Current research in neurobiology最新文献

{"title":"Altered pattern separation in Goto-Kakizaki rats","authors":"Chelsey C. Damphousse,&nbsp;Jaclyn K. Medeiros,&nbsp;Nicole E. Micks,&nbsp;Diano F. Marrone","doi":"10.1016/j.crneur.2023.100082","DOIUrl":"10.1016/j.crneur.2023.100082","url":null,"abstract":"<div><p>Type 2 diabetes mellitus has steadily increased in prevalence over the past five decades. Among the health risks associated with this disorder are cognitive decline and are increased risk of developing dementia. To further investigate the link between diabetes and cognition, here we test memory performance and hippocampal function in the Goto-Kakizaki (GK) rat, a robust model of diabetes. Relative to age-matched Wistar rats, GK rats show impairments in a conjunctive memory task that requires discriminating objects not only on the basis of their physical characteristics, but also on the basis of where and when they were last seen. Concomitant to these deficits are changes in the pattern of expression of <em>Egr1</em> (an immediate-early gene critical for memory) in dentate gyrus granule cells, consistent with dentate hypoactivity leading to unstable hippocampal representations. These data support the hypothesis that diabetes confers a phenotype of accelerated senescence on the hippocampus, and help to link this disorder with changes in hippocampal circuits.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100082"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10123129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progranulin is an FMRP target that influences macroorchidism but not behaviour in a mouse model of Fragile X Syndrome","authors":"Benjamin Life ,&nbsp;Luis E.B. Bettio ,&nbsp;Ilse Gantois ,&nbsp;Brian R. Christie ,&nbsp;Blair R. Leavitt","doi":"10.1016/j.crneur.2023.100094","DOIUrl":"10.1016/j.crneur.2023.100094","url":null,"abstract":"<div><p>A growing body of evidence has implicated progranulin in neurodevelopment and indicated that aberrant progranulin expression may be involved in neurodevelopmental disease. Specifically, increased progranulin expression in the prefrontal cortex has been suggested to be pathologically relevant in male <em>Fmr1</em> knockout (<em>Fmr1</em> KO) mice, a mouse model of Fragile X Syndrome (FXS). Further investigation into the role of progranulin in FXS is warranted to determine if therapies that reduce progranulin expression represent a viable strategy for treating patients with FXS. Several key knowledge gaps remain. The mechanism of increased progranulin expression in <em>Fmr1</em> KO mice is poorly understood and the extent of progranulin's involvement in FXS-like phenotypes in <em>Fmr1</em> KO mice has been incompletely explored. To this end, we have performed a thorough characterization of progranulin expression in <em>Fmr1</em> KO mice. We find that the phenomenon of increased progranulin expression is post-translational and tissue-specific. We also demonstrate for the first time an association between progranulin mRNA and FMRP, suggesting that progranulin mRNA is an FMRP target. Subsequently, we show that progranulin over-expression in <em>Fmr1</em> wild-type mice causes reduced repetitive behaviour engagement in females and mild hyperactivity in males but is largely insufficient to recapitulate FXS-associated behavioural, morphological, and electrophysiological abnormalities. Lastly, we determine that genetic reduction of progranulin expression on an <em>Fmr1</em> KO background reduces macroorchidism but does not alter other FXS-associated behaviours or biochemical phenotypes.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"5 ","pages":"Article 100094"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b7/45/main.PMC10319828.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9796670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficient viral expression of a chemogenetic receptor in the old-world monkey amygdala","authors":"Walter Lerchner ,&nbsp;Kiana Dash ,&nbsp;Deborah Rose ,&nbsp;Mark.A.G. Eldridge ,&nbsp;Kathryn.M. Rothenhoefer ,&nbsp;Xuefeng Yan ,&nbsp;Vincent.D. Costa ,&nbsp;Bruno Averbeck ,&nbsp;Barry.J. Richmond","doi":"10.1016/j.crneur.2023.100091","DOIUrl":"10.1016/j.crneur.2023.100091","url":null,"abstract":"<div><p>Genetically encoded synthetic receptors, such as the chemogenetic and optogenetic proteins, are powerful tools for functional brain studies in animals. In the primate brain, with its comparatively large, intricate anatomical structures, it can be challenging to express transgenes, such as the hM4Di chemogenetic receptor, in a defined anatomical structure with high penetrance. Here, we compare parameters for lentivirus vector injections in the rhesus monkey amygdala. We find that four injections of 20 μl, infused at 0.5 μl/min, can achieve neuronal hM4Di expression in 50–100% of neurons within a 60 mm³ volume, without observable damage from overexpression. Increasing the number of hM4Di_CFP lentivirus injections to up to 12 sites per hemisphere, resulted in 30%–40% neuronal coverage of the overall amygdala volume, with coverage reaching 60% in some subnuclei. Manganese Chloride was mixed with lentivirus and used as an MRI marker to verify targeting accuracy and correct unsuccessful injections in these experiments. In a separate monkey we visualized, in vivo<em>,</em> viral expression of the hM4Di receptor protein in the amygdala, using Positron Emission Tomography. Together, these data show efficient and verifiable expression of a chemogenetic receptor in old-world monkey amygdala.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100091"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c2/29/main.PMC10313863.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unilateral caudate inactivation increases motor impulsivity in rhesus monkeys","authors":"Mark A.G. Eldridge ,&nbsp;Maya C. Smith ,&nbsp;Scott Hunter Oppler ,&nbsp;Jonah E. Pearl ,&nbsp;Jalene Y. Shim ,&nbsp;Walter Lerchner ,&nbsp;Barry J. Richmond","doi":"10.1016/j.crneur.2023.100085","DOIUrl":"10.1016/j.crneur.2023.100085","url":null,"abstract":"<div><p>Impulsivity, the tendency to react quickly and without consideration of consequences, is correlated with asymmetry in the volume of the caudate nucleus in human patients. In this study, we sought to determine whether the induction of functional asymmetry in the caudate nucleus of monkeys would produce phenomenologically comparable behavior. We found that unilateral suppression of the ventral caudate nucleus increases impulsive behavior in rhesus monkeys. Impulsivity was modeled by the subjects’ inability to maintain hold of a touch-sensitive bar until presentation of an imperative signal. Two methods were used to suppress activity in the caudate region. First, muscimol was locally infused. Second, a viral construct expressing the hM₄Di DREADD (designer receptor exclusively activated by designer drug) was injected at the same site. Clozapine N-oxide and deschloroclozapine activate the DREADD to suppress neuronal activity. Both methods of suppression, pharmacological and chemogenetic, increased the rate of early bar releases, a behavior we interpret to indicate impulsivity. Thus, we demonstrate a causal relationship between caudate asymmetry and impulsivity.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100085"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b5/d5/main.PMC10313876.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optogenetic stimulation of the primary visual cortex drives activity in the visual association cortex","authors":"Michael Ortiz-Rios ,&nbsp;Beshoy Agayby ,&nbsp;Fabien Balezeau ,&nbsp;Marcus Haag ,&nbsp;Samy Rima ,&nbsp;Jaime Cadena-Valencia ,&nbsp;Michael C. Schmid","doi":"10.1016/j.crneur.2023.100087","DOIUrl":"10.1016/j.crneur.2023.100087","url":null,"abstract":"<div><p>Developing optogenetic methods for research in non-human primates (NHP) is important for translational neuroscience and for delineating brain function with unprecedented specificity. Here we assess, in macaque monkeys, the selectivity by which optogenetic stimulation of the primary visual cortex (V1) drives the local laminar and widespread cortical connectivity related to visual perception. Towards this end, we transfected neurons with light-sensitive channelrhodopsin in dorsal V1. fMRI revealed that optogenetic stimulation of V1 using blue light at 40 Hz increased functional activity in the visual association cortex, including areas V2/V3, V4, motion-sensitive area MT and frontal eye fields, although nonspecific heating and eye movement contributions to this effect could not be ruled out. Neurophysiology and immunohistochemistry analyses confirmed optogenetic modulation of spiking activity and opsin expression with the strongest expression in layer 4-B in V1. Stimulating this pathway during a perceptual decision task effectively elicited a phosphene percept in the receptive field of the stimulated neurons in one monkey. Taken together, our findings demonstrate the great potential of optogenetic methods to drive the large-scale cortical circuits of the primate brain with high functional and spatial specificity.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100087"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10313868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9745788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterisation of functional deficits induced by AAV overexpression of alpha-synuclein in rats","authors":"F. Gubinelli ,&nbsp;L. Sarauskyte ,&nbsp;C. Venuti ,&nbsp;I. Kulacz ,&nbsp;G. Cazzolla ,&nbsp;M. Negrini ,&nbsp;D. Anwer ,&nbsp;I. Vecchio ,&nbsp;F. Jakobs ,&nbsp;F.P. Manfredsson ,&nbsp;M. Davidsson ,&nbsp;A. Heuer","doi":"10.1016/j.crneur.2022.100065","DOIUrl":"10.1016/j.crneur.2022.100065","url":null,"abstract":"<div><h3>Background</h3><p>In the last decades different preclinical animal models of Parkinson's disease (PD) have been generated, aiming to mimic the progressive neuronal loss of midbrain dopaminergic (DA) cells as well as motor and non-motor impairment. Among all the available models, AAV-based models of human alpha-synuclein (h-aSYN) overexpression are promising tools for investigation of disease progression and therapeutic interventions.</p></div><div><h3>Objectives</h3><p>The goal with this work was to characterise the impairment in motor and non-motor domains following nigrostriatal overexpression of h-aSYN and correlate the behavioural deficits with histological assessment of associated pathology.</p></div><div><h3>Methods</h3><p>Intranigral injection of an AAV9 expressing h-aSYN was compared with untreated animals, 6-OHDA and AAV9 expressing either no transgene or GFP. The animals were assessed on a series of simple and complex behavioural tasks probing motor and non-motor domains. Post-mortem neuropathology was analysed using immunohistochemical methods.</p></div><div><h3>Results</h3><p>Overexpression of h-aSYN led to progressive degeneration of DA neurons of the SN and axonal terminals in the striatum (STR). We observed extensive nigral and striatal pathology, resembling that of human PD brain, as well as the development of stable progressive deficit in simple motor tasks and in non-motor domains such as deficits in motivation and lateralised neglect.</p></div><div><h3>Conclusions</h3><p>In the present work we characterized a rat model of PD that closely resembles human PD pathology at the histological and behavioural level. The correlation of cell loss with behavioural performance enables the selection of rats which can be used in neuroprotective or neurorestorative therapies.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100065"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/06/33/main.PMC9827042.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9899919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methods for shipping live primary cortical and hippocampal neuron cultures from postnatal mice","authors":"Ferass M. Sammoura ,&nbsp;Dina Popova ,&nbsp;Ayeshia Morris ,&nbsp;Ronald P. Hart ,&nbsp;Jason R. Richardson","doi":"10.1016/j.crneur.2022.100069","DOIUrl":"10.1016/j.crneur.2022.100069","url":null,"abstract":"<div><p>Primary neuronal cultures have proven to be a powerful tool for studying mechanisms in neuroscience. It is technically challenging and expensive to reproduce high quality viable neuronal cultures. Laboratories that are not experienced or equipped to prepare primary neuron cultures may have difficulty producing consistent cultures for experiments. It has previously been shown that live rat embryonic hippocampal cultures can be shipped from laboratories that produce them. Here, we show that variations to this procedure allow for shipping postnatal mouse cultures of hippocampal and cortical primary neurons using standard commercial couriers. We also show that after shipping, primary neurons are viable, express synaptic markers, and demonstrate physiological activity, making them relevant models over immortalized cell lines. Among the many applications of this technique would be the preparation of cultured neurons from transgenic mouse lines in one laboratory and sharing them with distant collaborators, reducing variability.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100069"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fb/3e/main.PMC9794877.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10531950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal evaluation of the functional connectivity changes in the secondary somatosensory cortex (S2) of the monkey brain during acute stroke","authors":"Chun-Xia Li ,&nbsp;Frank Tong ,&nbsp;Doty Kempf ,&nbsp;Leonard Howell ,&nbsp;Xiaodong Zhang","doi":"10.1016/j.crneur.2023.100097","DOIUrl":"10.1016/j.crneur.2023.100097","url":null,"abstract":"<div><h3>Background</h3><p>Somatosensory deficits are frequently seen in acute stroke patients and may recover over time and affect functional outcome. However, the underlying mechanism of function recovery remains poorly understood. In the present study, progressive function alteration of the secondary somatosensory cortex (S2) and its relationship with regional perfusion and neurological outcome were examined using a monkey model of stroke.</p></div><div><h3>Methods and materials</h3><p>Rhesus monkeys (n = 4) were induced with permanent middle cerebral artery occlusion (pMCAo). Resting-state functional MRI, dynamic susceptibility contrast perfusion MRI, diffusion-weighted, T₁ and T₂ weighted images were collected before surgery and at 4–6, 48, and 96 h post stroke on a 3T scanner. Progressive changes of relative functional connectivity (FC), cerebral blood flow (CBF), and CBF/Tmax (Time to Maximum) of affected S2 regions were evaluated. Neurological deficits were assessed using the Spetzler approach.</p></div><div><h3>Results</h3><p>Ischemic lesion was evidently seen in the MCA territory including S2 in each monkey. Relative FC of injured S2 regions decreased substantially following stroke. Spetzler scores dropped substantially at 24 h post stroke but slightly recovered from Day 2 to Day 4. Relative FC progressively increased from 6 to 48 and 96 h post stroke and correlated significantly with relative CBFand CBF/Tmax changes.</p></div><div><h3>Conclusion</h3><p>The present study revealed the progressive alteration of function connectivity in S2 during acute stroke. The preliminary results suggested the function recovery might start couple days post occlusion and collateral circulation might play a key role in the recovery of somatosensory function after stroke insult. The relative function connectivity in S2 may provide additional information for prediction of functional outcome in stroke patients.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"5 ","pages":"Article 100097"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c5/e7/main.PMC10315998.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9792740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The systemic inhibition of the terminal complement system reduces neuroinflammation but does not improve motor function in mouse models of CMT1A with overexpressed PMP22","authors":"Iliana Michailidou ,&nbsp;Jeroen Vreijling ,&nbsp;Matthijs Rumpf ,&nbsp;Maarten Loos ,&nbsp;Bastijn Koopmans ,&nbsp;Nina Vlek ,&nbsp;Nina Straat ,&nbsp;Cedrick Agaser ,&nbsp;Thomas B. Kuipers ,&nbsp;Hailiang Mei ,&nbsp;Frank Baas ,&nbsp;Kees Fluiter","doi":"10.1016/j.crneur.2023.100077","DOIUrl":"https://doi.org/10.1016/j.crneur.2023.100077","url":null,"abstract":"<div><p>Charcot-Marie-Tooth disease type 1A (CMT1A) is the most prevalent hereditary demyelinating neuropathy. This autosomal, dominantly inherited disease is caused by a duplication on chromosome 17p which includes the peripheral myelin protein 22 (PMP22) gene. There is clinical evidence that the disability in CMT1A is to a large extend due to axonal damage rather than demyelination. Over-expression of <em>PMP22</em> is recently thought to impede cholesterol trafficking causing a total shutdown of local cholesterol and lipid synthesis in the Schwann cells, thus disturbing their ability to remyelinate. But there is a large variety in disease burden between CMT1A patients with the same genetic defect, indicating the presence of modifying factors that affect disease severity. One of these potential factors is the immune system. Several reports have described patients with co-occurrence of CMT1A with chronic inflammatory demyelinating disease or Guillain-Barré syndrome. We have previously shown in multiple animal models that the innate immune system and specifically the terminal complement system is a driver of inflammatory demyelination. To test the contribution of the terminal complement system to neuroinflammation and disease progression in CMT1A, we inhibited systemic complement C6 in two transgenic mouse models for CMT1A, the C3-<em>PMP22</em> and C3-<em>PMP22</em> c-JunP0Cre models. Both models over-express human <em>PMP22</em>, and one (C3-<em>PMP22</em> c-JunP0Cre) also has a Schwann cell-specific knockout of c-Jun, a crucial regulator of myelination controlling autophagy. We found that systemic inhibition of C6 using antisense oligonucleotides affects the neuroinflammation, Rho GTPase and ERK/MAPK signalling pathways in the CMT1A mouse models. The cholesterol synthesis pathway remained unaffected. Analysis of motor function during treatment with C6 antisense oligonucleotides did not reveal any significant improvement in the CMT1A mouse models. This study shows that the contribution of the terminal complement system to progressive loss of motor function in the CMT1A mouse models tested is limited.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"4 ","pages":"Article 100077"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49774897","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}

{"title":"Serotonergic mediation of the brain-wide neurogenesis: Region-dependent and receptor-type specific roles on neurogenic cellular transformation","authors":"Yuki Higuchi,&nbsp;Hiroyuki Arakawa","doi":"10.1016/j.crneur.2023.100102","DOIUrl":"10.1016/j.crneur.2023.100102","url":null,"abstract":"<div><p>Brain serotonin (5-hydroxytryptamine, 5-HT) is a key molecule for the mediation of depression-related brain states, but the neural mechanisms underlying 5-HT mediation need further investigation. A possible mechanism of the therapeutic antidepressant effects is neurogenic cell production, as stimulated by 5-HT signaling. Neurogenesis, the proliferation of neural stem cells (NSCs), and cell differentiation and maturation occur across brain regions, particularly the hippocampal dentate gyrus and the subventricular zone, throughout one's lifespan. 5-HT plays a major role in the mediation of neurogenic processes, which in turn leads to the therapeutic effect on depression-related states. In this review article, we aim to identify how the neuronal 5-HT system mediates the process of neurogenesis, including cell proliferation, cell-type differentiation and maturation. First, we will provide an overview of the neurogenic cell transformation that occurs in brain regions containing or lacking NSCs. Second, we will review brain region-specific mechanisms of 5-HT-mediated neurogenesis by comparing regions localized to NSCs, i.e., the hippocampus and subventricular zone, with those not containing NSCs. Highlighting these 5-HT mechanisms that mediate neurogenic cell production processes in a brain-region-specific manner would provide unique insights into the role of 5-HT in neurogenesis and its associated effects on depression.</p></div>","PeriodicalId":72752,"journal":{"name":"Current research in neurobiology","volume":"5 ","pages":"Article 100102"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10458724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10109824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}