The Stimulatory Effect of 5HT and the Role of the Paraventricular Nucleus on PMS Induced Ovulation in the Immature Rat

1979 ◽  
Vol 28 (6) ◽  
pp. 415-424 ◽  
Author(s):  
C.A. Wilson ◽  
C.A. Endersby
Keyword(s):  
Paraventricular Nucleus ◽  
Immature Rat ◽  
Induced Ovulation

Follicle-stimulating hormone-dependent estrogen secretion by rat Sertoli cells in vitro: Modulation by calcium

1991 ◽  
Vol 125 (3) ◽  
pp. 280-285 ◽  
Author(s):  
J. Alan Talbot ◽  
Ann Lambert ◽  
Robert Mitchell ◽  
Marek Grabinski ◽  
David C. Anderson ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Culture Medium ◽  
Follicle Stimulating Hormone ◽  
Dibutyryl Camp ◽  
Immature Rat ◽  
Estradiol Secretion ◽  
Old Rats ◽  
Stimulating Hormone

Abstract We have investigated the role of Ca2+ in the control of FSH-induced estradiol secretion by Sertoli cells isolated from 8-10 days old rats. Exogenous Ca2+ (4-8 mmol/1) inhibited FSH-stimulated E2 secretion such that, with 8 mmol/l Ca2+ and FSH (8 IU/l) E2 secretion decreased from 2091±322 to 1480±84 pmol/l (p<0.002), whilst chelation of Ca2+ in the culture medium with EGTA (3 mmol/l) increased E2 secretion from 360±45 to 1242±133 pmol/l) in the absence of FSH. Further, EGTA (3 mmol/l) markedly potentiated FSH (8 IU/l), forskolin (1 μmol/l) and dibutyryl cAMP (1 mmol/l)-stimulated E2 secretion. Addition of the Ca2+ ionophores, ionomycin (2-5 μmol/l) and A23187 (2 μmol/l), inhibited FSH (8 IU/l)-stimulated E2 secretion by >80%. The effect of ionomycin was totally reversible, whereas that of A23187 was irreversible. Ionomycin (5 μmol/l) had no effect on EGTA-induced E2 secretion in the absence of FSH, but reduced EGTA-provoked E2 secretion by 59% in the presence of FSH (8 IU/l). Similarly, forskolin- and dibutyryl cAMP-provoked E2 production was inhibited 46-50% by ionomycin (5 μmol/l). We conclude that FSH-induced E2 secretion from immature rat Sertoli cells is modulated by intra- and extracellular Ca2+.

POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE
Keyword(s):  
Inhibitory Action ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Immature Rat ◽  
Rat Strain ◽  
Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

Role of vasopressin in sympathetic response to paraventricular nucleus stimulation in anesthetized rats

1994 ◽  
Vol 266 (1) ◽  
pp. R228-R236 ◽  
Author(s):  
S. C. Malpas ◽  
J. H. Coote
Keyword(s):  
Paraventricular Nucleus ◽  
Neuronal Cell ◽  
Detection Algorithm ◽  
Homocysteic Acid ◽  
Renal Sympathetic Nerve Activity ◽  
Anesthetized Rats ◽  
Neuronal Cell Bodies ◽  
Peak Detection Algorithm ◽  
Glass Micropipette

Vasopressin may play an extrahypothalamic role in the central control of the cardiovascular system, specifically acting as a spinal neurotransmitter in the pathway where the paraventricular nucleus (PVN) alters sympathetic outflow. In this study, the effect of stimulating neuronal cell bodies in the PVN on renal sympathetic nerve activity (RSNA) and the possible involvement of vasopressin in the pathway was investigated in anesthetized rats. The PVN was stimulated by microinjection with 0.2 M D,L-homocysteic acid via a glass micropipette, and the hemodynamic and sympathetic responses were recorded. A computerized sympathetic peak-detection algorithm was applied to recordings of sympathetic discharges to retrieve information about the characteristics of RSNA during PVN stimulation. The algorithm scanned the series of RSNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RSNA peak had been detected, its corresponding amplitude and peak-to-peak interval were calculated. PVN stimulation consistently increased the amplitude of RSNA (mean 30 +/- 5.6% over control), arterial pressure, and the peak-to-peak interval of discharges. A V1 vasopressin antagonist intrathecally administered as a 500-pmol dose was subsequently able to completely block the hemodynamic response (blood pressure increase of 14 +/- 5%) and a 35 +/- 6% increase in RSNA in response to PVN stimulation and intrathecal vasopressin. Thus spinal vasopressin is likely to be a neurotransmitter involved in the cardiovascular regulation involving the PVN.

Ovarian increase in kinin-generating capacity in PMSG/hCG-primed immature rat

1986 ◽  
Vol 251 (3) ◽  
pp. E362-E365 ◽  
Author(s):  
L. L. Espey ◽  
D. H. Miller ◽  
H. S. Margolius
Keyword(s):  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Wistar Rats ◽  
Immature Rat ◽  
Induced Ovulation ◽  
Generating Capacity ◽  
Phosphate Buffered Saline ◽  
Ovulatory Process

Ovarian kinin-generating capacity was determined during induced ovulation in immature Wistar rats. The onset of ovulation was monitored by counting the number of ova in the oviducts at 2-h intervals after the administration of human chorionic gonadotropin (hCG). Ova began to appear in significant numbers at 14 h after hCG, with an average of 7.6 +/- 2.3 ova/rat. By 16 h after hCG, the oviducts contained 32.7 +/- 4.1 ova/rat. The ovaries from each group of animals were homogenized in phosphate-buffered saline, and extracts of this tissue were incubated for 200 min to allow the generation of kinins from endogenous kininogen. The amount of kinin generated by this procedure was measured by radioimmunoassay. At 0 h (i.e., just before the administration of hCG), the ovaries contained 5.90 +/- 0.60 pg kinin/micrograms protein per 200 min in the ovarian extract. By 4 h after hCG, the kinins increased significantly (P less than 0.05) to 13.16 +/- 3.61 pg kinin/micrograms protein. The kinins progressively increased (P less than 0.001) to 67.88 +/- 23.26 pg kinin/micrograms protein by 16 h after hCG. Indomethacin and cycloheximide significantly inhibited both kinin-generating activity and ovulation. These data suggest that kinin-forming activity and kinins may have a role in the ovulatory process of mammals.

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.

ANG II-induced excitation of paraventricular nucleus magnocellular neurons: a role for glutamate interneurons

2004 ◽  
Vol 286 (5) ◽  
pp. R894-R902 ◽  
Author(s):  
K. J. Latchford ◽  
A. V. Ferguson
Keyword(s):  
Paraventricular Nucleus ◽  
Kynurenic Acid ◽  
Neuronal Excitability ◽  
Critical Role ◽  
Ang Ii ◽  
Magnocellular Neurons ◽  
Whole Cell Patch Clamp ◽  
Electrolyte Homeostasis ◽  
Hypothalamic Slices

The hypothalamic paraventricular nucleus (PVN) plays a critical role in cardiovascular and neuroendocrine regulation. ANG II (ANG) acts throughout the periphery in the maintenance of fluid-electrolyte homeostasis and has also been demonstrated to act as a neurotransmitter in PVN exerting considerable influence on neuronal excitability in this nucleus. The mechanisms underlying the ANG-mediated excitation of PVN magnocellular neurons have yet to be determined. We have used whole cell patch-clamp techniques in hypothalamic slices to examine the effects of ANG on magnocellular neurons. Application of ANG resulted in a depolarization of magnocellular neurons, a response that was abolished in TTX, suggesting an indirect mechanism of action. Interestingly, ANG also increased the frequency of excitatory postsynaptic potentials/currents in magnocellular neurons, an effect that was abolished after application of the glutamate antagonist kynurenic acid. ANG was without effect on the amplitude of excitatory postsynaptic currents, suggesting a presynaptic action on an excitatory interneuron within PVN. The ANG-induced depolarization was shown to be sensitive to kynurenic acid, revealing the requisite role of glutamate in mediating the ANG-induced excitation of magnocellular neurons. These observations indicate that the ANGergic excitation of magnocellular PVN neurons are dependent on an increase in glutamatergic input and thus highlight the importance of a glutamate interneuron in mediating the effects of this neurotransmitter.

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