Frontiers in Neuroendocrinology最新文献

This manuscript proposes that melanin-concentrating hormone (MCH) in the medial preoptic area (MPOA) is an neurochemical signal evolved to trigger the declining process of maternal care. MCH in the MPOA appears only after parturition and is progressively increased with the progression of lactation, while maternal behavior declines progressively. Intra-MPOA injection of MCH decreases active maternal responses. MCH is also highly responsive to infant characteristics and maternal condition. Behavioral changes induced by MCH in late postpartum period are conducive to the decline of infant-directed maternal behavior. The MPOA MCH system may mediate the maternal behavior decline by suppressing the maternal approach motivation and/or increasing maternal withdrawal via its inhibitory action onto the mesolimbic dopamine D₁/D₂ receptors and its stimulating action on serotonin 5-HT_2C receptors in the ventral tegmental area. Research into the MCH maternal effects will enhance our understanding of the neurochemical mechanisms underlying the maternal behavior decline.

Astrocytes are now recognized as integral components of neural circuits, regulating their maturation, activity and plasticity. Neuroendocrinology has provided fertile ground for revealing the diverse strategies used by astrocytes to regulate the physiological and behavioural outcomes of neural circuit activity in response to internal and environmental inputs. However, the development of astrocytes in the hypothalamus has received much less attention than in other brain regions such as the cerebral cortex and spinal cord. In this review, we synthesize our current knowledge of astrogenesis in the hypothalamus across various life stages. A distinctive feature of hypothalamic astrogenesis is that it persists all throughout lifespan, and involves multiple cellular sources corresponding to radial glial cells during early development, followed by tanycytes, parenchymal progenitors and locally dividing astrocytes. Astrogenesis in the hypothalamus is closely coordinated with the maturation of hypothalamic neurons. This coordination is exemplified by recent findings in neurons producing gonadotropin-releasing hormone, which actively shape their astroglial environment during infancy to integrate functionally into their neural network and facilitate sexual maturation, a process vulnerable to endocrine disruption. While hypothalamic astrogenesis shares common principles with other brain regions, it also exhibits specific features in its dynamics and regulation, both at the inter- and intra-regional levels. These unique properties emphasize the importance of further exploration. Additionally, we discuss the experimental strategies used to assess astrogenesis in the hypothalamus and their potential bias and limitations. Understanding the mechanisms of hypothalamic astrogenesis throughout life will be crucial for comprehending the development and function of the hypothalamus under both physiological and pathological conditions.

The hypothalamus is a key link in neuroendocrine regulations, which are provided by neuropeptides and dopamine. Until the late 1980 s, it was believed that, along with peptidergic neurons, hypothalamus contained dopaminergic neurons. Over time, it has been shown that besides dopaminergic neurons expressing the dopamine transporter and dopamine-synthesizing enzymes − tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) − the hypothalamus contains neurons expressing only TH, only AADC, both enzymes or only dopamine transporter. The end secretory product of TH neurons is L-3,4-dihydroxyphenylalanine, while that of AADC neurons and bienzymatic neurons lacking the dopamine transporter is dopamine. During ontogenesis, especially in the perinatal period, monoenzymatic neurons predominate in the hypothalamic neuroendocrine centers. It is assumed that L-3,4-dihydroxyphenylalanine and dopamine are released into the neuropil, cerebral ventricles, and blood vessels, participating in the regulation of target cell differentiation in the perinatal period and the functioning of target cells in adulthood.

Over the past two decades, there has been increasing evidence for the importance of rapid-onset actions of corticosteroid hormones in the brain. Here, we highlight the distinct rapid corticosteroid actions that regulate excitatory and inhibitory synaptic transmission in the hypothalamus, the hippocampus, basolateral amygdala, and prefrontal cortex. The receptors that mediate rapid corticosteroid actions are located at or close to the plasma membrane, though many of the receptor characteristics remain unresolved. Rapid-onset corticosteroid effects play a role in fast neuroendocrine feedback as well as in higher brain functions, including increased aggression and anxiety, and impaired memory retrieval. The rapid non-genomic corticosteroid actions precede and complement slow-onset, long-lasting transcriptional actions of the steroids. Both rapid and slow corticosteroid actions appear to be indispensable to adapt to a continuously changing environment, and their imbalance can increase an individual’s susceptibility to psychopathology.