scholarly journals The Role of Intracerebroventricular Administration of Leptin in the Stimulation of Prothyrotropin Releasing Hormone Neurons in the Hypothalamic Paraventricular Nucleus

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3296-3306 ◽  
Author(s):  
Mario Perello ◽  
Ronald C. Stuart ◽  
Eduardo A. Nillni
Keyword(s):  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Intracerebroventricular Administration ◽  
Releasing Hormone ◽  
Stimulation Of

Effect of different types of stressors on peptide messenger ribonucleic acids in the hypothalamic paraventricular nucleus

1993 ◽  
Vol 128 (6) ◽  
pp. 485-492 ◽  
Author(s):  
Sandra Ceccatelli ◽  
Catello Orazzo
Keyword(s):  
Paraventricular Nucleus ◽  
Immobilization Stress ◽  
Thyrotropin Releasing Hormone ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Ribonucleic Acids ◽  
Releasing Hormone ◽  
Different Types

Using in situ hybridization we have studied the effects of different types of stressors, such as ether, immobilization, cold and swimming, on the expression of several peptide messenger ribonucleic acids (mRNAs) in the hypothalamic paraventricular nucleus of adult male rats. Paraventricular nucleus sections were hybridized using synthetic oligonucleotide probes complementary to mRNA for corticotropin-releasing hormone, neurotensin, enkephalin and thyrotropin-releasing hormone. A clear upregulation of neurotensin mRNA was seen after ether and, to a lesser extent, after immobilization stress, whereas after the two other stressors neurotensin mRNA was undetectable, as in control rats. An increase in enkephalin mRNA was observed in a selective region of the dorsal part of the medioparvocellular subdivision of the paraventricular nucleus only after ether and immobilization stress. No significant changes were seen in corticotropin-releasing hormone and thyrotropin-releasing hormone mRNA levels in any of the experimental paradigms. The present results show selective changes for various peptide mRNAs in the paraventricular nucleus after various types of stress. Significant effects could be demonstrated only on neurotensin and enkephalin mRNA after ether and immobilization stress. This suggests that adaptive changes in the rate of synthesis, processing and transport of the peptide may develop over a longer period of time.

scholarly journals The role of SOCS3 in the hypothalamic paraventricular nucleus in rat model of inflammatory pain

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Na Meng ◽  
Ning-Ning Ji ◽  
Ziming Zhou ◽  
Yicheng Qian ◽  
Yu Tang ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Rat Model ◽  
Inflammatory Pain ◽  
Hypothalamic Paraventricular Nucleus

scholarly journals Regulation of Serine (Ser)-31 and Ser40 Tyrosine Hydroxylase Phosphorylation during Morphine Withdrawal in the Hypothalamic Paraventricular Nucleus and Nucleus Tractus Solitarius-A2 Cell Group: Role of ERK1/2

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5780-5793 ◽  
Author(s):  
Cristina Núñez ◽  
M. Luisa Laorden ◽  
M. Victoria Milanés
Keyword(s):  
Tyrosine Hydroxylase ◽  
Paraventricular Nucleus ◽  
Nucleus Tractus Solitarius ◽  
Morphine Withdrawal ◽  
Hypothalamic Paraventricular Nucleus ◽  
Cell Group ◽  
Erk Activation ◽  
Catecholamine Biosynthesis ◽  
Hpa Axis Activity

Our previous studies have shown that naloxone-induced morphine withdrawal increases the hypothalamic-pituitary-adrenocortical (HPA) axis activity, which is dependent on a hyperactivity of noradrenergic pathways [nucleus tractus solitarius (NTS) A2] innervating the hypothalamic paraventricular nucleus (PVN). Short-term regulation of catecholamine biosynthesis occurs through phosphorylation of tyrosine hydroxylase (TH), which enhances enzymatic activity. In the present study, the effect of morphine withdrawal on site-specific TH phosphorylation in the PVN and NTS-A2 was determined by quantitative blot immunolabeling and immunohistochemistry using phosphorylation state-specific antibodies. We show that naloxone-induced morphine withdrawal phosphorylates TH at Serine (Ser)-31 but not Ser40 in PVN and NTS-A2, which is associated with both an increase in total TH immunoreactivity in NTS-A2 and an enhanced TH activity in the PVN. In addition, we demonstrated that TH neurons phosphorylated at Ser31 coexpress c-Fos in NTS-A2. We then tested whether pharmacological inhibition of ERK activation by ERK kinase contributes to morphine withdrawal-induced phosphorylation of TH at Ser31. We show that the ability of morphine withdrawal to stimulate phosphorylation at this seryl residue is reduced by SL327, an inhibitor of ERK1/2 activation. These results suggest that morphine withdrawal increases noradrenaline turnover in the PVN, at least in part, via ERK1/2-dependent phosphorylation of TH at Ser31.

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