatal pathway, underscoring the importance of studying this pathway for treatment and recovery after TBI.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"845 ","pages":"Article 138070"},"PeriodicalIF":2.5000,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Traumatic brain injury, alone or with striatal hemorrhage-like extension, transiently decreases GABA and glutamate levels along motor deficits in the rat striatum: an in vivo study\",\"authors\":\"Alberto Avila-Luna , Rodrigo Cruz-Castro , Antonio Verduzco-Mendoza , Adriana Olmos-Hernández , Arturo Gálvez-Rosas , Alfonso Alfaro-Rodríguez , José-Antonio Arias-Montaño , Antonio Bueno-Nava\",\"doi\":\"10.1016/j.neulet.2024.138070\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>The cerebral cortex is connected to the striatum via the axons of the pyramidal glutamatergic neurons, and this pathway is intimately involved in motor function. In the striatum, glutamatergic afferents initiate the activity of GABAergic medium spiny neurons. This study addressed whether traumatic brain injury (TBI) affects GABA and glutamate extracellular levels in the dorsal striatum as an indicator of effects on the cortico-striatal pathway, in rats with motor deficits and recovered animals. Animals were assigned to a sham group, a TBI-alone group, and a TBI + striatal injury group (local injection of a FeCl<sub>2</sub> solution to mimic hemorrhagic lesion). In the TBI-alone and TBI + striatal injury groups, motor deficits were accompanied by decreased extracellular GABA and glutamate levels in the striatum at 3 days post-injury. The TBI + striatal injury group showed higher motor deficits, which lasted 7 days longer, and GABA levels were significantly different compared to the TBI alone group. At 18 days post-injury, in recovered rats from the TBI-alone group GABA and glutamate levels returned to control levels. Alterations in extracellular GABA and glutamate levels indicate damage to the cortico-striatal pathway, underscoring the importance of studying this pathway for treatment and recovery after TBI.</div></div>\",\"PeriodicalId\":19290,\"journal\":{\"name\":\"Neuroscience Letters\",\"volume\":\"845 \",\"pages\":\"Article 138070\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-11-28\",\"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/S030439402400449X\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Letters","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S030439402400449X","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Traumatic brain injury, alone or with striatal hemorrhage-like extension, transiently decreases GABA and glutamate levels along motor deficits in the rat striatum: an in vivo study
The cerebral cortex is connected to the striatum via the axons of the pyramidal glutamatergic neurons, and this pathway is intimately involved in motor function. In the striatum, glutamatergic afferents initiate the activity of GABAergic medium spiny neurons. This study addressed whether traumatic brain injury (TBI) affects GABA and glutamate extracellular levels in the dorsal striatum as an indicator of effects on the cortico-striatal pathway, in rats with motor deficits and recovered animals. Animals were assigned to a sham group, a TBI-alone group, and a TBI + striatal injury group (local injection of a FeCl2 solution to mimic hemorrhagic lesion). In the TBI-alone and TBI + striatal injury groups, motor deficits were accompanied by decreased extracellular GABA and glutamate levels in the striatum at 3 days post-injury. The TBI + striatal injury group showed higher motor deficits, which lasted 7 days longer, and GABA levels were significantly different compared to the TBI alone group. At 18 days post-injury, in recovered rats from the TBI-alone group GABA and glutamate levels returned to control levels. Alterations in extracellular GABA and glutamate levels indicate damage to the cortico-striatal pathway, underscoring the importance of studying this pathway for treatment and recovery after TBI.
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.