Journal: Molecular Psychiatry
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Abbreviation
Mol. Psychiatry
Publisher
Nature
37 results
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Publications 1 - 10 of 37
- Hypervulnerability of the adolescent prefrontal cortex to nutritional stress via reelin deficiencyItem type: Journal Article
Molecular PsychiatryLabouesse, Marie A.; Lassalle, Olivier; Richetto, Juliet; et al. (2017) - Introducing neurofilament light chain measure in psychiatry: current evidence, opportunities, and pitfallsItem type: Review Article
Molecular PsychiatryBavato, Francesco; Barro, Christian; Schnider, Laura K.; et al. (2024)The recent introduction of new-generation immunoassay methods allows the reliable quantification of structural brain markers in peripheral matrices. Neurofilament light chain (NfL), a neuron-specific cytoskeletal component released in extracellular matrices after neuroaxonal impairment, is considered a promising blood marker of active brain pathology. Given its sensitivity to a wide range of neuropathological alterations, NfL has been suggested for the use in clinical practice as a highly sensitive, but unspecific tool to quantify active brain pathology. While large efforts have been put in characterizing its clinical profile in many neurological conditions, NfL has received far less attention as a potential biomarker in major psychiatric disorders. Therefore, we briefly introduce NfL as a marker of neuroaxonal injury, systematically review recent findings on cerebrospinal fluid and blood NfL levels in patients with primary psychiatric conditions and highlight the opportunities and pitfalls. Current evidence suggests an elevation of blood NfL levels in patients with major depression, bipolar disorder, psychotic disorders, anorexia nervosa, and substance use disorders compared to physiological states. However, blood NfL levels strongly vary across diagnostic entities, clinical stage, and patient subgroups, and are influenced by several demographic, clinical, and analytical factors, which require accurate characterization. Potential clinical applications of NfL measure in psychiatry are seen in diagnostic and prognostic algorithms, to exclude neurodegenerative disease, in the assessment of brain toxicity for different pharmacological compounds, and in the longitudinal monitoring of treatment response. The high inter-individual variability of NfL levels and the lack of neurobiological understanding of its release are some of the main current limitations. Overall, this primer aims to introduce researchers and clinicians to NfL measure in the psychiatric field and to provide a conceptual framework for future research directions. - The autism brain imaging data exchange: Towards a large-scale evaluation of the intrinsic brain architecture in autismItem type: Journal Article
Molecular PsychiatryDi Martino, Adriana; Yan, Chaogan G.; Li, Qingyang; et al. (2014) - Paternal experience impacts cognitive function in offspring: a pre-existing conceptItem type: Other Journal Item
Molecular PsychiatryBohacek, Johannes; Weber-Stadlbauer, Ulrike; Mansuy, Isabelle (2017) - Dysfunction of ventral tegmental area GABA neurons causes mania-like behaviorItem type: Journal Article
Molecular PsychiatryYu, Xiao; Ba, Wei; Zhao, Guangchao; et al. (2021)The ventral tegmental area (VTA), an important source of dopamine, regulates goal- and reward-directed and social behaviors, wakefulness, and sleep. Hyperactivation of dopamine neurons generates behavioral pathologies. But any roles of non-dopamine VTA neurons in psychiatric illness have been little explored. Lesioning or chemogenetically inhibiting VTA GABAergic (VTA(Vgat)) neurons generated persistent wakefulness with mania-like qualities: locomotor activity was increased; sensitivity to D-amphetamine was heightened; immobility times decreased on the tail suspension and forced swim tests; and sucrose preference increased. Furthermore, after sleep deprivation, mice with lesioned VTA(Vgat)neurons did not catch up on lost sleep, even though they were starting from a sleep-deprived baseline, suggesting that sleep homeostasis was bypassed. The mania-like behaviors, including the sleep loss, were reversed by valproate, and re-emerged when treatment was stopped. Lithium salts and lamotrigine, however, had no effect. Low doses of diazepam partially reduced the hyperlocomotion and fully recovered the immobility time during tail suspension. The mania like-behaviors mostly depended on dopamine, because giving D1/D2/D3 receptor antagonists reduced these behaviors, but also partially on VTA(Vgat)projections to the lateral hypothalamus (LH). Optically or chemogenetically inhibiting VTA(Vgat)terminals in the LH elevated locomotion and decreased immobility time during the tail suspension and forced swimming tests. VTA(Vgat)neurons help set an animal's (and perhaps human's) mental and physical activity levels. Inputs inhibiting VTA(Vgat)neurons intensify wakefulness (increased activity, enhanced alertness and motivation), qualities useful for acute survival. In the extreme, however, decreased or failed inhibition from VTA(Vgat)neurons produces mania-like qualities (hyperactivity, hedonia, decreased sleep). - A novel murine model to study the impact of maternal depression and antidepressant treatment on biobehavioral functions in the offspringItem type: Journal Article
Molecular PsychiatryScarborough, Joseph; Mueller, Flavia S.; Weber-Stadlbauer, Ulrike; et al. (2021)Antenatal psychopathology negatively affects obstetric outcomes and exerts long-term consequences on the offspring's wellbeing and mental health. However, the precise mechanisms underlying these associations remain largely unknown. Here, we present a novel model system in mice that allows for experimental investigations into the effects of antenatal depression-like psychopathology and for evaluating the influence of maternal pharmacological treatments on long-term outcomes in the offspring. This model system in based on rearing nulliparous female mice in social isolation prior to mating, leading to a depressive-like state that is initiated before and continued throughout pregnancy. Using this model, we show that the maternal depressive-like state induced by social isolation can be partially rescued by chronic treatment with the selective serotonin reuptake inhibitor, fluoxetine (FLX). Moreover, we identify numerous and partly sex-dependent behavioral and molecular abnormalities, including increased anxiety-like behavior, cognitive impairments and alterations of the amygdalar transcriptome, in offspring born to socially isolated mothers relative to offspring born to mothers that were maintained in social groups prior to conception. We also found that maternal FLX treatment was effective in preventing some of the behavioral and molecular abnormalities emerging in offspring born to socially isolated mothers. Taken together, our findings suggest that the presence of a depressive-like state during preconception and pregnancy has sex-dependent consequences on brain and behavioral functions in the offspring. At the same time, our study highlights that FLX treatment in dams with a depression-like state can prevent abnormal behavioral development in the offspring. - Increased pregenual anterior cingulate glucose and lactate concentrations in major depressive disorderItem type: Journal Article
Molecular PsychiatryErnst, Jutta; Hock, Andreas; Henning, Anke; et al. (2017) - Disentangling the role of NAc D1 and D2 cells in hedonic eatingItem type: Journal Article
Molecular PsychiatryGuillaumin, Mathilde C.C.; Viskaitis, Paulius; Bracey, Eva; et al. (2023)Overeating is driven by both the hedonic component ('liking') of food, and the motivation ('wanting') to eat it. The nucleus accumbens (NAc) is a key brain center implicated in these processes, but how distinct NAc cell populations encode 'liking' and 'wanting' to shape overconsumption remains unclear. Here, we probed the roles of NAc D1 and D2 cells in these processes using cell-specific recording and optogenetic manipulation in diverse behavioral paradigms that disentangle reward traits of 'liking' and 'wanting' related to food choice and overeating in healthy mice. Medial NAc shell D2 cells encoded experience-dependent development of 'liking', while D1 cells encoded innate 'liking' during the first food taste. Optogenetic control confirmed causal links of D1 and D2 cells to these aspects of 'liking'. In relation to 'wanting', D1 and D2 cells encoded and promoted distinct aspects of food approach: D1 cells interpreted food cues while D2 cells also sustained food-visit-length that facilitates consumption. Finally, at the level of food choice, D1, but not D2, cell activity was sufficient to switch food preference, programming subsequent long-lasting overconsumption. By revealing complementary roles of D1 and D2 cells in consumption, these findings assign neural bases to 'liking' and 'wanting' in a unifying framework of D1 and D2 cell activity. - Erratum: Fluoxetine effects on molecular, cellular and behavioral endophenotypes of depression are driven by the living environmentItem type: Other Journal Item
Molecular PsychiatryAlboni, Silvia; Van Dijk, R. Maarten; Poggini, Silvia; et al. (2017) - Transgenerational disruption of functional 5-HT1AR-induced connectivity in the adult mouse brain by traumatic stress in early lifeItem type: Journal Article
Molecular PsychiatryRazoux, F.; Russig, H.; Mueggler, T.; et al. (2017)
Publications 1 - 10 of 37