{"title":"Fluoxetine, but not paroxetine, alters the jaw-closing muscle activity during non-rapid eye movement sleep in mice","authors":"Minako Ikeda , Ayako Mochizuki , Takafumi Kato , Shiro Nakamura , Kiyomi Nakayama , Masanori Dantsuji , Kazuyoshi Baba , Tomio Inoue","doi":"10.1016/j.neures.2024.09.004","DOIUrl":"10.1016/j.neures.2024.09.004","url":null,"abstract":"<div><div>Sleep bruxism is an involuntary, exaggerated jaw-closing activity during sleep. Selective serotonin reuptake inhibitor (SSRI) use is a risk factor for bruxism. However, the effect of various SSRIs on masseter (jaw-closing) muscle activity remains unclear. Here, we examined the effects of long-term administration of two SSRIs, fluoxetine (FLX) and paroxetine (PRX), for 14 days on masseter muscle activity during wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep for 24 h in mice. Vigilance states were scored based on electroencephalographic, electrooculography and neck electromyographic (EMG) activities. The EMG activity of the masseter muscle was quantified in 6 h periods. FLX and PRX did not affect the duration of the three vigilance states. Both drugs significantly prolonged the REM sleep episode duration while decreasing the number of episodes. FLX significantly increased REM sleep onset latency. Neither FLX nor PRX affected the mean masseter EMG activity during wakefulness. FLX significantly increased the relative time of masseter muscle activity in NREM sleep during 02:00–08:00 and 08:00–14:00, while PRX did not affect three vigilance states. Overall, FLX had a limited but significant effect on masseter muscle activity in NREM sleep during specific periods.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"210 ","pages":"Pages 51-61"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350802","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":"Deciphering the spectrum of astrocyte diversity: Insights into molecular, morphological, and functional dimensions in health and neurodegenerative diseases","authors":"Fumito Endo","doi":"10.1016/j.neures.2024.07.008","DOIUrl":"10.1016/j.neures.2024.07.008","url":null,"abstract":"<div><div>Astrocytes are the most abundant and morphologically complex glial cells that play active roles in the central nervous system (CNS). Recent research has identified shared and region-specific astrocytic genes and functions, elucidated the cellular origins of their regional diversity, and uncovered the molecular networks for astrocyte morphology, which are essential for their functional complexity. Reactive astrocytes exhibit a wide range of functional diversity in a context-specific manner in CNS disorders. This review discusses recent advances in understanding the molecular and morphological diversity of astrocytes in healthy individuals and those with neurodegenerative diseases, such as Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"210 ","pages":"Pages 1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889830","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":"Functional segregation and dynamic integration of the corticotectal descending signal in rat","authors":"Hikaru Sugino, Sho Tanno, Tatsumi Yoshida, Yoshikazu Isomura, Riichiro Hira","doi":"10.1016/j.neures.2024.09.002","DOIUrl":"10.1016/j.neures.2024.09.002","url":null,"abstract":"<div><div>The superior colliculus (SC) receives inputs from various brain regions in a layer- and radial subregion-specific manner, but whether the SC exhibits subregion-specific dynamics remains unclear. To address this issue, we recorded the spiking activity of single SC neurons while photoactivating cortical areas in awake head-fixed Thy1-ChR2 rats. We classified 309 neurons that responded significantly into 8 clusters according to the response dynamics. Among them, neurons with monophasic excitatory responses (7–12 ms latency) that returned to baseline within 20 ms were commonly observed in the optic and intermediate gray layers of centromedial and centrolateral SC. In contrast, neurons with complex polyphasic responses were commonly observed in the deep layers of the anterolateral SC. Cross-correlation analysis suggested that the complex pattern could be only partly explained by an internal circuit of the deep gray layer. Our results indicate that medial to centrolateral SC neurons simply relay cortical activity, whereas neurons in the deep layers of the anterolateral SC dynamically integrate inputs from the cortex, SNr, CN, and local circuits. These findings suggest a spatial gradient in SC integration, with a division of labor between simple relay circuits and those integrating complex dynamics.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"210 ","pages":"Pages 38-50"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292170","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":"SARM1 is essential for NMDA receptor-dependent endocytosis of AMPA receptors in hippocampal neurons","authors":"Misaki Morishita , Shinji Matsuda","doi":"10.1016/j.neures.2024.09.005","DOIUrl":"10.1016/j.neures.2024.09.005","url":null,"abstract":"<div><div>Long-term depression (LTD) is a form of synaptic plasticity thought to be the cellular basis of experience-dependent learning and memory. LTD is caused by an activity-dependent decrease in cell surface α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPA receptors) at the postsynaptic sites. However, the mechanism through which AMPA receptors are removed from the cell surface via neuronal activity is not fully understood. In this study, we showed that small interfering RNA (siRNA)-mediated knockdown of sterile alpha and toll/interleukin receptor motif containing 1 (SARM1) in cultured hippocampal neurons prevented the N-methyl-d-aspartate (NMDA)-induced reduction in cell surface AMPA receptors. However, the control RNA did not affect NMDA-mediated AMPA receptor trafficking. Overexpression of the siRNA-resistant form of SARM1 in SARM1-knocked-down neurons restored AMPA receptor trafficking. However, overexpression of SARM1, which lacks the mitochondrial transport signal, in the SARM1-knocked-down neurons did not restore NMDA-dependent AMPA receptor endocytosis. Moreover, the inhibition of the NADase activity of SARM1 blocked the NMDA-induced reduction of cell surface AMPA receptors. These results suggest that both the mitochondrial localization and NADase activity of SARM1 are essential for NMDA receptor-dependent AMPA receptor internalization in the hippocampal neurons.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"210 ","pages":"Pages 28-37"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350803","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":"Modulation of empathic abilities by the interplay between estrogen receptors and arginine vasopressin","authors":"Rui Du , Ting Liang , Guofang Lu","doi":"10.1016/j.neures.2024.09.001","DOIUrl":"10.1016/j.neures.2024.09.001","url":null,"abstract":"<div><div>This review examines the complex interactions between estrogen receptors α and β (ERα and ERβ) and arginine vasopressin (AVP), delving into their significant roles in modulating empathy, a critical psychological component in human social dynamics. Empathy, integrating affective and cognitive elements, is anchored in neural regions like the amygdala and prefrontal cortex. ERα and ERβ, pivotal in estrogen regulation, influence neurotransmitter dynamics and neural network activities, crucial for empathic development. AVP, key in regulating water balance, blood pressure, and social behaviors, interplays with these receptors, profoundly impacting empathic responses. The study highlights that ERα predominantly enhances empathy, especially affective empathy, by stimulating AVP synthesis and release. In contrast, ERβ may diminish empathy in certain contexts by suppressing AVP expression and activity. The intricate interplay, homeostatic balance, and mutual conversion between ERα and ERβ in AVP regulation are identified as challenging yet crucial areas for future research. These findings provide essential insights into the neurobiological underpinnings of empathy, offering new avenues for therapeutic interventions in social cognitive disorders and emotional dysregulation.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"210 ","pages":"Pages 11-18"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154672","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}
Yuchen Xu , Lily Zhang , Yan Yan , Wenbiao Xiao , Wei Zou , Zhaohui Luo , Bo Xiao , Hongyu Long
{"title":"MicroRNA-33 regulates the synaptic plasticity-related gene ARC in temporal lobe epilepsy","authors":"Yuchen Xu , Lily Zhang , Yan Yan , Wenbiao Xiao , Wei Zou , Zhaohui Luo , Bo Xiao , Hongyu Long","doi":"10.1016/j.neures.2024.08.003","DOIUrl":"10.1016/j.neures.2024.08.003","url":null,"abstract":"<div><div>This study aimed to elucidate the expression patterns of miR-33 and ARC in both a rat model of temporal lobe epilepsy (TLE) and human TLE patients, to explore the role of miR-33 in epilepsy onset through its regulation of ARC expression in the hippocampus. Our findings, supported by a Dual-Luciferase reporter assay, suggest that miR-33 can bind to the 3′ UTR region of ARC. We observed that miR-33 levels were reduced at 1 hour and 60 days post-seizure, while ARC expression notably increased at these time points. In the hippocampal CA1 and CA3 regions of post-seizure rats, ARC expression significantly exceeded that of control groups. Following the transfection of HEK cells with a miR-33 mimic, there was a decrease in both ARC mRNA and protein levels, whereas the group treated with a miR-33 inhibitor displayed the opposite effect. RNA sequencing in TLE patients revealed a similar miR-33 and ARC interaction. The regulation of Arc expression by miR-33 suggests that Arc may be a target gene of miR-33 in the context of epilepsy. Our findings indicate that miR-33 downregulation could contribute to the dysregulation of Arc expression observed in TLE, potentially influencing the disease process. Further studies are required to establish the exact role of miR-33-mediated Arc regulation in the development of epilepsy.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"210 ","pages":"Pages 19-27"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109950","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":"Stress and parental behaviors.","authors":"Yifan Wang, Dayu Lin","doi":"10.1016/j.neures.2024.12.004","DOIUrl":"10.1016/j.neures.2024.12.004","url":null,"abstract":"<p><p>In nearly all mammalian species, newborn pups are weak and vulnerable, relying heavily on care and protection from parents for survival. Thus, developmentally hardwired neural circuits are in place to ensure the timely expression of parental behaviors. Furthermore, several neurochemical systems, including estrogen, oxytocin, and dopamine, facilitate the emergence and expression of parental behaviors. However, stress can adversely affect these systems, impairing parental behaviors. In this review, we will summarize our current knowledge regarding the impact of stress on pup-directed behavior circuits that lead to infant neglect, abuse, and, in extreme cases, killing. We will discuss various stressors that influence parental behaviors at different life stages and how stress induces changes in the neurochemical systems that support parental care, ultimately leading to its poor performance.</p>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824391","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":"Cell type census in cerebral cortex reveals species-specific brain function and connectivity.","authors":"Kohei Onishi, Tomomi Shimogori","doi":"10.1016/j.neures.2024.11.008","DOIUrl":"10.1016/j.neures.2024.11.008","url":null,"abstract":"<p><p>The cerebral cortex contains a diverse array of functional regions that are conserved across species, such as primary somatosensory and primary visual cortex. However, despite this conservation, these regions exhibit different connectivity and functions in various species. It is hypothesized that these differences arise from distinct cell types within the conserved regions. To uncover these species-specific differences, investigating gene expression at the cellular level can reveal unique cell types. In this review, we highlight recent research on the molecular mechanisms that govern the formation of specific cell types in the rodent primary somatosensory cortex. Furthermore, we explore how these conserved molecular mechanisms are observed across different brain regions in various species. These findings offer new insights into the diversity and evolutionary background of neural circuit formation in the mammalian cortex.</p>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792136","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}
Hyeokjun Kwon , Eunchong Hong , Yong Sup Lee , Jae Hoon Cheong , Hee Jin Kim , Soyoung Kim , Jaesuk Yun
{"title":"Augmentation of intracranial self-stimulation induced by amphetamine-like drugs in Period circadian regulator 2 knockout mice is associated with intracellular Ca2+ levels","authors":"Hyeokjun Kwon , Eunchong Hong , Yong Sup Lee , Jae Hoon Cheong , Hee Jin Kim , Soyoung Kim , Jaesuk Yun","doi":"10.1016/j.neures.2024.07.007","DOIUrl":"10.1016/j.neures.2024.07.007","url":null,"abstract":"<div><div>Over the past decade, new psychoactive substances (NPS) have emerged in the illegal drug market and have continued to attract attention from the international community. Among these, amphetamine-like NPS, classified as stimulants, constitute a significant proportion. However, the pharmacological characteristics and mechanisms underlying addiction to amphetamine-like NPS remain poorly understood. Given that circadian rhythms are linked to the brain stimulation effects of methamphetamine (METH) and amphetamine, we investigated the effects of METH, 1-(4-methoxyphenyl)-N-methylpropan-2-amine (PMMA), and 1-(benzofuran-5-yl)-N-ethylpropan-2-amine (5-EAPB) on intracranial self-stimulation (ICSS) in wild-type (WT) or Period circadian regulator 2 knockout mice. Amphetamine-like drugs increase intracellular Ca<sup>2+</sup> levels to provoke dopamine release, so we examined the impact of <em>Per2</em> knockdown on intracellular Ca<sup>2+</sup> levels in PC12 cells to elucidate a potential mechanism underlying NPS-induced ICSS enhancement. Our ICSS results showed that METH and PMMA significantly increased brain stimulation in <em>Per2</em> knockout mice compared to WT mice. Similarly, METH and PMMA induced higher Ca<sup>2+</sup> fluorescence intensity in <em>Per2</em> knockdown PC12 cells than in control cells. In contrast, 5-EAPB did not produce significant changes in either ICSS or Ca<sup>2+</sup> signaling. These findings suggest that <em>Per2</em> plays a crucial role in the brain stimulation effects of amphetamine-like drugs through the regulation of intracellular Ca<sup>2+</sup>.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"209 ","pages":"Pages 34-41"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879196","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":"Correlations of brain structure with the social behavior of 15q11-13 duplication mice, an animal model of autism","authors":"Zhilei Zhao , Naohiro Okada , Sho Yagishita , Noriaki Yahata , Nobuhiro Nitta , Sayaka Shibata , Yoshifumi Abe , Susumu Morita , Eureka Kumagai , Kenji F. Tanaka , Tetsuya Suhara , Toru Takumi , Kiyoto Kasai , Seiichiro Jinde","doi":"10.1016/j.neures.2024.07.009","DOIUrl":"10.1016/j.neures.2024.07.009","url":null,"abstract":"<div><div>Duplication of chromosome 15q11–13 has been reported to be one of the most frequent cytogenetic copy number variations in autism spectrum disorder (ASD), and a mouse model of paternal 15q11–13 duplication was generated, termed <em>15q dup</em> mice. While previous studies have replicated some of the behavioral and brain structural phenotypes of ASD separately, the relationship between brain structure and behavior has rarely been examined. In this study, we performed behavioral experiments related to anxiety and social behaviors and magnetic resonance imaging (MRI) using the same set of <em>15q dup</em> and wild-type mice. <em>15q dup</em> mice showed increased anxiety and a tendency toward alterations in social behaviors, as reported previously, as well as variability in terms of sociability. MRI analysis revealed that a lower sociability index was correlated with a smaller gray matter volume in the right medial entorhinal cortex. These results may help to understand how variability in behavioral phenotypes of ASD arises even in individuals with the same genetic background and to determine the individual differences in neurodevelopmental trajectory correlated with specific brain structures that underlie these phenotypes.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"209 ","pages":"Pages 42-49"},"PeriodicalIF":2.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889800","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}