scholarly journals Refeeding-Activated Glutamatergic Neurons in the Hypothalamic Paraventricular Nucleus (PVN) Mediate Effects of Melanocortin Signaling in the Nucleus Tractus Solitarius (NTS)

Endocrinology ◽  
2012 ◽  
Vol 153 (8) ◽  
pp. 3804-3814 ◽  
Author(s):  
Praful S. Singru ◽  
Gábor Wittmann ◽  
Erzsébet Farkas ◽  
Györgyi Zséli ◽  
Csaba Fekete ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Nucleus Tractus Solitarius ◽  
Glutamate Transporter ◽  
Hypothalamic Paraventricular Nucleus ◽  
Double Labeling ◽  
Axon Terminals ◽  
Glutamatergic Neurons ◽  
Prolonged Fast ◽  
Melanocortin Signaling

We previously demonstrated that refeeding after a prolonged fast activates a subset of neurons in the ventral parvocellular subdivision of the paraventricular nucleus (PVNv) as a result of increased melanocortin signaling. To determine whether these neurons contribute to satiety by projecting to the nucleus tractus solitarius (NTS), the retrogradely transported marker substance, cholera toxin-β (CTB), was injected into the dorsal vagal complex of rats that were subsequently fasted and refed for 2 h. By double-labeling immunohistochemistry, CTB accumulation was found in the cytoplasm of the majority of refeeding-activated c-Fos neurons in the ventral parvocellular subdivision of the hypothalamic paraventricular nucleus (PVNv). In addition, a large number of refeeding-activated c-Fos-expressing neurons were observed in the lateral parvocellular subdivision (PVNl) that also contained CTB and were innervated by axon terminals of proopiomelanocortin neurons. To visualize the location of neuronal activation within the NTS by melanocortin-activated PVN neurons, α-MSH was focally injected into the PVN, resulting in an increased number of c-Fos-containing neurons in the PVN and in the NTS, primarily in the medial and commissural parts. All refeeding-activated neurons in the PVNv and PVNl expressed the mRNA of the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), indicating their glutamatergic phenotype, but only rare neurons contained oxytocin. These data suggest that melanocortin-activated neurons in the PVNv and PVNl may contribute to refeeding-induced satiety through effects on the NTS and may alter the sensitivity of NTS neurons to vagal satiety inputs via glutamate excitation.

scholarly journals Orexin depolarizes rat hypothalamic paraventricular nucleus neurons

2001 ◽  
Vol 281 (4) ◽  
pp. R1114-R1118 ◽  
Author(s):  
Tetsuro Shirasaka ◽  
Satoshi Miyahara ◽  
Takato Kunitake ◽  
Qing-Hua Jin ◽  
Kazuo Kato ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Brain Slices ◽  
Hypothalamic Paraventricular Nucleus ◽  
Dependent Manner ◽  
Patch Clamp Recording ◽  
Concentration Dependent Manner ◽  
Whole Cell Patch Clamp ◽  
Orexin Receptors ◽  
Bath Application

Orexins, also called hypocretins, are newly discovered hypothalamic peptides that are thought to be involved in various physiological functions. In spite of the fact that orexin receptors, especially orexin receptor 2, are abundant in the hypothalamic paraventricular nucleus (PVN), the effects of orexins on PVN neurons remain unknown. Using a whole cell patch-clamp recording technique, we investigated the effects of orexin-B on PVN neurons of rat brain slices. Bath application of orexin-B (0.01–1.0 μM) depolarized 80.8% of type 1 ( n = 26) and 79.2% of type 2 neurons tested ( n = 24) in the PVN in a concentration-dependent manner. The effects of orexin-B persisted in the presence of TTX (1 μM), indicating that these depolarizing effects were generated postsynaptically. Addition of Cd2+(1 mM) to artificial cerebrospinal fluid containing TTX (1 μM) significantly reduced the depolarizing effect in type 2 neurons. These results suggest that orexin-B has excitatory effects on the PVN neurons mediated via a depolarization of the membrane potential.

scholarly journals Differential Effects of Refeeding on Melanocortin-Responsive Neurons in the Hypothalamic Paraventricular Nucleus

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4329-4335 ◽  
Author(s):  
Edith Sánchez ◽  
Praful S. Singru ◽  
Runa Acharya ◽  
Monica Bodria ◽  
Csaba Fekete ◽  
...  
Keyword(s):  
Gene Expression ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Early Action ◽  
Sprague Dawley Rats ◽  
Melanocortin Signaling ◽  
Agouti Related Protein ◽  
Serum Tsh

To explore the effect of refeeding on recovery of TRH gene expression in the hypothalamic paraventricular nucleus (PVN) and its correlation with the feeding-related neuropeptides in the arcuate nucleus (ARC), c-fos immunoreactivity (IR) in the PVN and ARC 2 h after refeeding and hypothalamic TRH, neuropeptide Y (NPY) and agouti-related protein (AGRP) mRNA levels 4, 12, and 24 h after refeeding were studied in Sprague-Dawley rats subjected to prolonged fasting. Despite rapid reactivation of proopiomelanocortin neurons by refeeding as demonstrated by c-fos IR in ARC α-MSH-IR neurons and ventral parvocellular subdivision PVN neurons, c-fos IR was present in only 9.7 ± 1.1% hypophysiotropic TRH neurons. Serum TSH levels remained suppressed 4 and 12 h after the start of refeeding, returning to fed levels after 24 h. Fasting reduced TRH mRNA compared with fed animals, and similar to TSH, remained suppressed at 4 and 12 h after refeeding, returning toward normal at 24 h. AGRP and NPY gene expression in the ARC were markedly elevated in fasting rats, AGRP mRNA returning to baseline levels 12 h after refeeding and NPY mRNA remaining persistently elevated even at 24 h. These data raise the possibility that refeeding-induced activation of melanocortin signaling exerts differential actions on its target neurons in the PVN, an early action directed at neurons that may be involved in satiety, and a later action on hypophysiotropic TRH neurons involved in energy expenditure, potentially mediated by sustained elevations in AGRP and NPY. This response may be an important homeostatic mechanism to allow replenishment of depleted energy stores associated with fasting.

A Slow Transient Potassium Current Expressed in a Subset of Neurosecretory Neurons of the Hypothalamic Paraventricular Nucleus

2000 ◽  
Vol 84 (4) ◽  
pp. 1814-1825 ◽  
Author(s):  
Jason A. Luther ◽  
Katalin Cs. Halmos ◽  
Jeffrey G. Tasker
Keyword(s):  
Paraventricular Nucleus ◽  
Potassium Current ◽  
Outward Current ◽  
Retrograde Transport ◽  
Neurosecretory Cells ◽  
Firing Frequency ◽  
Hypothalamic Paraventricular Nucleus ◽  
Transient Outward Current ◽  
Type I ◽  
Double Labeling

Type I putative magnocellular neurosecretory cells of the hypothalamic paraventricular nucleus (PVN) express a prominent transient outward rectification generated by an A-type potassium current. Described here is a slow transient outward current that alters cell excitability and firing frequency in a subset of type I PVN neurons (38%). Unlike most of the type I neurons (62%), the transient outward current in these cells was composed of two kinetically separable current components, a fast activating, fast inactivating component, resembling an A-type potassium current, and a slowly activating [10–90% rise time: 20.4 ± 12.8 (SE) ms], slowly inactivating component (time constant of inactivation: τ = 239.0 ± 66.1 ms). The voltage dependence of activation and inactivation and the sensitivity to block by 4-aminopyridine (5 mM) and tetraethylammonium chloride (10 mM) of the fast and slow components were similar. Compared to the other type I neurons, the neurons that expressed the slow transient outward current were less excitable when hyperpolarized, requiring larger current injections to elicit an action potential (58.5 ± 13.2 vs. 15.4 ± 2.4 pA; 250-ms duration; P < 0.01), displaying a longer delay to the first spike (184.9 ± 15.7 vs. 89.7 ± 8.8 ms with 250- to 1,000-ms, 50-pA current pulses; P < 0.01), and firing at a lower frequency (18.7 ± 4.6 vs. 37.0 ± 5.5 Hz with 100-pA current injections; P < 0.05). These data suggest that a distinct subset of type I PVN neurons express a novel slow transient outward current that leads to a lower excitability. Based on double labeling following retrograde transport of systemically administered fluoro-gold and intracellular injection of biocytin, these cells are neurosecretory and are similar morphologically to magnocellular neurosecretory cells, although it remains to be determined whether they are magnocellular neurons.

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.

scholarly journals 11β-Hydroxysteroid Dehydrogenase Type 2 Activity in Hypothalamic Paraventricular Nucleus Modulates Sympathetic Excitation

Hypertension ◽  
2006 ◽  
Vol 48 (1) ◽  
pp. 127-133 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Yu-Ming Kang ◽  
Yang Yu ◽  
Shun-Guang Wei ◽  
Thomas J. Schmidt ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Hydroxysteroid Dehydrogenase ◽  
Hypothalamic Paraventricular Nucleus

Galanin- but not galanin-like peptide-containing axon terminals innervate hypophysiotropic TRH-synthesizing neurons in the hypothalamic paraventricular nucleus

2004 ◽  
Vol 1002 (1-2) ◽  
pp. 43-50 ◽  
Author(s):  
Gábor Wittmann ◽  
Sumit Sarkar ◽  
Erik Hrabovszky ◽  
Zsolt Liposits ◽  
Ronald M. Lechan ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Axon Terminals
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