Neuropsychopharmacology最新文献

{"title":"Astrocytic RARγ mediates hippocampal astrocytosis and neurogenesis deficits in chronic retinoic acid-induced depression.","authors":"Huixian Huang, Wensi Lu, Ran Luo, Yinyun Zeng, Yuqin Zhang, Xiaohong Su, Xinyi Zhang, Bo Tian, Xuemin Wang","doi":"10.1038/s41386-024-01983-3","DOIUrl":"https://doi.org/10.1038/s41386-024-01983-3","url":null,"abstract":"<p><p>Accumulating clinical evidence indicates that chronic exposure to retinoic acid (RA) may lead to depressive symptoms and even increase the risk of suicidal behavior, which severely limits the clinical long-term application of RA. The exact mechanisms through which RA contributes to the onset of depression remain largely unclear. Here, we administered intraperitoneal injections of all-trans RA to male C57BL/6 J mice over a period of 21 days. Mice subjected to chronic RA exposure displayed depressive-like behaviors, accompanied by impaired hippocampal neurogenesis and heightened RA receptor gamma (RARγ) levels in the ventral hippocampus (vHip). The administration of an RARγ antagonist effectively mitigated these RA-induced neurogenesis impairments and depressive-like behaviors. Chronic exposure to RA was also observed to promote hippocampal astrocytosis and increase astrocytic Rarγ expression in the ventral dentate gyrus (vDG) of hippocampus. Notably, astrocytic RARγ in the vDG was found to be a key factor in the observed hippocampal astrocytosis and neurogenesis impairments, and depressive-like behaviors. Chronic exposure to RA resulted in increased extracellular glutamate levels in neural stem cells (NSCs), accompanied by a decrease in glutamate transporter 1 (GLT-1) expression. Enhancing astrocytic GLT-1 expression was found to alleviate both hippocampal astrocytosis and depressive-like behaviors caused by RA. These findings underscore the critical role of astrocytic RARγ-GLT-1 axis in the development of hippocampal astrocytosis, neurogenesis impairments, and depressive symptoms, suggesting that targeting RARγ-GLT-1 could potentially offer an effective therapeutic approach for depression.</p>","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142146040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-level therapeutic actions of cannabidiol in ketamine-induced schizophrenia psychopathology in male rats.","authors":"Charalampos Brakatselos, Alexia Polissidis, George Ntoulas, Michail-Zois Asprogerakas, Olga Tsarna, Anastasia Vamvaka-Iakovou, Gerasimos Nakas, Anastasios Delis, Petros Tzimas, Leandros Skaltsounis, Joana Silva, Foteini Delis, Joao Filipe Oliveira, Ioannis Sotiropoulos, Katerina Antoniou","doi":"10.1038/s41386-024-01977-1","DOIUrl":"https://doi.org/10.1038/s41386-024-01977-1","url":null,"abstract":"<p><p>Repeated administration of ketamine (KET) has been used to model schizophrenia-like symptomatology in rodents, but the psychotomimetic neurobiological and neuroanatomical underpinnings remain elusive. In parallel, the unmet need for a better treatment of schizophrenia requires the development of novel therapeutic strategies. Cannabidiol (CBD), a major non-addictive phytocannabinoid has been linked to antipsychotic effects with unclear mechanistic basis. Therefore, this study aims to clarify the neurobiological substrate of repeated KET administration model and to evaluate CBD's antipsychotic potential and neurobiological basis. CBD-treated male rats with and without prior repeated KET administration underwent behavioral analyses, followed by multilevel analysis of different brain areas including dopaminergic and glutamatergic activity, synaptic signaling, as well as electrophysiological recordings for the assessment of corticohippocampal and corticostriatal network activity. Repeated KET model is characterized by schizophrenia-like symptomatology and alterations in glutamatergic and dopaminergic activity mainly in the PFC and the dorsomedial striatum (DMS), through a bi-directional pattern. These observations are accompanied by glutamatergic/GABAergic deviations paralleled to impaired function of parvalbumin- and cholecystokinin-positive interneurons, indicative of excitation/inhibition (E/I) imbalance. Moreover, CBD counteracted the schizophrenia-like behavioral phenotype as well as reverted prefrontal abnormalities and ventral hippocampal E/I deficits, while partially modulated dorsostriatal dysregulations. This study adds novel insights to our understanding of the KET-induced schizophrenia-related brain pathology, as well as the CBD antipsychotic action through a region-specific set of modulations in the corticohippocampal and costicostrtiatal circuitry of KET-induced profile contributing to the development of novel therapeutic strategies focused on the ECS and E/I imbalance restoration.</p>","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142146041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal exposure to the mineralocorticoid receptor antagonist spironolactone disrupts hippocampal area CA2 connectivity and alters behavior in mice.","authors":"Stephanie M Jones, Sarah Jo Sleiman, Katharine E McCann, Alan K Jarmusch, Georgia M Alexander, Serena M Dudek","doi":"10.1038/s41386-024-01971-7","DOIUrl":"https://doi.org/10.1038/s41386-024-01971-7","url":null,"abstract":"<p><p>In the brain, the hippocampus is enriched with mineralocorticoid receptors (MR; Nr3c2), a ligand-dependent transcription factor stimulated by the stress hormone corticosterone in rodents. Recently, we discovered that MR is required for the acquisition and maintenance of many features of mouse area CA2 neurons. Notably, we observed that immunofluorescence for the vesicular glutamate transporter 2 (vGluT2), likely representing afferents from the supramammillary nucleus (SuM), was disrupted in the embryonic, but not postnatal, MR knockout mouse CA2. To test whether pharmacological perturbation of MR activity in utero similarly disrupts CA2 connectivity, we implanted slow-release pellets containing the MR antagonist spironolactone in mouse dams during mid-gestation. After confirming that at least one likely active metabolite crossed from the dams' serum into the embryonic brains, we found that spironolactone treatment caused a significant reduction of CA2 axon fluorescence intensity in the CA1 stratum oriens, where CA2 axons preferentially project, and that vGluT2 staining was significantly decreased in both CA2 and dentate gyrus in spironolactone-treated animals. We also found that spironolactone-treated animals exhibited increased reactivity to novel objects, an effect similar to what is seen with embryonic or postnatal CA2-targeted MR knockout. However, we found no difference in preference for social novelty between the treatment groups. We infer these results to suggest that persistent or more severe disruptions in MR function may be required to interfere with this type of social behavior. These findings do indicate, though, that developmental disruption in MR signaling can have persistent effects on hippocampal circuitry and behavior.</p>","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLP-1 receptor agonist exenatide uncouples food intake from hedonic and anticipatory regulation in non-human primates: insights from an operant meal schedule paradigm.","authors":"Balázs Knakker, Judit Inkeller, Péter Kovács, Balázs Lendvai, István Hernádi","doi":"10.1038/s41386-024-01981-5","DOIUrl":"https://doi.org/10.1038/s41386-024-01981-5","url":null,"abstract":"<p><p>Glucagon-like peptide 1 (GLP-1), a neuroendocrine signal of energy balance and satiety, has a major role in regulating food intake behaviour. Here we investigated the effects of the GLP-1 agonist exenatide on palatability-driven feeding regulation in adult male rhesus macaques (n = 5) using a novel operant food intake paradigm with four meal schedule conditions where two types of pellets with different palatability values were offered as meal in all combinations in two consecutive daily feeding sessions (S1 and S2). In control conditions, a strong, palatability-driven anticipatory effect was found in S1, followed by a complementary positive contrast effect in S2. After acute subcutaneous treatment with 1 µg/kg dose of exenatide 1 h before S1, food intake decreased to the same very low level in all meal schedule conditions in S1, completely erasing the previously observed anticipatory effect. Conversely, exenatide induced hypoglycaemia in an anticipatory meal schedule dependent pattern. Interestingly, the previously observed positive contrast effect was spared in S2, with a weaker residual effect specifically on the consumption of the more palatable pellet type. To conclude, the food intake reducing effects of exenatide may temporally evolve from strong anorectic to weak anhedonic modulations, where hedonic experience and anticipation during the early anorectic phase is conserved but uncoupled from food intake behaviour.</p>","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic efficacy of the BKCa channel opener chlorzoxazone in a mouse model of Fragile X syndrome","authors":"Celeste Ferraguto,&nbsp;Marion Piquemal-Lagoueillat,&nbsp;Valerie Lemaire,&nbsp;Maïté M. Moreau,&nbsp;Stefania Trazzi,&nbsp;Beatrice Uguagliati,&nbsp;Elisabetta Ciani,&nbsp;Sandrine S. Bertrand,&nbsp;Eric Louette,&nbsp;Bruno Bontempi,&nbsp;Susanna Pietropaolo","doi":"10.1038/s41386-024-01956-6","DOIUrl":"10.1038/s41386-024-01956-6","url":null,"abstract":"Fragile X syndrome (FXS) is an X-linked neurodevelopmental disorder characterized by several behavioral abnormalities, including hyperactivity, anxiety, sensory hyper-responsiveness, and autistic-like symptoms such as social deficits. Despite considerable efforts, effective pharmacological treatments are still lacking, prompting the need for exploring the therapeutic value of existing drugs beyond their original approved use. One such repurposed drug is chlorzoxazone which is classified as a large-conductance calcium-dependent potassium (BKCa) channel opener. Reduced BKCa channel functionality has been reported in FXS patients, suggesting that molecules activating these channels could serve as promising treatments for this syndrome. Here, we sought to characterize the therapeutic potential of chlorzoxazone using the Fmr1-KO mouse model of FXS which recapitulates the main phenotypes of FXS, including BKCa channel alterations. Chlorzoxazone, administered either acutely or chronically, rescued hyperactivity and acoustic hyper-responsiveness as well as impaired social interactions exhibited by Fmr1-KO mice. Chlorzoxazone was more efficacious in alleviating these phenotypes than gaboxadol and metformin, two repurposed treatments for FXS that do not target BKCa channels. Systemic administration of chlorzoxazone modulated the neuronal activity-dependent gene c-fos in selected brain areas of Fmr1-KO mice, corrected aberrant hippocampal dendritic spines, and was able to rescue impaired BKCa currents recorded from hippocampal and cortical neurons of these mutants. Collectively, these findings provide further preclinical support for BKCa channels as a valuable therapeutic target for treating FXS and encourage the repurposing of chlorzoxazone for clinical applications in FXS and other related neurodevelopmental diseases.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"49 13","pages":"2032-2041"},"PeriodicalIF":6.6,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kappa opioid receptor availability predicts severity of anhedonia in schizophrenia","authors":"Mark Slifstein,&nbsp;Wenchao Qu,&nbsp;Roberto Gil,&nbsp;Jodi J. Weinstein,&nbsp;Greg Perlman,&nbsp;Thomas Jaworski-Calara,&nbsp;Jiayan Meng,&nbsp;Bao Hu,&nbsp;Scott J. Moeller,&nbsp;Guillermo Horga,&nbsp;Anissa Abi-Dargham","doi":"10.1038/s41386-024-01975-3","DOIUrl":"10.1038/s41386-024-01975-3","url":null,"abstract":"The kappa opioid receptor (KOR) and its endogenous agonist dynorphin have been implicated in multiple psychiatric conditions including psychotic disorders. We tested the hypotheses that kappa expression is elevated and associated with psychotic symptoms in schizophrenia. We measured kappa expression in unmedicated patients with schizophrenia (7 female, 6 male) and matched controls (7 female, 6 male) with positron emission tomography (PET). We also acquired a measurement of cumulative dopamine activity over the life span in the same subjects using neuromelanin sensitive MRI. We hypothesized that neuromelanin accumulation would be higher in patients than controls and that in patients there would be a positive association between KOR availability and neuromelanin accumulation. Fourteen patients and thirteen controls were enrolled. Whole brain dynamic PET imaging data using the KOR selective tracer [18F]LY245998 were acquired. Distribution volume (VT) was measured with region of interest analysis in 14 brain regions. Neuromelanin accumulation in midbrain dopaminergic nuclei was assessed in the same subjects. Positive and negative symptoms were measured by a clinical psychologist. We did not observe group level differences in KOR expression, neuromelanin accumulation or relationships of these to positive symptoms. Unexpectedly, we did observe strong positive associations between KOR expression and symptoms of anhedonia in the patients (Pearson r &gt; 0.7, uncorrected p &lt; 0.01 in 8 cortical brain regions). We also observed moderate associations between KOR expression and neuromelanin levels in patients. In conclusion, we did not observe a relationship between kappa and symptoms of psychosis but the observed relationship to the negative symptom of anhedonia is in line with recent work testing kappa antagonism as a therapy for anhedonia in depression.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"49 13","pages":"2087-2093"},"PeriodicalIF":6.6,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41386-024-01975-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute sleep disruption reduces fear memories in male and female mice.","authors":"Allison R Foilb, Elisa M Taylor-Yeremeeva, Brett D Schmidt, Kerry J Ressler, William A Carlezon","doi":"10.1038/s41386-024-01978-0","DOIUrl":"10.1038/s41386-024-01978-0","url":null,"abstract":"<p><p>Sleep problems are a prominent feature of mental health conditions including post-traumatic stress disorder (PTSD). Despite its potential importance, the role of sleep in the development of and/or recovery from trauma-related illnesses is not understood. Interestingly, there are reports that sleep disruption immediately after a traumatic experience can reduce fear memories, an effect that could be utilized therapeutically in humans. While the mechanisms of this effect are not completely understood, one possible explanation for these findings is that immediate sleep disruption interferes with consolidation of fear memories, rendering them weaker and more sensitive to intervention. Here, we allowed fear-conditioned mice to sleep immediately after fear conditioning during a time frame (18 h) that includes and extends beyond periods typically associated with memory consolidation before subjecting them to 6-h of sleep disruption. Mice exposed to this delayed regimen showed dramatic reductions in fear during tests conducted immediately after sleep disruption, as well as 24 h later. This sleep disruption regimen also increased levels of mRNA encoding brain-derived neurotrophic factor (BDNF), a molecule implicated in neuroplasticity, in the basolateral amygdala (BLA), a brain area implicated in fear and its extinction. These findings raise the possibility that the effects of our delayed sleep disruption regimen are not due to disruption of memory consolidation, but instead are caused by BDNF-mediated neuroadaptations within the BLA that actively suppress expression of fear. Treatments that safely reduce expression of fear memories would have considerable therapeutic potential in the treatment of conditions triggered by trauma.</p>","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142093633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and correlates of irritability among U.S. adults","authors":"Roy H. Perlis,&nbsp;Ata Uslu,&nbsp;Jonathan Schulman,&nbsp;Aliayah Himelfarb,&nbsp;Faith M. Gunning,&nbsp;Nili Solomonov,&nbsp;Mauricio Santillana,&nbsp;Matthew A. Baum,&nbsp;James N. Druckman,&nbsp;Katherine Ognyanova,&nbsp;David Lazer","doi":"10.1038/s41386-024-01959-3","DOIUrl":"10.1038/s41386-024-01959-3","url":null,"abstract":"This study aimed to characterize the prevalence of irritability among U.S. adults, and the extent to which it co-occurs with major depressive and anxious symptoms. A non-probability internet survey of individuals 18 and older in 50 U.S. states and the District of Columbia was conducted between November 2, 2023, and January 8, 2024. Regression models with survey weighting were used to examine associations between the Brief Irritability Test (BITe5) and sociodemographic and clinical features. The survey cohort included 42,739 individuals, mean age 46.0 (SD 17.0) years; 25,001 (58.5%) identified as women, 17,281 (40.4%) as men, and 457 (1.1%) as nonbinary. A total of 1218(2.8%) identified as Asian American, 5971 (14.0%) as Black, 5348 (12.5%) as Hispanic, 1775 (4.2%) as another race, and 28,427 (66.5%) as white. Mean irritability score was 13.6 (SD 5.6) on a scale from 5 to 30. In linear regression models, irritability was greater among respondents who were female, younger, had lower levels of education, and lower household income. Greater irritability was associated with likelihood of thoughts of suicide in logistic regression models adjusted for sociodemographic features (OR 1.23, 95% CI 1.22–1.24). Among 1979 individuals without thoughts of suicide on the initial survey assessed for such thoughts on a subsequent survey, greater irritability was also associated with greater likelihood of thoughts of suicide being present (adjusted OR 1.17, 95% CI 1.12–1.23). The prevalence of irritability and its association with thoughts of suicide suggests the need to better understand its implications among adults outside of acute mood episodes.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"49 13","pages":"1-8"},"PeriodicalIF":6.6,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41386-024-01959-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute effects of R-MDMA, S-MDMA, and racemic MDMA in a randomized double-blind cross-over trial in healthy participants.","authors":"Isabelle Straumann, Isidora Avedisian, Aaron Klaiber, Nimmy Varghese, Anne Eckert, Deborah Rudin, Dino Luethi, Matthias E Liechti","doi":"10.1038/s41386-024-01972-6","DOIUrl":"10.1038/s41386-024-01972-6","url":null,"abstract":"<p><p>Racemic 3,4-methylenedioxymethamphetamine (MDMA) acutely increases mood, feelings of empathy, trust, and closeness to others and is investigated to assist psychotherapy. Preclinical research indicates that S-MDMA releases monoamines and oxytocin more potently than R-MDMA, whereas R-MDMA more potently stimulates serotonin 5-hydroxytryptamine-2A receptors. S-MDMA may have more stimulant properties, and R-MDMA may be more psychedelic-like. However, acute effects of S- and R-MDMA have not been examined in a controlled human study. We used a double-blind, randomized, placebo-controlled, crossover design to compare acute effects of MDMA (125 mg), S-MDMA (125 mg), R-MDMA (125 mg and 250 mg), and placebo in 24 healthy participants. Outcome measures included subjective, autonomic, and adverse effects, pharmacokinetics, and plasma oxytocin, prolactin, and cortisol concentrations. S-MDMA (125 mg) induced greater subjective effects (\"stimulation,\" \"drug high,\" \"happy,\" \"open\") and higher increases in blood pressure than R-MDMA (both 125 and 250 mg) and MDMA (125 mg). Unexpectedly, R-MDMA did not produce more psychedelic-like effects than S-MDMA. S-MDMA increased plasma prolactin more than MDMA, and S-MDMA increased plasma cortisol and oxytocin more than MDMA and R-MDMA. The plasma elimination half-life of S-MDMA was 4.1 h after administration. The half-life of R-MDMA was 12 and 14 h after the administration of 125 and 250 mg, respectively. Half-lives for S-MDMA and R-MDMA were 5.1 h and 11 h, respectively, after racemic MDMA administration. Concentrations of the CYP2D6-formed MDMA-metabolite 4-hydroxy-3-methoxymethamphetamine were lower after R-MDMA administration compared with S-MDMA administration. The pharmacokinetic findings are consistent with the R-MDMA-mediated inhibition of CYP2D6. Stronger stimulant-like effects of S-MDMA in the present study may reflect the higher potency of S-MDMA rather than qualitative differences between S-MDMA and R-MDMA. Equivalent acute effects of S-MDMA, MDMA, and R-MDMA can be expected at doses of 100, 125, and 300 mg, respectively, and need to be investigated.Trial registration: ClinicalTrials.gov identifier: NCT05277636.</p>","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142046935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new prism next to motherhood’s light: uncovering changes in neural function following childbirth","authors":"Henry W. Chase","doi":"10.1038/s41386-024-01967-3","DOIUrl":"10.1038/s41386-024-01967-3","url":null,"abstract":"Childbirth has far-reaching consequences for the mother’s neural structure and function. In new research, Lotter and colleagues perform a comprehensive evaluation of neural function, hormone levels, and mood within a longitudinal design of post-partum women. The authors implicate new candidate neural processes following childbirth, which may have implications for resilience from and susceptibility to psychiatric disorders during this time.","PeriodicalId":19143,"journal":{"name":"Neuropsychopharmacology","volume":"49 12","pages":"1805-1806"},"PeriodicalIF":6.6,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41386-024-01967-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142009133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}