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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Dimitrov, Eugene Usdin, Ted Björn |
| Description | Country affiliation: United States Author Affiliation: Dimitrov E ( Section on Fundamental Neuroscience, National Institute of Mental Health, Bethesda, Maryland 20892, USA.) |
| Abstract | Neurons in the subparafascicular area at the caudal border of the thalamus that contain the neuropeptide tuberoinfundibular peptide of 39 residues (TIP39) densely innervate several hypothalamic areas, including the paraventricular nucleus (PVN). These areas contain a matching distribution of TIP39's receptor, the parathyroid hormone receptor 2 (PTH2R). Frequent PTH2R coexpression with a vesicular glutamate transporter (VGlut2) suggests that TIP39 could presynaptically regulate glutamate release. By using immunohistochemistry we found CRH-ir neurons surrounded by PTH2R-ir fibers and TIP39-ir axonal projections in the PVN area of the mouse brain. Labeling hypothalamic neuroendocrine neurons by peripheral injection of fluorogold in PTH2R-lacZ knock-in mice showed that most PTH2Rs are on PVN and peri-PVN interneurons and not on neuroendocrine cells. Double fluorescent in situ hybridization revealed a high level of coexpression between PTH2R and VGlut2 mRNA by cells located in the PVN and nearby brain areas. Local TIP39 infusion (100 pmol) robustly increased pCREB-ir in the PVN and adjacent perinuclear zone. It also increased plasma corticosterone and decreased plasma prolactin. These effects of TIP39 on pCREB-ir, corticosterone, and prolactin were abolished by coinfusion of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonopentanoic acid (AP-5; 30 pmol each) and were absent in PTH2R knockout mice. Basal plasma corticosterone was slightly decreased in TIP39 knockout mice just before onset of their active phase. The present data indicate that the TIP39 ligand/PTH2 receptor system provides facilitatory regulation of the hypothalamic-pituitary-adrenal axis via hypothalamic glutamatergic neurons and that it may regulate other neuroendocrine systems by a similar mechanism. |
| File Format | HTM / HTML |
| ISSN | 00219967 |
| e-ISSN | 10969861 |
| DOI | 10.1002/cne.22462 |
| Journal | Journal of Comparative Neurology |
| Issue Number | 21 |
| Volume Number | 518 |
| Language | English |
| Publisher | Wiley |
| Publisher Date | 2010-11-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Neurology Glutamic Acid Metabolism Hypothalamo-hypophyseal System Neurons Neuropeptides Paraventricular Hypothalamic Nucleus Cytology Pituitary-adrenal System Animals Corticosterone Corticotropin-releasing Hormone Mice Mice, Inbred C57bl Mice, Knockout Genetics Receptor, Parathyroid Hormone, Type 2 Vesicular Glutamate Transport Protein 2 Research Support, N.i.h., Extramural |
| Content Type | Text |
| Resource Type | Article |
| Subject | Neuroscience |
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