That the brain is a target for hormones is a well established fact. Today we also know that brains can secrete the whole gamut of peptides and steroid hormones, i.e., pregnanes and pregnenes. Considering that the ancestral neuron was a neurosecreting cell, this is not surprising. As CRH and cortisol secretion occur in situ in nervous systems, the intriguing possibility that anxio-depressive syndromes may be associated with paracrine effects of these compounds on the brain should now be considered. The concept of stress as a specific reaction of the nueroendocrine system to nocuous stimuli is re-examined in light of new evidence. The fundamental importance of historical, social, and psychological contexts in evaluating hormonal actions is emphasized. Problems emerging from the attempt to search for specific biological markers in different psychiatric disorders are discussed. The suggestion is made that, rather than to categorize nosological entities, biological dysfunctions should be elated with psychological abnormalities.
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Front Aging Neurosci
January 2025
Department of Psychology and Neuroscience, Baylor University, Waco, TX, United States.
Assessing sex as a biological variable is critical to determining the influence of environmental and lifestyle risks and protective factors mediating behavior and neuroplasticity across the lifespan. We investigated sex differences in affective behavior, memory, and hippocampal neurogenesis following short- or long-term exposure to exercise or chronic mild stress in young and aged mice. Male and female mice were assigned control, running, or chronic stress rearing conditions for 1 month (young) or for 15 months (aged), then underwent a behavioral test battery to assess activity, affective behavior, and memory.
View Article and Find Full Text PDFMol Neurobiol
January 2025
Cellular and Molecular Neurobiology and Drug Targeting Laboratory, Department of Zoology, Indira Gandhi National Tribal University, Amarkantak-484 887, MP, India.
Depression is one of the most disabling mental disorders worldwide and characterized by symptoms including worthlessness, anhedonia, sleep, and appetite disturbances. Recently, studies have suggested that tryptophan (Trp) metabolism plays a key role in depressed mood through serotonin and kynurenine pathway involving enzyme tryptophan 5-monooxygenase (TPH) and indoleamine-2,3-dioxygenase (IDO) respectively. Moreover, during neuroinflammation, IDO is activated by proinflammatory cytokines and affects neurogenesis, cognition, disturbed hypothalamic-pituitary-adrenal (HPA) axis, and gut homeostasis by altering the gut bacteria and its metabolites like Trp derivatives.
View Article and Find Full Text PDFCell Biol Toxicol
January 2025
Laboratory of Neurobiology, Hebei Medical University, Shijiazhuang, 050017, China.
Esketamine, a newly developed antidepressant, is the subject of this research which seeks to explore its impact on depressive symptoms in neuropathic pain mice and the potential molecular mechanisms involved. Through transcriptome sequencing and bioinformatics analysis combined with in vivo studies, it was identified that esketamine markedly boosts the levels of the m6A methyltransferase METTL3 and the AMPA receptor GluA1 subunit. Esketamine activates METTL3, allowing it to bind with GluA1 mRNA, promoting m6A modification, thereby enhancing GluA1 expression at synapses.
View Article and Find Full Text PDFJMIR Form Res
January 2025
CIRCLE - Complex Intervention Research in Health and Care, Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden.
Background: Parents of children treated for cancer may experience psychological difficulties including depression, anxiety, and posttraumatic stress. Digital interventions, such as internet-administered cognitive behavioral therapy, offer an accessible and flexible means to support parents. However, engagement with and adherence to digital interventions remain a significant challenge, potentially limiting efficacy.
View Article and Find Full Text PDFJ Headache Pain
January 2025
Department of Neurology, University of Utah, 383 Colorow Drive, Salt Lake City, UT, 84108, USA.
A key unanswered question in migraine neurobiology concerns the mechanisms that make the brain of migraineurs susceptible to cortical spreading depression (CSD, a spreading depolarization that underlies migraine aura and may trigger the migraine pain mechanisms). Important insights into this question can be obtained by studying the mechanisms of facilitation of CSD initiation in genetic mouse models of the disease. These models, all generated from families with hereditary migraine, allow the investigation of the functional consequences of disease-causing mutations at the molecular, cellular, synaptic and neural circuit levels.
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