bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Role of Oxytocin Release in the Mediobasal Hypothalamus of the Sheep in Relation to Female Sexual Receptivity
Authors: Kendrick K. M. , Fabre‐Nys C. , Blache D. , Goode J. A. , Broad K. D. 
Published: September 2006

Abstract In vivo microdialysis and retrodialysis were used to investigate the role of oxytocin (OXY) release in the mediobasal hypothalamus (MBH) of the ewe in the control of sexual receptivity. Initial experiments showed that OXY release was significantly increased in ovariectomized animals treated with progesterone and oestradiol when they were sexually receptive towards males and received intromissions. No such increases were seen during tests where the ewes were receptive but the males were prevented from achieving intromission. By contrast, OXY release was significantly reduced in tests where the ewes were not receptive to the male. In a second experiment artificial vaginocervical stimulation (VCS) was found to significantly increase OXY release when the animals were treated with oestradiol and this effect was potentiated by progesterone priming. OXY release in the MBH was not significantly altered by VCS in the presence of progesterone priming alone. Plasma OXY concentrations were significantly increased by VCS following all three hormone treatments but no one treatment was significantly more effective than another. Noradrenaline release in the MBH was only significantly increased following VCS when progesterone priming was given before oestradiol treatment. No effects of VCS on release of GABA, glutamate or dopamine were seen but their basal concentrations were significantly increased by the combined steroid treatment compared to oestradiol alone. In a third experiment it was found that OXY (10 μM) infused bilaterally into the MBH of receptive ewes, by retrodialysis, significantly decreased sexual receptivity and increased the release of noradrenaline and GABA. Finally, in a fourth experiment is was shown that multiple intromissions significantly reduced sexual receptivity.These results show that OXY release in the MBH is increased by natural or artificial VCS and that this is modulated by sex steroids. The inhibitory action of OXY infusions into the MBH on sexual receptivity suggests that a functional role of this peptide within this brain region might be to mediate decreases in sexual receptivity which we observed following multiple intromissions. It is probable that the behavioural effects of this peptide are primarily mediated directly rather than through a modulation of noradrenaline and GABA release.
Oxytocin Pretreatment Enhances Arginine Vasopressin‐lnduced Motor Disturbances and Arginine Vasopressin‐lnduced Phosphoinositol Hydrolysis in Rat Septum: A Cross‐Sensitization Phenomenon
Authors: Poulin Paule , Pittman Quentin J. 
Published: September 2006

AbstractThe recent observation that the central oxytocin (OT) receptor has high affinity for both OT and arginine vasopressin (AVP) raises the possibility that it may be involved in some of the central actions of AVP. Repeated intracerebroventricular (icv) injections of AVP in rats evoke an unusual sensitization phenomenon in that a first exposure to the peptide enhances the sensitivity (sensitization) of the brain to a second exposure. This report investigates the possibility that the OT receptor may be involved in the mediation of the phenomenon of sensitization, using OT, a specific OT receptor agonist, [Thr4, Gly7]OT, and a specific OT receptor antagonist, d(CH2)5, [Tyr(Me)2, Thr4, Tyr‐NH29]OVT (compound 6; cpd 6), as well as a V1 AVP receptor antagonist, d(CH2)5Tyr(Me)AVP. Peptides were injected icv in conscious, adult male Sprague‐Dawley rats. The data showed that: 1) a first icv AVP injection (10 pmol/5μl) enhanced the sensitivity of the rat brain to the motor response of a second AVP injection (10 pmol/5 μl) given 24 h later; 2) injection of d(CH2)5Tyr(Me)AVP (100 pmol/5 μl icv) but not cpd 6, (100 pmol/5 μl icv) 2 min prior to the first AVP injection, blocked AVP‐induced sensitization; 3) a first injection of OT or [Thr4, Gly7]OT (10 pmol/5 μl) enhanced the sensitivity of the brain to the motor actions of a subsequent AVP injection given 24 h later; 4) the magnitude of this cross‐sensitization induced by OT pretreatment varied with dose and appeared to be ten times more potent than the sensitization induced by a first AVP injection; 5) injection of cpd 6 (100 pmol/5 μl) but not d(CH2)5Tyr(Me)AVP (100 pmol/5 μl icv) 2 min prior to the first OT injection (1 pmol/5 μl) blocked the cross‐sensitization induced by OT; 6) an injection of OT (100 to 1,000 pmol/5 μl) or [Thr4, Gly7]OT (10 pmol/5 μl) in rats that had been cross‐sensitized with OT or [Thr4, Gly7]OT pretreatment did not evoke enhanced motor responses; 7) OT injected 2 min prior to the second AVP injection in AVP‐sensitized rats did not block the enhanced AVP‐induced motor responses; 8) AVP‐induced [3H]inositol monophosphate accumulation in septal slices was also enhanced in rats cross‐sensitized by OT pretreatment.These results suggest that while pre‐exposure of the rat brain to both AVP and OT alters the responsiveness of the rat brain to subsequent AVP exposures, AVP sensitization appears to be mediated via the V1 AVP receptor, whereas cross‐sensitization by OT may be mediated via the OT receptor. The ability of OT to alter the responsiveness of the rat brain to subsequent AVP injection suggests a role for this peptide in modulating central AVP actions.
Colchicine‐lnduced Accumulation of Estrogen Receptor and Progestin Receptor Immunoreactivity in Atypical Areas in Guinea‐Pig Brain
Authors: Blaustein Jeffrey D. , Olster Deborah H. 
Published: September 2006

AbstractUsing immunocytochemical techniques, cells containing estrogen and progestin receptors have been observed in many discrete regions of the guinea‐pig forebrain, including the mediobasal hypothalamus and preoptic area. While most reaction product is located within cell nuclei, we have reported abundant reaction product in perikaryal cytoplasm and neuronal processes as well. Ultrastructural analysis has revealed the presence of estrogen and progestin receptors in atypical subcellular sites within the hypothalamus, including dendrites and axon terminals. In order to determine if microtubule‐dependent intracellular transport is involved in intraneuronal transport of steroid hormone receptors, ovariectomized guinea‐pigs were injected intracerebroventricularly with the microtubule inhibitor, colchicine, and brain sections at the level of the hypothalamus were immunostained for estrogen receptors. This treatment resulted in the appearance of estrogen receptor immunoreactivity in the paraventricular and mediodorsal thalamic region, areas typically devoid of estrogen receptor‐immunoreactive cells in guinea‐pigs. In a second study on progestin receptors, we observed the colchicine‐induced accumulation of progestin receptor immunoreactivity in the paraventricular thalamic, mediodorsal thalamic and lateral dorsal thalamic areas as well as in the medial amygdala, all areas typically devoid of progestin receptor immunoreactivity. While estradiol injection induced progestin receptor immunoreactivity in the hypothalamus and preoptic area as described previously, it had no effect on the colchicine‐induced accumulation in the thalamus and amygdala. These results provide evidence that in some neurons, progestin receptors and estrogen receptors are transported intracellularly, apparently at a rapid enough rate that they do not ordinarily accumulate within the perikaryon.
Potential Corticotropin‐Releasing Factor Pathways in the Rat Brain as Determined by Bilateral Electrolytic Lesions of the Central Amygdaloid Nucleus and the Paraventricular Nucleus of the Hypothalamus
Authors: Koegler‐Muly Susan M. , Owens Michael J. , Ervin Gregory N. , Kilts Clinton D. , Nemeroff Charles B. 
Published: September 2006

AbstractThe projection fields of corticotropin‐releasing factor (CRF)‐containing perikarya in the rat central nervous system were studied using a combination of electrolytic lesions, microdissection and radioimmunoassay. The effects of bilateral electrolytic lesions of the central nucleus of the amygdala (Ce) or the paraventricular nucleus (PVN) of the hypothalamus were measured by a sensitive and specific radioimmunoassay. Following lesions of the Ce, CRF concentrations in the locus ceruleus (LC) were significantly decreased. Following lesions of the PVN, CRF concentrations in the median eminence were markedly decreased (>85%), with smaller but consistent reductions of CRF in the hippocampus as well. In contrast to the Ce lesions, PVN lesions resulted in increases in CRF concentratixhtmlons in the LC.These results further confirm the projection of CRF‐containing cells from the PVN to the median eminence, provide evidence for a PVN‐hippocampal CRF pathway, and suggest that the PVN modulates CRF neurons innervating the LC. Moreover, the existence of a CRF‐containing pathway from the Ce to the LC appears likely, and such a circuit may play a role in the behavioral and physiological responses to stress.
Substance P Inhibits the Release of Anterior Pituitary Adrenocorticotrophin via a Central Mechanism Involving Corticotrophin‐Releasing Factor‐Containing Neurons in the Hypothalamic Paraventricular Nucleus
Authors: Larsen Philip J. , Jessop David , Patel Hemant , Lightman Stafford L. , Chowdrey Hardial S. 
Published: September 2006

AbstractChronic osmotic stimulation influences the hypothalamo‐adenohypophysial axis by inhibiting the synthesis of hypothalamic corticotrophin‐releasing factor (CRF‐41) and subsequently the secretion of basal and adrenalectomy‐elevated adrenocorticotrophin from the adenohypophysis. In the present study, we used a substance P antagonist to test the hypothesis that this inhibition is mediated centrally by substance P or other tachykinins. In control rats and rats given 2% saline to drink for 12 days, intracerebroventricular administration of a substance P antagonist elevated plasma adrenocorticotrophin and corticosterone levels. Using quantitative in situ hybridization histochemistry, it was also demonstrated that CRF mRNA increased in the medial parvocellular division of the paraventricular nucleus of saline‐treated as well as control rats 6 h after intracerebroventricular administration of the antagonist, while vasopressin mRNA in the medial parvocellular division of the paraventricular nucleus was increased in the control animals only. These results provide evidence that central endogenous substance P has an inhibitory influence over the synthesis and release of CRF‐41 both under normal conditions and during a chronic osmotic stimulus.
Altered Ratios of Beta‐Endorphin : Beta‐Lipotropin Released from Anterior Lobe Corticotropes with Increased Secretory Drive. I. Effects of Diminished Glucocorticoid Secretion
Authors: Young Elizabeth A. , Przewlocki Ryszard , Patel Paresh , Watson Stanley J. , Akil Huda 
Published: September 2006

AbstractPrevious studies have demonstrated that acute stress or ovine corticotropin‐releasing hormone (oCRH) in vivo, or oCRH in vitro, stimulates release of β‐endorphin over β‐lipotropin from anterior pituitary corticotropes. This occurs despite the predominance of β‐lipotropin in corticotrope peptide stores. In vitro studies with primary anterior pituitary cultures suggested that chronic exposure to oCRH results in a shift towards more β‐lipotropin secretion into the media than with short‐term exposure. The current studies explored whether increased secretory drive in vivo results in a similar shift towards more β‐lipotropin. We used removal of glucocorticoids by adrenalectomy or metyrapone blockade of corticosterone synthesis, to stimulate endogenous secretion of CRH and vasopressin. Both treatments resulted in shifts of the ratio of β‐endorphin: β‐lipotropin in plasma of experimental animals in comparison to the sham‐treated control rats. In vitro testing with oCRH of anterior lobe cultures from adrenalectomized or metyrapone‐treated rats demonstrated similar effects of these treatments on the ratio of β‐endorphin : β‐lipotropin. These changes occurred despite similar ratios of β‐endorphin : β‐lipotropin in anterior pituitary peptide stores.
Testosterone Enhances GABA and Taurine but not N‐Methyl‐D,L‐Aspartate Stimulation of Gonadotropin Secretion in the Goldfish: Possible Sex Steroid Feedback Mechanisms
Authors: Trudeau V. L. , Sloley B. D. , Peter R. E. 
Published: September 2006

AbstractThe effects of gonadal steroids on GABA‐, taurine (TAU)‐ and N‐methyl‐D, L‐aspartate (NMA)‐induced gonadotropin‐II (GTH‐II) release were investigated in male and female goldfish in vivo. In sexually regressed goldfish (both sexes mixed), intraperitoneal implantation for 5 to 10 days with solid Silastic pellets containing testosterone (100 μg/g), oestradiol (100 μg/g) or progesterone (100 μg/g) was previously shown to elevate serum sex steroid levels to values comparable to those in sexually mature animals, and to potentiate gonadotropin‐releasing hormone‐stimulated GTH‐II release. In the present study, testosterone but not oestradiol or progesterone enhanced the stimulatory effects of exogenous GABA (100 μg/g) on GTH‐II release in vivo. TAU (1 mg/g) stimulated GTH‐II release in sexually regressed mixed sex and sexually recrudescent male goldfish, and both testosterone and oestradiol implantation enhanced GTH‐II release induced by TAU. The glutamate agonist NMA (25 to 50 μg/g) was also found to stimulate GTH‐II release; however it was relatively less effective in elevating serum GTH‐II levels than GABA and TAU, and its effects were not modulated by sex steroid treatments. Pretreatment of goldfish with α‐methyl‐p‐tyrosine to deplete brain and pituitary catecholam‐ines did not affect NMA action on GTH‐II release. Our results indicate that GABA, TAU and NMA are involved in the neuroendocrine regulation of GTH‐II release in goldfish, and support the idea that testosterone participates in the positive feedback regulation of pituitary gonadotropin release in a non‐mammalian vertebrate by enhancing GABA‐ and TAU‐stimulated GTH release in vivo.
Development of Gonadotrophs and Thyrotrophs in the Female Foetal Sheep Pituitary: Immunocytochemical Localization Studies
Authors: Thomas Gregory B. , McNeilly Alan S. , Brooks A. Nigel 
Published: September 2006

AbstractIn order to investigate the ontogenesis of cell types in the pituitary gland, anterior pituitaries were collected from female foetal sheep at days 70, 100 and 130 of gestation (term = 145 days). Cells containing the common α‐subunit and the specific β‐subunits of luteinizing hormone (LH), follicle‐stimulating hormone (FSH) and thyroid‐stimulating hormone (TSH) were immunolocalized using the avidin‐biotin immunoperoxidase technique. LHβ‐containing cells were first detected in the foetal pituitary by day 70 of gestation. The number and intensity of staining of these LHβ cells increased by day 100 but had declined again by day 130. Immunopositive a‐subunit and FSHβ cells appeared by day 100 of gestation and had further increased in number and staining intensity by day 130. Cells containing TSHβ were present at day 70 and progressively increased in abundance and intensity through gestation. These data indicate that the development of LH‐ and FSH‐containing cells in the female foetal sheep pituitary is differentially regulated during foetal life, and that in the sheep free a‐subunit is not produced in significant amounts before the specific β‐subunits.
Application of a Percoll Density Gradient to Separate and Enrich Porcine Pituitary Cell Types
Authors: Torronteras R. , Castaño J. P. , Ruiz‐Navarro A. , Gracia‐Navarro F. 
Published: September 2006

AbstractThe application of a Percoll density gradient cell separation procedure to the pituitary gland of neonatal, prepubertal and mature pigs is described. After enzymatic dispersion, cell viability was 90% to 98% as determined by uptake of Trypan Blue. Recovery of dissociated cells after application of the gradient ranged from 80% to 95%. The dissociated cells were separated in several fractions that were characterized immunocytochemically using different antisera. We obtained highly enriched fractions of gonadotrope (gonadotropins), somatotrope (growth hormone) and lactotrope (prolactin) cells for each age. Concentration of the cell types (purity) was higher than 60% in the following fractions: 1) gonadotropin cells, fraction 15 (1.033 g/cc of density) from mature animals; 2) growth hormone cells, fraction 3 (1.121 g/cc of density) from neonatal animals and fraction 9 (1.087 g/cc) from prepubertal animals; and 3) prolactin cells, fraction 7 (1.094 g/cc) and 10 (1.082 g/cc) from neonatal animals and fraction 14 (1.051 g/cc) from mature pigs. In thyrotrope (thyroid‐stimulating hormone) and corticotrope (adrenocorticotropin) cells, enriched fractions were also obtained, although the values of purity were lower (20% to 58%). In conclusion, the proposed cell separation and enrichment technique is suitable for the isolation, purification and examination of porcine pituitary cell types and subpopulations, and offers major advantages such as simplicity, rapidity, efficiency and reproducible results.
Neuroanatomical and Physiological Evidence for the Involvement of Pituitary Adenylate Cyclase‐Activating Polypeptide in the Regulation of the Distal Lobe of the Frog Pituitary
Authors: Yon Laurent , Jeandel Lydie , Chartrel Nicolas , Feuilloley M. , Conlon J. Michael , Arimura Akira , Fournier Alain , Vaudry Hubert 
Published: September 2006

AbstractPituitary adenylate cyclase‐activating polypeptide (PACAP) is a 38 amino‐acid peptide which belongs to the glucagon/secretin/ vasoactive intestinal peptide superfamily. The sequence of PACAP is identical in all mammalian species studied so far but frog PACAP differs by one amino‐acid from mammalian PACAP. The aim of the present study was to investigate the presence of PACAP in the hypothalamo‐pituitary complex of the frog Rana ridibunda and to determine the biological activity of frog PACAP on homologous pituitary cells. The distribution of PACAP‐containing neurons and fibers was examined by the indirect immunofluores‐cence method using an antiserum raised against the N‐terminal region of the peptide. In the hypothalamus, PACAP‐immunoreactive perikarya were localized in the preoptic nucleus and the dorsal and ventral infundibular nuclei. Beaded nerve fibers were observed coursing from the ventral infundibular nucleus to the external vascular layer of the median eminence. A dense network of immunoreactive axons terminated in the vicinity of the capillaries of the hypophysial portal system. The neurointermediate lobe and the distal lobe of the pituitary were devoid of immunoreactive elements. The amount of PACAP‐like immunoreactive material in hypothalamus extracts was measured by radioimmunoassay; the apparent concentration of PACAP was 4.5 ng/mg protein. Synthetic frog PACAP38 and PACAP27 induced a similar dose‐dependent stimulation of cAMP production in isolated frog distal lobe pituitary fragments (ED50= 2 × 10−8 M). At the maximum dose tested (5 × 10−6 M), both frog PACAP38 and PACAP27 produced a 4‐fold increase in cAMP production. In contrast, the truncated form [Des‐His1frog PACAP38 did not affect adenylate cyclase activity demonstrating therefore that the N‐terminal histidyl residue is essential for the biological activity of the peptide. [Des‐His1]frog PACAP38 did not antagonize the stimulatory effect of frog PACAP38 or PACAP27 on cAMP production. Taken together, these data support the concept that, in amphibians as in mammals, PACAP may act as a hypophysiotropic neuropeptide.
Local Tetrodotoxin Blocks Chronic Stress Effects on Corticotropin‐Releasing Factor and Vasopressin Messenger Ribonucleic Acids in Hypophysiotropic Neurons
Authors: Sawchenko P. E. , Arias C. A. , Mortrud M. T. 
Published: September 2006

AbstractTo test the hypothesis that synaptic inputs to the paraventricular nucleus mediate stress‐induced increases in corticotropin‐releasing peptide expression in the paraventricular nucleus of the hypothalamus (PVH), relative levels of the mRNAs encodingv corticotropin‐releasing factor (CRF) and arginine vasopressin (AVP) were followed, in situ, in animals subjected to chronic footshock stress and concurrent local administration of tetrodotoxin or vehicle. Consistent with previous findings, a 7‐day exposure to chronic footshock resulted in a 2.1‐fold increase in CRF mRNA levels in the parvocellular division of the PVH. The footshock paradigm also resulted in at least a 41% increase in AVP transcripts in this same region; this effect was localized predominantly to CRF‐immunoreactive neurons. The Stressor did not significantly alter AVP mRNA levels in the magnocellular division of the PVH. Tetrodotoxin, administered to the PVH via osmotic minipump, blocked the stress‐induced rise in CRF and AVP mRNAs, but had no significant effect on basal levels of these transcripts. The results support the view that maintenance of the enhanced central drive on pituitary‐adrenal activity seen in response to chronic stress is mediated via neural inputs to the PVH.
Involvement of Central Corticotropin‐Releasing Factor (CRF) in Suckling‐Induced Inhibition of Luteinizing Hormone Secretion in Lactating Rats
Authors: Walker Claire‐Dominique , Dallman Mary F. , Palmer Abraham A. , Steele Marianne K. 
Published: September 2006

AbstractThe lack of ovulation and the inhibition of reproductive functions observed in many species during lactation is closely related to the intensity of the suckling stimulus. However, the mechanisms by which suckling inhibits hypothalamic GnRH and pituitary LH secretion in rats are still unclear. Since we recently demonstrated that suckling is a persistent stimulus to the adrenococortical system of the rat, we tested the hypothesis that suckling‐induced activation of central CRF release may mediate the associated inhibition of GnRH secretion. Lactating females were ovariectomized (OVX) on day 2 of lactation, and equipped with icv guide cannula on day 2 and indwelling jugular catheters on day 5 before testing on day 7. Lactating females were separated from their pups for 24 h prior to the suckling test with the following pretreatments: 1) icv injection with artificial CSF (aCSF) or a specific CRF antagonist, alpha‐helical CRF (9–41), (25μg/rat, CRF‐AX) 15 min prior to pup reunion or 2) iv injection of normal sheep serum (NSS) or CRF antiserum (CRF‐AB) 4 h prior to pup reunion. Plasma ACTH, LH and PRL concentrations were determined prior to and at various intervals after pup reunion. After 3 h of suckling, LH and PRL responses to a bolus injection of GnRH (10 ng/rat) were measured; a bolus injection of Angiotensin II (All, 5 μg/rat) was administered after 4 h to test for ACTH responses. Non‐lactating females injected with GnRH and All were used as controls.In animals treated icv with aCSF or iv with NSS, the suckling stimulus resulted in increased ACTH and PRL secretion with a decrease in LH release. Iv CRF‐AB abolished the increase in ACTH, but did not affect the increase in PRL nor the decrease in LH secretion. In contrast, and in support of our hypothesis, icv CRF‐AX abolished the suckling‐induced decline in LH secretion without altering the increase in PRL and ACTH secretion. Finally, we did not observe lactation‐related changes in LH (or PRL) responses to a bolus GnRH injection or in ACTH responses to All stimulation.Our results suggest that: 1) central CRF release is involved in the decrease in LH secretion which occurs following suckling in lactating females, and 2) the changes in LH secretion during suckling are not mediated by an effect of CRF at the median eminence or by acute changes in pituitary responsiveness to GnRH.