{"title":"Paternal Deprivation and Female Biparental Family Rearing Induce Dendritic and Synaptic Changes in Octodon degus: II. Nucleus Accumbens.","authors":"Tony de Schultz, Katharina Braun, Joerg Bock","doi":"10.1159/000530050","DOIUrl":"https://doi.org/10.1159/000530050","url":null,"abstract":"<p><p>While the majority of studies on the importance of parental caregiving on offspring behavioral and brain development focus on the role of the mother, the paternal contribution is still an understudied topic. We investigated if growing up without paternal care affects dendritic and synaptic development in the nucleus accumbens of male and female offspring and if replacement of the father by a female caregiver \"compensates\" the impact of paternal deprivation. We compared (a) biparental rearing by father and mother, (b) monoparental care by a single mother, and (c) biparental rearing by two female caregivers. Quantitative analysis of medium-sized neurons in the nucleus accumbens revealed that growing up without father resulted in reduced spine number in both male and female offspring in the core region, whereas spine frequency was only reduced in females. In the shell region, reduced spine frequency was only found in males growing up in a monoparental environment. Replacement of the father by a female caregiver did not \"protect\" against the effects of paternal deprivation, indicating a critical impact of paternal care behavior on the development and maturation of neuronal networks in the nucleus accumbens.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"45 3","pages":"147-160"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9675235","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}
Lakshmi Shree Kulumani Mahadevan, Melissa Murphy, Marina Selenica, Elizabeth Latimer, Brent T Harris
{"title":"Clinicopathologic Characteristics of PANDAS in a Young Adult: A Case Report.","authors":"Lakshmi Shree Kulumani Mahadevan, Melissa Murphy, Marina Selenica, Elizabeth Latimer, Brent T Harris","doi":"10.1159/000534061","DOIUrl":"10.1159/000534061","url":null,"abstract":"<p><p>Pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS) is an acute onset or exacerbation of neuropsychiatric symptoms following a group A streptococcus infection. It is believed to be a result of autoimmune response to streptococcal infection, but there is insufficient evidence to fully support this theory. Although this disease is primarily thought to be a disease of childhood, it is reported to occur also in adults. PANDAS is a well-defined clinical entity, but the neuropathology of this condition has not been established yet. We describe the clinical course of a 26-year-old female diagnosed with PANDAS. She committed suicide and her brain was biobanked for further studies. We examined the banked tissue and performed special stains, immunohistochemical, and immunofluorescence analyses to characterize the neuropathology of this condition. Histology of the temporal lobes, hippocampus, and basal ganglia shows mild gliosis and Alzheimer's type II astrocytes. Acute hypoxic ischemic changes were noted in hippocampus CA1 and CA2 areas. Immunostaining shows increased parenchymal/perivascular GFAP staining and many vessels with mild increases in CD3-, CD4-, and CD25-stained lymphocytes in the basal ganglia. The findings suggest that CD4- and CD25-positive T cells might have an important role in understanding the neuroinflammation and pathogenesis of this condition. The case represents the first neuropathological evaluation report for PANDAS.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"335-341"},"PeriodicalIF":2.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10753865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10224138","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}
Allison Vreeland, Denise Calaprice, Noga Or-Geva, Richard E Frye, Dritan Agalliu, Herbert M Lachman, Christopher Pittenger, Stefano Pallanti, Kyle Williams, Meiqian Ma, Margo Thienemann, Antonella Gagliano, Elizabeth Mellins, Jennifer Frankovich
{"title":"Postinfectious Inflammation, Autoimmunity, and Obsessive-Compulsive Disorder: Sydenham Chorea, Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal Infection, and Pediatric Acute-Onset Neuropsychiatric Disorder.","authors":"Allison Vreeland, Denise Calaprice, Noga Or-Geva, Richard E Frye, Dritan Agalliu, Herbert M Lachman, Christopher Pittenger, Stefano Pallanti, Kyle Williams, Meiqian Ma, Margo Thienemann, Antonella Gagliano, Elizabeth Mellins, Jennifer Frankovich","doi":"10.1159/000534261","DOIUrl":"10.1159/000534261","url":null,"abstract":"<p><p>Postinfectious neuroinflammation has been implicated in multiple models of acute-onset obsessive-compulsive disorder including Sydenham chorea (SC), pediatric acute-onset neuropsychiatric syndrome (PANS), and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). These conditions are associated with a range of autoantibodies which are thought to be triggered by infections, most notably group A streptococci (GAS). Based on animal models using huma sera, these autoantibodies are thought to cross-react with neural antigens in the basal ganglia and modulate neuronal activity and behavior. As is true for many childhood neuroinflammatory diseases and rheumatological diseases, SC, PANS, and PANDAS lack clinically available, rigorous diagnostic biomarkers and randomized clinical trials. In this review article, we outline the accumulating evidence supporting the role neuroinflammation plays in these disorders. We describe work with animal models including patient-derived anti-neuronal autoantibodies, and we outline imaging studies that show alterations in the basal ganglia. In addition, we present research on metabolites, which are helpful in deciphering functional phenotypes, and on the implication of sleep in these disorders. Finally, we encourage future researchers to collaborate across medical specialties (e.g., pediatrics, psychiatry, rheumatology, immunology, and infectious disease) in order to further research on clinical syndromes presenting with neuropsychiatric manifestations.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"361-374"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41145233","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":"Caspase-3 Inhibition toward Perinatal Protection of the Developing Brain from Environmental Stress.","authors":"Anna Arjun Kaji, Masaaki Torii, Seiji Ishii","doi":"10.1159/000529125","DOIUrl":"10.1159/000529125","url":null,"abstract":"<p><p>Throughout our lives, we are exposed to a variety of hazards, such as environmental pollutants and chemical substances that affect our health, and viruses and bacteria that cause infectious diseases. These external factors that are undesirable to an organism are called environmental stress. During the perinatal period, when neural networks are drastically reorganized and refined, the tolerance of the developing brain to various environmental stresses is lower than in adulthood. Thus, exposure to environmental stress during this vulnerable period is strongly associated with cognitive and behavioral deficits in later life. Recent studies have uncovered various mechanisms underlying the adverse impacts of environmental stress during the perinatal period on brain development. In this mini-review, we will present the findings from these studies, focusing on caspase-mediated apoptotic and nonapoptotic effects of environmental stress, and discuss several compounds that mitigate these caspase-mediated effects as examples of potential therapeutic approaches.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"45 2","pages":"66-75"},"PeriodicalIF":2.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10521911/pdf/nihms-1929477.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10471380","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}
S. Levison, Christian P. Speer Würzburg, J. Loturco, P. Bhide, J. Lauder, A. Obenaus, J. Pasquini
{"title":"Front & Back Matter","authors":"S. Levison, Christian P. Speer Würzburg, J. Loturco, P. Bhide, J. Lauder, A. Obenaus, J. Pasquini","doi":"10.1159/000527001","DOIUrl":"https://doi.org/10.1159/000527001","url":null,"abstract":"","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44994498","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}
M. Ardalan, Tetyana Chumak, Alexandra Quist, Seyedeh Marziyeh Jabbari Shiadeh, Anna-Jean Mallard, A. Rafati, C. Mallard
{"title":"Sex-Dependent Gliovascular Interface Abnormality in the Hippocampus following Postnatal Immune Activation in Mice","authors":"M. Ardalan, Tetyana Chumak, Alexandra Quist, Seyedeh Marziyeh Jabbari Shiadeh, Anna-Jean Mallard, A. Rafati, C. Mallard","doi":"10.1159/000525478","DOIUrl":"https://doi.org/10.1159/000525478","url":null,"abstract":"The neuro-gliovascular unit is a crucial structure for providing a balanced well-functioning environment for neurons and their synapses. Activation of the immune system during the developmental period is believed to affect the gliovascular unit, which may trigger neurodevelopmental and neurological/neuropsychiatric diseases. In this study, we hypothesized that vulnerability of the male brain to a neonatal insult was conditioned by sex-dependent differences in the impairment of the hippocampal gliovascular unit. Male and female C57BL/6J pups received lipopolysaccharide (LPS) (1 mg/kg) or saline on postnatal day (P) 5. Brains were collected at P12 and morphological quantifications of hippocampal fibrillary glial acid protein (GFAP+) astrocytes and ionized calcium-binding adaptor molecule 1 protein (Iba1+) microglia were performed by using 3-D image analysis together with measuring the length of CD31+ and aquaporin-4 (AQP4+) vessels. We found a significant increase in the length of CD31+ capillaries in the male LPS group compared to the saline group; however, coverage of capillaries by astrocytic end-feet (AQP4+) was significantly reduced. In contrast, there was a significant increase in AQP4+ capillary length in female pups 1 week after LPS injection. GFAP+ astrocytes via morphological changes in the hippocampus showed significant enhancement in the activity 1 week following LPS injection in male mice. We propose that neonatal inflammation could induce susceptibility to neurodevelopmental disorders through modification of hippocampal gliovascular interface in a sex-dependent manner.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"44 1","pages":"320 - 330"},"PeriodicalIF":2.9,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42804155","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":"Neurologic Consequences of Neonatal Necrotizing Enterocolitis","authors":"Jonathan A. Berken, Jill Chang","doi":"10.1159/000525378","DOIUrl":"https://doi.org/10.1159/000525378","url":null,"abstract":"Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease of the premature infant with high mortality and morbidity. Children who survive NEC have been shown to demonstrate neurodevelopmental delay, with significantly worse outcomes than from prematurity alone. The pathways leading to NEC-associated neurological impairments remain unclear, limiting the development of preventative and protective strategies. This review aims to summarize the existing clinical and experimental studies related to NEC-associated brain injury. We describe the current epidemiology of NEC, reported long-term neurodevelopmental outcomes among survivors, and proposed pathogenesis of brain injury in NEC. Highlighted are the potential connections between hypoxia-ischemia, nutrition, infection, gut inflammation, and the developing brain in NEC.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"44 1","pages":"295 - 308"},"PeriodicalIF":2.9,"publicationDate":"2022-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48450723","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}
Rebecca H Morris, G. Chabrier, S. Counsell, I. McGonnell, C. Thornton
{"title":"Differential Effects of Urban Particulate Matter on BV2 Microglial-Like and C17.2 Neural Stem/Precursor Cells","authors":"Rebecca H Morris, G. Chabrier, S. Counsell, I. McGonnell, C. Thornton","doi":"10.1159/000524829","DOIUrl":"https://doi.org/10.1159/000524829","url":null,"abstract":"Air pollution affects the majority of the world’s population and has been linked to over 7 million premature deaths per year. Exposure to particulate matter (PM) contained within air pollution is associated with cardiovascular, respiratory, and neurological ill health. There is increasing evidence that exposure to air pollution in utero and in early childhood is associated with altered brain development. However, the underlying mechanisms for impaired brain development are not clear. While oxidative stress and neuroinflammation are documented consequences of PM exposure, cell-specific mechanisms that may be triggered in response to air pollution exposure are less well defined. Here, we assess the effect of urban PM exposure on two different cell types, microglial-like BV2 cells and neural stem/precursor-like C17.2 cells. We found that, contrary to expectations, immature C17.2 cells were more resistant to PM-mediated oxidative stress and cell death than BV2 cells. PM exposure resulted in decreased mitochondrial health and increased mitochondrial ROS in BV2 cells which could be prevented by MitoTEMPO antioxidant treatment. Our data suggest that not only is mitochondrial dysfunction a key trigger in PM-mediated cytotoxicity but that such deleterious effects may also depend on cell type and maturity.","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":"44 1","pages":"309 - 319"},"PeriodicalIF":2.9,"publicationDate":"2022-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41532716","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}