Developmental Neuroscience最新文献

{"title":"Aquaporins: Bridging Normal Brain Development and Neurodevelopmental Disorder Mechanisms.","authors":"Fateme Azizi, Wing Ki Chan, Maryam Ardalan","doi":"10.1159/000545512","DOIUrl":"https://doi.org/10.1159/000545512","url":null,"abstract":"<p><p>Homeostasis of water content in the brain during fetal development is of crucial physiological importance. Aquaporins play a critical role in brain water homeostasis, and normal brain development, and have implications for understanding and potentially treating neurodevelopmental disorders. In this review, we provide a comprehensive overview of aquaporins (AQPs) and their critical roles in the central nervous system (CNS) and various neurodevelopmental disorders. Specifically, AQP4, AQP11 and AQP9 play a crucial role in water transport in the brain, maintaining water homeostasis, and facilitating water movement across cell membranes. The review highlights how disruptions in aquaporin expression and function may contribute to various neurodevelopmental disorders, including autism and Fragile X syndrome. These disruptions can affect blood-brain barrier integrity, neuroinflammation, and synaptic function, suggesting that AQPs could be potential therapeutic targets for these conditions.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143732834","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":"Selective injury of thalamocortical tract in neonatal rats impairs forelimb use: model validation and behavioral effects.","authors":"Tong Chun Wen, Michelle Corkrum, Jason B Carmel","doi":"10.1159/000544990","DOIUrl":"https://doi.org/10.1159/000544990","url":null,"abstract":"<p><strong>Introduction: </strong>Unilateral brain injury in neonates results in largely contralateral hand function impairment in children. Most research investigating neurorehabilitation targets for movement recovery has focused on the effects of brain injury on descending motor systems, especially the corticospinal tract. However, a recent human study demonstrated that sensory tract injury may have larger effects on dexterity than motor tract injury. In this study, we first developed a model of sensory tract injury in neonatal rats by targeting the thalamocortical tract, and then we used this model to assess the effects of sensory lesions on paw use.</p><p><strong>Methods: </strong>In the postnatal day 7 rats, we used three types of lesions to the thalamocortical tract: periventricular blood injection, photothrombotic lesion, and electrolytic lesion. To test the sensitivity and specificity of these techniques, viral tracers were injected into the primary sensory or motor cortex immediately after injury.</p><p><strong>Results: </strong>Electrolytic lesions were the most specific and reproducible for inducing a lesion compared to the other two methods. Electrolytic lesions disrupted 63% of the thalamocortical tract, while sparing the adjacent corticospinal tract in the internal capsule. Given that electrolytic lesions were the most specific and sensitive for targeting the thalamocortical tract, this model was used for behavioral experiments to measure the impact of sensory tract lesion on dexterity. The cylinder exploration and pasta handling tests were used to test the changes of forelimb use at 8 weeks after electrolytic lesion when the rats reached maturity. Lesions to the thalamocortical tract were associated with a significant decrease in the use of the contralateral forelimb in the cylinder task, and the degree of impairment positively correlated with the degree of injury.</p><p><strong>Conclusion: </strong>Overall, specific sensory system lesions of the thalamocortical tract impair forelimb use, suggesting a key role for skilled movement.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711968","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":"Acute onset neuropsychiatric conditions in children and adolescents following SARS-CoV-2 infection: a case series.","authors":"Mohamed T Jasser, Thomas Ferland, Thomas Bocian, Matthew Goff, Abigail Gauch, Michael V Heinz, Elizabeth Joffrey, Richard Morse, Daniel Albert, Jennifer Frankovich, Juliette C Madan","doi":"10.1159/000545349","DOIUrl":"https://doi.org/10.1159/000545349","url":null,"abstract":"<p><p>Neuropsychiatric symptoms following SARS-CoV-2 infection have been described in a substantial proportion of adult patients, both acute, sub-acute and chronic. Understanding of the neurological and neuropsychiatric sequelae of this virus is an emerging field of study with rapidly evolving descriptions of its impact on the central and peripheral nervous system. Here, we report a series of pediatric patients presenting with acute onset neuropsychiatric symptoms following SARS-CoV-2 infection who received comprehensive medical and psychiatric evaluation and treatment in our research-based Neuroimmune Psychiatric Disorders Program. We provide a review of the research available to date regarding potential mechanisms underlying neuroinflammatory consequences of this endemic infection. Opportunities for further investigations of mechanisms, evaluations and impactful treatments following SARS-CoV-2 infection are described. The pediatric cases presented share acute onset of OCD, psychosis, tics, neurobehavioral and physiological symptoms, with significant response to treatments targeting inflammation in combination with psychiatric and psychological interventions. Ongoing study and identification of this phenomenon of abrupt neuropsychiatric changes following SARS-CoV-2 infection may lead to more effective treatments with potential application to broader populations.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-22"},"PeriodicalIF":2.3,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143701989","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":"Branched Chain Amino Acid Metabolism in Developmental Brain Injury: Putative Mechanisms and Therapeutic Potential.","authors":"Margaret M Cassidy, Marc Yudkoff, Rebecca C Ahrens-Nicklas, Ana G Cristancho","doi":"10.1159/000545099","DOIUrl":"https://doi.org/10.1159/000545099","url":null,"abstract":"<p><strong>Background: </strong>Branched chain amino acid (BCAA) metabolism plays roles in various cellular processes, including energy homeostasis, anabolic signaling, and production of glutamate, the primary excitatory neurotransmitter. Emerging evidence also suggests BCAA metabolism has relationships to inflammatory and hypoxic cellular responses. Recent work in adult and adolescent clinical populations has suggested that BCAA dietary supplementation may improve outcomes associated with traumatic brain injury (TBI). Given these links, examining the putative mechanisms and potential therapeutic applications of modulating dietary BCAA content in the context of inflammatory and hypoxic developmental brain injury may reveal mechanisms for intervention in affected infants.</p><p><strong>Summary: </strong>Inflammatory and hypoxic brain injury influence the dynamics of BCAA metabolism in the fetal brain. Inflammatory insults to the developing brain may increase BCAA catabolism downstream of the branched chain ketoacids (BCKAs). The effect of altered BCAA metabolism on the pathophysiology of inflammatory developmental brain injury is currently unclear but may play a role in microglial response. Hypoxic brain injury seems to increase BCAA concentration in fetal brain, possibly because of re-amination of BCKAs to the parent BCAAs, or via increased protein breakdown during hypoxia.</p><p><strong>Key messages: </strong>The apparent relationship between aberrant BCAA metabolism and inflammation or hypoxia warrants consideration of BCAA supplementation or restriction as a strategy for attenuating developmental brain injury that is associated with these pathologic events. This approach could entail alterations of maternal diet during pregnancy or the feeding of infant formula that is fortified with or restricted in BCAA. These types of interventions have been safely and effectively employed in cases of inborn errors of BCAA metabolism, suggesting feasibility in infant populations. Both in vitro and pre-clinical work is necessary to elucidate how BCAA supplementation or restriction may affect the sequelae of inflammatory and hypoxic developmental brain injury.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-22"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607048","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":"Auditory deficits in a mouse model of first-trimester prenatal alcohol exposure.","authors":"Mark Jessup, Abigail Tice, Addison McNeill, Avery Tangen, Maya L Liu, Deirdre M McCarthy, Pradeep G Bhide, Jennifer L Steiner, Yuan Wang","doi":"10.1159/000545065","DOIUrl":"https://doi.org/10.1159/000545065","url":null,"abstract":"<p><p>Prenatal alcohol exposure (PAE) can lead to a wide spectrum of deficits in growth and neurological function, and there is an established link between PAE and auditory dysfunction. However, the effects of PAE on auditory development are complex and vary depending on the age and pattern of alcohol exposure. In this study, we developed a mouse model of PAE during the first half of the gestational period, mimicking alcohol consumption during the first trimester of pregnancy in humans. This exposure did not affect overall growth or induce anxiety-related symptoms in the offspring, as indicated by normal body weight change and largely unchanged behaviors in the open field and elevated zero maze tests. However, several aspects of auditory function were affected by PAE. Offspring born from prenatal alcohol-exposed dams displayed smaller auditory brainstem responses (ABRs) at 2-month-old as compared to those from control dams, suggesting weakened neuron synchronization within auditory brainstem circuits. Additionally, a reduction in the reproducibility of ABR peaks III/IV was observed in PAE offspring. In contrast, the overall hearing sensitivity and neuron transmission was not affected by PAE, as evaluated by ABR thresholds or peak latencies. In an acoustic startle test, PAE offspring failed to display prepulse inhibition to low levels of prepulses more frequently than control offspring at both 2 weeks old and 2 months old, suggesting an early-onset and lasting deficit in auditory gating or sound level differentiation. Together, these results demonstrate that mice exposed to alcohol during early gestation have largely preserved auditory responses but show significant alterations in specific features of auditory processing.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-29"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607044","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":"Caffeine as a treatment for perinatal hypoxic-ischemic brain injury - the potential risks and benefits.","authors":"Kelly Qishan Zhou, Flora Lam, Laura Bennet, Alistair J Gunn, Joanne O Davidson","doi":"10.1159/000545126","DOIUrl":"https://doi.org/10.1159/000545126","url":null,"abstract":"<p><p>It is well established that therapeutic hypothermia improves outcomes for infants with moderate-severe hypoxic-ischemic encephalopathy in high-income counties. However, ~29 % of the infants treated with therpeutic hypothermia still have adverse outcome. Additionally, therapeutic hypothermia is not recommended as a treatment for infants with HIE in low- and middle-income countries. Therefore, there is an urgent need to develop alternative treatments for infants with HIE in middle- and low-income countries, as well as additive treatments to therapeutic hypothermia in high-income countries. Caffeine is widely used as an agent to prevent apnea in preterm infants, and more recently, it has been investigated as a potential neuroprotective treatment for perinatal hypoxic-ischemic brain injury, but the preclinical evidence so far has been mixed. Furthermore, there are concerns that caffeine, which is an adenosine receptor antagonist, could abolish the endogenous neuroprotective effects of adenosine, during and after hypoxia-ischemia. Further studies, particularly in large animal translational models of hypoxic-ischemic brain injury are required to establish the safety and efficacy of caffeine in this setting before conducting large randomized controlled trials.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-18"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607088","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":"Obsessive Compulsive Disorder associated with Autoimmunity in Youth: Clinical Course before and after Rituximab+/- Adjunctive Immunomodulation.","authors":"Jennifer Frankovich, Denise Calaprice, Meiqian Ma, Olivia Knight, Kate Miles, Cindy Manko, Joseph D Hernandez, Jesse Sandberg, Bahare Farhadian, Yuhuan Xie, Melissa Silverman, Juliette Madan, Vibeke Strand, Kiki Chang, Margo Thienemann","doi":"10.1159/000544993","DOIUrl":"https://doi.org/10.1159/000544993","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Multiple lines of evidence suggest that some cases of OCD are underlain by autoimmune and/or inflammatory processes that act on the brain to create neuropsychiatric symptomatology. However, studies of immunomodulatory treatments for such cases are sparse. Here we present consecutive cases of presumed-neuroimmune OCD in youth that have been treated with rituximab +/- adjunctive immunomodulatory treatments.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Of the 458 cases evaluated by our clinic between September 15, 2012 and January 6, 2023, 23 patients were treated with rituximab +/- adjunctive immunomodulation orchestrated by our team (based on evidence of autoimmunity) and were followed routinely by the outpatient clinic team. Patients who presented for a second opinion and were not diagnosed, treated, and/or followed by our outpatient clinic (n=5) or did not have OCD (n=1) are not included. We present the immunological and psychiatric profiles (prior to treatment), selection criteria for use of rituximab, rituximab treatment protocol, recovery status, and reasons for discontinuation (if applicable). Data was obtained from chart review of clinical records. Determination of recovery status was confirmed by the clinical team caring for the patients; patients were classified as: did not recover, partial recovery (PR), or full recovery (FR). Since multiple treatments (psychotherapy, psychiatric medication, and immunomodulation) together contributed to recovery, the team additionally assessed attribution of response to rituximab and details are documented.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Patients were between ages of 4 and 20 at initiation of rituximab treatment. All suffered from severe, debilitating neuropsychiatric symptoms prior to rituximab initiation in the context of evidence for systemic autoimmunity. Approximately 70% had an unequivocal recovery following treatment with rituximab (+/- induction and adjunctive immunomodulation) which in most cases allowed the patients to achieve normal levels of function and cease psychotropic medications. Interpretation of attribution in many cases is complicated by the use of induction and adjunct immunomodulation. Most patients experienced transient increases in symptoms before improving; 11 experienced mild self-limited infusion-related reactions, and 14 experienced hypogammaglobulinemia. No patient had an organ or life-threatening reaction or infection following rituximab. One patient developed recurrent sinusitis following rituximab and thus rituximab was stopped despite neuropsychiatric improvements, then rituximab was restarted later due to recrudescence of psychiatric symptoms; the approval to use rituximab with IVIG permitted its use. Patients who received adjunctive immunomodulation (IVIG, methotrexate, leflunomide, etc.) had a higher likelihood of achieving recovery (FR or PR) after rituximab (Fisher's Exact Test, one-sided, p&lt;0.0001).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion and conclusions: &lt;/st","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-26"},"PeriodicalIF":2.3,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598345","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":"Androgen aggravates chorioamnionitis-induced white matter brain injury and neurobehavioral impairments in males.","authors":"Seline Vancolen, Mathilde Chevin, Marie-Julie Allard, Nour Bouzidi, Bernard Robaire, Guillaume Sébire","doi":"10.1159/000545074","DOIUrl":"https://doi.org/10.1159/000545074","url":null,"abstract":"<p><strong>Introduction: </strong>Group B Streptococcus (GBS) colonization lead to placental infection and inflammation, known as chorioamnionitis (CA). Fetal exposure to CA is linked to elevated risks of neurobehavioral impairments in offspring, including autism spectrum disorder, which is more prominent in males than females. In our preclinical model of GBS-induced CA, males exhibited heightened placental inflammation compared to females, correlating with more severe subsequent neurobehavioral impairments. We hypothesize that androgens upregulate the placental immune response in male fetuses, potentially contributing to GBS-induced autistic-like traits in male offspring. Our previous findings demonstrated that there were reduced pro-inflammatory cytokines and polymorphonuclear cell infiltration in flutamide (androgen receptor antagonist) plus GBS-infected compared to vehicle plus GBS-infected placenta. In this study we investigated the effect of end gestational androgen blockade on brain injury patterns and neurobehavioral outcomes in offspring in utero exposed to GBS CA.</p><p><strong>Methods: </strong>Lewis dams received daily injections of vehicle or flutamide from gestational day (G) 18 to 21, followed by saline or inactivated GBS injections from G19 to 21. Behavioral assessments were conducted from postnatal day (P) 9 to 40 and brains were dissected on P50.</p><p><strong>Results: </strong>Behavioral assessments revealed impaired social interactions in CA-exposed vs unexposed male rats. These impairments were not observed in flutamide-treated rats. Histological analysis of forebrains at P50 showed lateral forebrain ventricle enlargement and reduced periventricular white matter thickness, namely the corpus callosum and external capsule in offspring exposed to CA contrasting with an improvement in these outcomes observed in flutamide treated rats. Exposure to CA reduced the density of CC-1+ oligodendrocytes in the external capsule whereas flutamide mitigated this reduction in offspring at P50.</p><p><strong>Conclusion: </strong>These findings suggest a significant role for androgens in the skewed sex ratio observed in developmental impairments resulting from perinatal inflammation, underscoring the need for personalized sex-specific neuroprotective therapies.  .</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558713","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":"Effects of light exposure duration on severity and long-term neurodevelopment following photothrombotic stroke in a neonate.","authors":"Arya Jithoo, Tayla Penny, Shu Wen Wen, Althea R Suthya, Yen Pham, Amy E Sutherland, Connie H Y Wong, Suzanne L Miller, Courtney A McDonald","doi":"10.1159/000544994","DOIUrl":"https://doi.org/10.1159/000544994","url":null,"abstract":"<p><p>Introduction Perinatal stroke causes lasting neurological deficits and there are currently no effective treatment options. Established animal models of perinatal stroke do not always mimic the clinical presentation of neonatal injury or are technically challenging to perform. The photothrombotic (PT) stroke model is a minimally invasive method that replicates focal ischemic injury. Few studies have applied the PT model in neonatal contexts, and none have examined both short- and long-term effects across varying injury severities. This study aimed to optimise a protocol to create a mild model of perinatal stroke and subsequently characterize injury progression, neuropathological impact, and motor deficits over time. Methods On post-natal day (PND) 10 we used the PT method to induce perinatal stroke in rat pups. Pups were exposed to various light exposure times (10, 20 or 30 minutes) to determine the optimal time needed to produce a mild and reproducible cortical stroke injury. Behavioural assessments were conducted on days 4, 10, 20, and 30 post-injury. Brains were collected for analysis on days 3 and 40 post-injury. Results 3 days post-injury, the 20 and 30-minute group had significant focal lesions and microbleeds were present in each of the PT groups. All PT groups showed significant neuron loss in the penumbra and the thalamus, and microglia activation in multiple brain regions. As 30 minutes of light exposure showed extensive cortical tissue loss (>70%), we excluded the 30-minute group from long-term assessment. 40 days post-injury, the 10 and 20-minute groups demonstrated significant tissue loss and neuronal loss in the penumbra and thalamus, but only the 20-minute group showed neuron loss in the hippocampus. The 10- and 20-minute groups both demonstrated ongoing motor deficits. Conclusion Our results demonstrate that increasing light exposure time in PT stroke results in a more severe stroke phenotype. 30 minutes of light exposure resulted in a severe injury at only 3 days post insult, therefore, was not further investigated. 10 and 20 minutes of light exposure had a similar effect at 3 days, however after 40 days the 20-minute exposure time created a moderate injury phenotype. From this study we propose that 10 minutes of light exposure is optimal to create a mild stroke phenotype and is associated with motor deficits and altered neuropathology. This injury phenotype provides a focal and reproducible injury, while still being mild enough to feasibly test therapeutics.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-30"},"PeriodicalIF":2.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558714","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":"Generating inhibitory neuron diversity through morphogenic patterning: From in vivo studies to new in vitro models.","authors":"Tanya Deutsch Guerrero, Chloé Borowski, Julien Ferent","doi":"10.1159/000545031","DOIUrl":"https://doi.org/10.1159/000545031","url":null,"abstract":"<p><p>The proper functioning of the central nervous system depends on the cooperation of distinct neuronal subtypes generated during development. Here, we review new insights provided by recent research and technological advances into the mechanisms underlying the generation of the remarkable diversity of inhibitory GABAergic neurons (INs). INs are generated in the ventral telencephalon or subpallium and migrate long distances to populate multiple brain regions. INs exhibit considerable morphological, molecular and electrophysiological diversity. This diversity is mediated by intrinsic and extrinsic factors, including secreted molecules (such as Sonic Hedgehog). This review examines the role of extrinsic factors in the establishment of distinct subpallial domains and the subsequent emergence of IN diversity. We begin by summarizing the in vivo morphogenesis of this process and then highlight the new technologies that allow us to revisit the role of morphogens in subpallial development and IN specification.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544390","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}