Pub Date : 2024-09-18DOI: 10.1177/10738584241276376
{"title":"Behavioral and neurochemical defects induced by maternal immune stimulation are reversed by N-acetylcysteine","authors":"","doi":"10.1177/10738584241276376","DOIUrl":"https://doi.org/10.1177/10738584241276376","url":null,"abstract":"","PeriodicalId":22806,"journal":{"name":"The Neuroscientist","volume":"19 1","pages":"519"},"PeriodicalIF":0.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142255595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-18DOI: 10.1177/10738584241276370
{"title":"Elkin1: the molecular identity of a light-touch transducer in sensory neurons","authors":"","doi":"10.1177/10738584241276370","DOIUrl":"https://doi.org/10.1177/10738584241276370","url":null,"abstract":"","PeriodicalId":22806,"journal":{"name":"The Neuroscientist","volume":"42 1","pages":"518"},"PeriodicalIF":0.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142255629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-18DOI: 10.1177/10738584241276376a
{"title":"A biomarker for treatment efficacy in social anxiety disorder","authors":"","doi":"10.1177/10738584241276376a","DOIUrl":"https://doi.org/10.1177/10738584241276376a","url":null,"abstract":"","PeriodicalId":22806,"journal":{"name":"The Neuroscientist","volume":"3 1","pages":"519"},"PeriodicalIF":0.0,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142255593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-29DOI: 10.1177/10738584241246530
Pengyu Zong, Nicholas Legere, Jianlin Feng, Lixia Yue
Glutamate excitotoxicity is a central mechanism contributing to cellular dysfunction and death in various neurological disorders and diseases, such as stroke, traumatic brain injury, epilepsy, schizophrenia, addiction, mood disorders, Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, pathologic pain, and even normal aging-related changes. This detrimental effect emerges from glutamate binding to glutamate receptors, including α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, N-methyl-d-aspartate receptors, kainate receptors, and GluD receptors. Thus, excitotoxicity could be prevented by targeting glutamate receptors and their downstream signaling pathways. However, almost all the glutamate receptor antagonists failed to attenuate excitotoxicity in human patients, mainly due to the limited understanding of the underlying mechanisms regulating excitotoxicity. Transient receptor potential (TRP) channels serve as ancient cellular sensors capable of detecting and responding to both external and internal stimuli. The study of human TRP channels has flourished in recent decades since the initial discovery of mammalian TRP in 1995. These channels have been found to play pivotal roles in numerous pathologic conditions, including excitotoxicity. In this review, our focus centers on exploring the intricate interactions between TRP channels and glutamate receptors in excitotoxicity.
{"title":"TRP Channels in Excitotoxicity","authors":"Pengyu Zong, Nicholas Legere, Jianlin Feng, Lixia Yue","doi":"10.1177/10738584241246530","DOIUrl":"https://doi.org/10.1177/10738584241246530","url":null,"abstract":"Glutamate excitotoxicity is a central mechanism contributing to cellular dysfunction and death in various neurological disorders and diseases, such as stroke, traumatic brain injury, epilepsy, schizophrenia, addiction, mood disorders, Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, pathologic pain, and even normal aging-related changes. This detrimental effect emerges from glutamate binding to glutamate receptors, including α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, N-methyl-d-aspartate receptors, kainate receptors, and GluD receptors. Thus, excitotoxicity could be prevented by targeting glutamate receptors and their downstream signaling pathways. However, almost all the glutamate receptor antagonists failed to attenuate excitotoxicity in human patients, mainly due to the limited understanding of the underlying mechanisms regulating excitotoxicity. Transient receptor potential (TRP) channels serve as ancient cellular sensors capable of detecting and responding to both external and internal stimuli. The study of human TRP channels has flourished in recent decades since the initial discovery of mammalian TRP in 1995. These channels have been found to play pivotal roles in numerous pathologic conditions, including excitotoxicity. In this review, our focus centers on exploring the intricate interactions between TRP channels and glutamate receptors in excitotoxicity.","PeriodicalId":22806,"journal":{"name":"The Neuroscientist","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140841861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-11DOI: 10.1177/10738584241245307
Nicola J. Smyllie, Michael H. Hastings, Andrew P. Patton
Almost every facet of our behavior and physiology varies predictably over the course of day and night, anticipating and adapting us to their associated opportunities and challenges. These rhythms are driven by endogenous biological clocks that, when deprived of environmental cues, can continue to oscillate within a period of approximately 1 day, hence circa- dian. Normally, retinal signals synchronize them to the cycle of light and darkness, but disruption of circadian organization, a common feature of modern lifestyles, carries considerable costs to health. Circadian timekeeping pivots around a cell-autonomous molecular clock, widely expressed across tissues. These cellular timers are in turn synchronized by the principal circadian clock of the brain: the hypothalamic suprachiasmatic nucleus (SCN). Intercellular signals make the SCN network a very powerful pacemaker. Previously, neurons were considered the sole SCN timekeepers, with glial cells playing supportive roles. New discoveries have revealed, however, that astrocytes are active partners in SCN network timekeeping, with their cell-autonomous clock regulating extracellular glutamate and GABA concentrations to control circadian cycles of SCN neuronal activity. Here, we introduce circadian timekeeping at the cellular and SCN network levels before focusing on the contributions of astrocytes and their mutual interaction with neurons in circadian control in the brain.
{"title":"Neuron-Astrocyte Interactions and Circadian Timekeeping in Mammals","authors":"Nicola J. Smyllie, Michael H. Hastings, Andrew P. Patton","doi":"10.1177/10738584241245307","DOIUrl":"https://doi.org/10.1177/10738584241245307","url":null,"abstract":"Almost every facet of our behavior and physiology varies predictably over the course of day and night, anticipating and adapting us to their associated opportunities and challenges. These rhythms are driven by endogenous biological clocks that, when deprived of environmental cues, can continue to oscillate within a period of approximately 1 day, hence circa- dian. Normally, retinal signals synchronize them to the cycle of light and darkness, but disruption of circadian organization, a common feature of modern lifestyles, carries considerable costs to health. Circadian timekeeping pivots around a cell-autonomous molecular clock, widely expressed across tissues. These cellular timers are in turn synchronized by the principal circadian clock of the brain: the hypothalamic suprachiasmatic nucleus (SCN). Intercellular signals make the SCN network a very powerful pacemaker. Previously, neurons were considered the sole SCN timekeepers, with glial cells playing supportive roles. New discoveries have revealed, however, that astrocytes are active partners in SCN network timekeeping, with their cell-autonomous clock regulating extracellular glutamate and GABA concentrations to control circadian cycles of SCN neuronal activity. Here, we introduce circadian timekeeping at the cellular and SCN network levels before focusing on the contributions of astrocytes and their mutual interaction with neurons in circadian control in the brain.","PeriodicalId":22806,"journal":{"name":"The Neuroscientist","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140571556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-05DOI: 10.1177/10738584241245304
Dorit Ben Shalom, Georgios P. Skandalakis
Merging functional evidence derived from studies of autism spectrum disorder and attention-deficit/hyperactivity disorder converges in four neural streams of the prefrontal cortex, hence suggesting a model of information processing through four streams: motor through Brodmann area (BA) 8, emotion through BA 9, memory through BA 10, and emotional-related sensory through BA 11. A growing body of functional data has been supporting this model of information processing. Nevertheless, the underlying structural connectivity was only recently unveiled by a population-based high-definition tractography study with data from 1,065 individuals. This update provides a brief overview of recent evidence supporting the anatomofunctional integration of the four streams of the prefrontal cortex and reviews the white matter fiber tracts subserving the four streams.
{"title":"Four Streams Within the Prefrontal Cortex: Integrating Structural and Functional Connectivity","authors":"Dorit Ben Shalom, Georgios P. Skandalakis","doi":"10.1177/10738584241245304","DOIUrl":"https://doi.org/10.1177/10738584241245304","url":null,"abstract":"Merging functional evidence derived from studies of autism spectrum disorder and attention-deficit/hyperactivity disorder converges in four neural streams of the prefrontal cortex, hence suggesting a model of information processing through four streams: motor through Brodmann area (BA) 8, emotion through BA 9, memory through BA 10, and emotional-related sensory through BA 11. A growing body of functional data has been supporting this model of information processing. Nevertheless, the underlying structural connectivity was only recently unveiled by a population-based high-definition tractography study with data from 1,065 individuals. This update provides a brief overview of recent evidence supporting the anatomofunctional integration of the four streams of the prefrontal cortex and reviews the white matter fiber tracts subserving the four streams.","PeriodicalId":22806,"journal":{"name":"The Neuroscientist","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140571635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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