Frontiers in Neuroendocrinology最新文献

There is a lack of understanding of the neural mechanisms regulating the rewarding effects of social interactions. A significant contributor to this lack of clarity is the diversity of social behaviors and animal models utilized to investigate mechanisms. Other sources of the lack of clarity are the diversity of brain regions that can regulate social reward and the diversity of signaling pathways that regulate reward. To provide some clarity into the mechanisms of social reward, this review focused on the brain region most implicated in reward for multiple stimuli, the nucleus accumbens, and surveyed (systematically reviewed) studies that investigated the relationship between social interaction and five signaling systems implicated in the regulation of reward and social behavior: oxytocin, vasopressin, serotonin, opioids and endocannabinoids. Moreover, all of these studies were organized by the type of social behavior studied: affiliative interactions, play behavior, aggression, social defeat, sex behavior, pair-bonding, parental behavior and social isolation. From this survey and organization, this review concludes that oxytocin, endocannabinoids and mu-opioid receptors in the nucleus accumbens positively regulate the rewarding social behaviors, and kappa-opioid receptors negatively regulate the rewarding social behaviors. The opposite profile is observed for these signaling systems for the aversive social behaviors. More studies are needed to investigate the directional role of the serotonin system in the nucleus accumbens in the regulation of many types of social behaviors, and vasopressin likely does not act in the nucleus accumbens in the regulation of the valence of social behaviors. Many of these different signaling systems are also interdependent of one another in the regulation of different types of social behaviors. Finally, the interaction of these signaling systems with dopamine in the nucleus accumbens is briefly discussed.

Estrogen fluctuations during the menstrual cycle, puberty, postpartum, or in the menopausal transition are associated with cognitive, affective, and behavioral effects. Additionally, estrogens are essential in hormonal contraception, menopausal hormone therapy, or gender-affirming hormone therapy. This systematic review summarizes findings on the role of estrogens for structure, function, and connectivity of human brain networks. We searched PubMed, Web of Science, and ScienceDirect for neuroimaging articles assessing estrogens published since 2008. We included 54 studies (N = 2,494 participants) on endogenous estrogen, and 28 studies (N = 1,740 participants) on exogenous estrogen conditions. Estrogen-related changes were reported for emotion, reward, memory, and resting-state networks, and in regional white and gray matter, with a particular neural plasticity in the hippocampus and amygdala. By examining study designs, imaging measures, and analysis methods, this review highlights the role of neuroimaging in advancing neuroendocrine and neurocognitive research, particularly promoting brain health for women and individuals with ovaries.

The complex interplay between the gut microbiota, sex hormones, and mental health is emerging as a pivotal factor in understanding and managing psychiatric disorders. Beyond their traditional roles, sex hormones exert profound effects on various physiological systems including the gut microbiota. Fluctuations in sex hormone levels, notably during the menstrual cycle, influence gut physiology and barrier function, shaping gut microbiota composition and immune responses. Conversely, the gut microbiota actively modulates sex hormone levels via enzymatic processes. This bidirectional relationship underscores the significance of the gut-brain axis in maintaining mental well-being. This review explores the multifaceted interactions between sex hormones, the gut microbiota, and mental health outcomes. We highlight the potential of personalized interventions in treating psychiatric disorders, particularly in vulnerable populations such as premenopausal women and individuals with depressive disorders. By elucidating these complex interactions, we aim to provide insights for future research into targeted interventions, enhancing mental health outcomes.

Sex-related differences characterize multiple sclerosis, an autoimmune, inflammatory and neurodegenerative disease displaying higher incidence in females as well as discrepancies in susceptibility and progression. Besides clinical specificities, molecular and cellular differences related to sex hormones were progressively uncovered improving our understanding of the mechanisms involved in this disabling disease. The most recent findings may give rise to the identification of novel therapeutic perspectives that could meet the urgent need for a treatment preventing the transition from the recurrent- to the progressive form of the disease. The present review is an update of our current knowledge about progestagens, androgens and estrogens in the context of CNS demyelination including their synthesis, the impact of their dysregulation, the preclinical and clinical data presently available, the main molecular dimorphisms related to these hormones and their age-related changes and relationship with failure of spontaneous remyelination, likely impacting the inexorable progression of multiple sclerosis towards irreversible disabilities.

Females diagnosed with Menstrually-related mood disorders (MRMDs) have more risk to develop postpartum depression (PPD). There are overlapping symptoms between MRMDs and PPD such as anxiety, depressed mood, irritability, that can contribute to a lower quality of life. MRMDs and PPD share components in their etiology such as dramatic hormonal oscillations, and alterations in Hypothalamus-Pituitary-Adrenal (HPA) axis activity that may impair GABAergic neurotransmission. As well, stressful events that impact HPA regulation may play an important role in the etiology of MRMDs and PPD. Here we review common hormone fluctuations across the menstrual cycle and pregnancy/postpartum to identify shared pathways that could contribute to greater sensitivity in people with MRMDs and PPD. This review summarizes hormone sensitivity, HPA axis activity and neurosteroids effects on GABAergic transmission and the potential role of chronic stress in developing MRMDs and PPD. In addition, other potential etiopathological factors, such as serotonin and the immune system, are discussed. Investigating the etiopathology of MRMDs and PDD will help to better understand the complexity of factors involved in these disorders that affect females across the reproductive years.

The levels of the key neurosteroid of pregnancy, allopregnanolone, are very high in the fetal and maternal brain compared to after birth. These levels are maintained by the placenta which forms a placental connection to fetal brain development. Maternal stresses depress placental synthesis resulting in a fall in allopregnanolone levels leading to deficits in myelination that continue into childhood. This contributes to an increased incidence of behavioural disorders. Supplementing neurosteroid action with allopregnanolone analogues or raising endogenous production with mitochondrial translocator protein (TSPO) ligands reverses these deficits. Preterm birth leads to an early dramatic loss of neurosteroid support for brain development leading to marked deficits in myelination and susceptibility to hypoxic-ischaemic injury. Postnatal treatment with the allopregnanolone analogue ganaxolone improves myelination and reduces hyperactive behaviour. TSPO ligands such as emapunil have been shown to improve oligodendrocyte maturation. These findings support the use of allopregnanolone supplementation approaches after pregnancy compromises to improve outcome.

Craniopharyngioma is a benign tumour affecting the hypothalamic and pituitary regions, which are involved in the production and secretion of oxytocin. We conducted a systematic review to assess dysregulation of the oxytocin system in craniopharyngioma and associations with neurobehavioural, eating, and metabolic abnormalities. Eight studies (n = 72 patients) were included. Evidence for dysfunction of the endogenous oxytocin system in craniopharyngioma is limited and mixed. While no significant differences in baseline salivary oxytocin concentrations were reported between patients with craniopharyngioma and controls, patients with craniopharyngioma were found to have blunted salivary oxytocin response following exercise stimulation and this was associated with greater state anxiety and higher BMI. Studies administering exogenous oxytocin are sparse and do not meet required standards. Hypothalamic damage may pose an additional mechanism of oxytocin dysregulation. Improving understanding of the oxytocin system in craniopharyngioma could be pivotal for exploring the potential therapeutic role of exogenous oxytocin in this condition.