A potent and specific growth hormone-releasing factor (GRF) was recently isolated and characterized from a human islet cell tumour of the pancreas that caused acromegaly. Antibodies raised against the synthetic replicate of this peptide have allowed the immunohistochemical identification of GRF-producing neurones within the primate central nervous system. Such neurones are found mainly in the arcuate nucleus in human and monkey hypothalamus, suggesting that this nucleus is a primary source of GRF. We have further investigated this hypothesis by studying the anatomical organization of GRF neurones in rat hypothalamus, using an antibody raised against the recently characterized rat hypothalamic GRF in normal animals and in animals neonatally treated with monosodium glutamate (MSG), a treatment which results in the selective destruction of arcuate nucleus neurones. We present here the results which show that GRF-producing neurones are located mainly in the arcuate nucleus of rats. MSG treatment results in the complete loss of GRF-immunoreactive cell bodies within this nucleus and provokes a selective disappearance of GRF-immunoreactive fibres in the median eminence. These results show that the arcuate nucleus is the origin of the GRF-containing fibres that project to the median eminence and establish the MSG-treated rat as an in vivo model for studying growth hormone secretion in the absence of neurohumoral GRF.
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http://dx.doi.org/10.1038/307272a0 | DOI Listing |
Andrology
January 2025
Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Background: Although some studies have revealed the close relationship between leptin and premature ejaculation in clinical practice, whether and how leptin participates in the regulation of ejaculatory behaviors are still unknown.
Objective: To explore the role of leptin on ejaculatory behaviors and its underlying mechanism.
Materials And Methods: Copulation behavior tests were performed after acute and chronic leptin administration at peripheral and central levels.
Nature
January 2025
Allen Institute for Brain Science, Seattle, WA, USA.
Endocrinology
November 2024
Laboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [IMBICE; Argentine Research Council (CONICET); Scientific Research Commission, Province of Buenos Aires (CIC-PBA); National University of La Plata], B1906APO La Plata, Buenos Aires, Argentina.
The GH secretagogue receptor (GHSR) and the glucagon-like peptide-1 receptor (GLP-1R) are G protein-coupled receptors with critical, yet opposite, roles in regulating energy balance. Interestingly, these receptors are expressed in overlapping brain regions. However, the extent to which they target the same neurons and engage in molecular crosstalk remains unclear.
View Article and Find Full Text PDFThyroid
December 2024
National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, Maryland, USA.
Thyroid hormones (TH) play a key role in fetal brain development. While severe thyroid dysfunction, has been shown to cause neurodevelopmental and reproductive disorders, the rising levels of TH-disruptors in the environment in the past few decades have increased the need to assess effects of subclinical (mild) TH insufficiency during gestation. Since embryos do not produce their own TH before mid-gestation, early development processes rely on maternal production.
View Article and Find Full Text PDFLife Sci
January 2025
Hospital & Institute of Obstetrics and Gynecology, Fudan University, Shanghai 200081, China; The Academy of Integrative Medicine, Fudan University, Shanghai 200081, China; Shanghai Key Laboratory of Female Reproductive Endocrine-related Disease, Shanghai 200081, China. Electronic address:
Polycystic ovary syndrome (PCOS) has been noticed as a neuroendocrine syndrome manifested by reproductive hormone dysregulation involving increased luteinizing hormone (LH) pulse frequency and an increased LH to follicle-stimulating hormone ratio, yet theory is just beginning to be established. Neuroglia located in the arcuate nucleus and median eminence (ARC-ME) that are close to gonadotropin-releasing hormone (GnRH) axon terminals, comprise the blood-brain barrier and fenestrated vessels implying their putative roles in the modulation of the abnormal GnRH pulse in PCOS. This review outlines the disturbances of neuron-glia networks that underlie hypothetically the deregulation of GnRH-LH release and impaired sex hormone negative feedback in PCOS.
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