bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Centrally Administered Oxytocin on the Association Between Cortical Electroencephalogram and Milk Ejection in the Rat
Authors: Wakerley J. B. , Foreman C. T. , Ingram C. D. 
Published: September 2006

AbstractThe milk‐ejection reflex of the rat is closely associated with synchronized activity of the cortical electroencephalogram (EEG), and the frequency of milk ejections has been shown to be greatly facilitated by central oxytocin. The following experiments were undertaken to examine the changes in the EEG during facilitation of the reflex by central oxytocin. Intracerebroventricular injection of 1 mU (2.2 ng) oxytocin during suckling caused a rapid increase in the frequency of milk ejections but no change in the predominantly synchronized pattern of the EEG. However, after a delay (11.3 ± 0.8 min, mean ± SE) there appeared to be an increasing proportion of desynchronization, which correlated with cessation of the facilitated milk‐ejection responses. Hence, the observed EEG desynchronization may signal activation of mechanisms inhibitory to the milk‐ejection reflex.In the absence of the suckling stimulus oxytocin also caused a change to desynchronization. However, this effect was more pronounced and commenced after a much shorter latency (1.7 ± 0.4 min, mean ± SE; P < 1.001), suggesting that the desynchronizing effect of oxytocin on the EEG can be attenuated by the suckling stimulus.These results demonstrate two phases in the action of central oxytocin in the suckled rat. During the initial phase, the milk‐ejection reflex is facilitated and although there may be a concomitant desynchronizing influence on the EEG this is prevented by the influence of the suckling stimulus. In the later phase, this desynchronizing influence predominates and is accompanied by cessation of milk‐ejection responses.Although milk ejections were generally restricted to periods of a synchronized EEG as previously reported, during the oxytocin‐induced change to desynchronization a number of milk ejections were observed to occur in the absence of a synchronized EEG. These results provide further evidence that the association between milk ejection and the EEG state is not an absolute causal relationship.
Triiodothyronine Regulates Insulin‐Like Growth Factor‐I Binding to Cultured Rat Pituitary Cells*
Authors: Geary E. Stewart , Lim Matthew , Ceda Gian Paolo , Ro Sandy , Rosenfeld Ron G. , Hoffman Andrew R. 
Published: September 2006

AbstractTriiodothyronine (T3) stimulates the synthesis of growth hormone and enhances the growth of neoplastic rat pituitary somatomam‐motrophs (GH cells) in culture. Moreover, T3 has been shown to stimulate the production and secretion of an autocrine growth factor by these cells. We have previously demonstrated the presence of specific receptors for insulin‐like growth factors (IGF) on GH cells. Since GH3 cells contain mRNA encoding IGF‐I, it has been suggested that IGF‐I might act in an autocrine fashion in these cells. Therefore, it was of interest to learn how T3 affects IGF‐I binding to GH3 cells. T3 increased [125I]IGF‐I binding in a time ‐ and dose‐dependent manner. After 48 h of exposure to T3, an increase in IGF‐I binding was seen with 10−11M T3, maximizing with 10−8M T3. When cells were exposed to 10−8 T3, [125I]IGF‐I binding reached a maximum of 218 ± 20.8% of control (±SEM, P < 0.002) after 72 h of incubation. Scatchard analysis indicated that T3 did not alter the Kd of IGF‐I for its receptor, but that the total receptor number was increased. Dexamethasone (10−7M) inhibited the T3‐induced increase in IGF‐I binding, but glucocorticoid alone did not substantially alter receptor number. No significant change in insulin or IGF‐II binding was seen after hormone treatment. 10−8 M T3 or IGF‐I increased the growth of the GH3 cells by ≥30%. Our data indicate that T3 upregulates IGF‐I binding in GH3 cells without altering insulin binding and thereby provides a means for enhancing potential autocrine regulation in this cell line.
The Expression of the Kallikrein Gene Family in the Rat Pituitary: Oestrogen Effects and the Expression of an Additional Family Member in the Neurointermediate Lobe
Authors: Clements Judith A. , Matheson Bronwyn A. , MacDonald Raymond J. , Funder John W. 
Published: September 2006

AbstractUsing a series of oligonucleotide probes (18 to 21 mers) specific for members of the rat kallikrein/tonin gene family (PS, S1, S2, S3, K1, P1), we have shown by Northern blot analysis that the oestrogen‐dependent kallikrein gene expressed in the male and female rat anterior pituitary is true kallikrein (PS). In addition, we have demonstrated that oestrogen treatment may also induce PS gene expression in the male and female rat neurointermediate lobe. None of the other five rat arginyl‐esteropeptidase genes so far described (S1, S2, S3, K1, P1) was found to be expressed in the anterior pituitary or neurointermediate lobe under these conditions. However, the demonstration of an additional hybridization signal in the male neurointermediate lobe using a relatively non‐specific PS gene probe suggests the expression of another, as yet uncharacterized, kallikrein gene family member in this tissue.
Electrical Stimulation of Specific Brainstem Nuclei Suppresses Growth Hormone‐Releasing Hormone‐Induced Growth Hormone Secretion in the Pentobarbital Anaesthetized Rat
Authors: Koibuchi Noriyuki , Kato Masakatsu , Kakegawa Tadao , Suzuki Mitsuo 
Published: September 2006

AbstractTo clarify the neural mechanism related to suppression of growth hormone (GH) secretion, biphasic electrical stimulation was delivered into several brainstem nuclei in the pentobarbital anaesthetized rat. A concentric bipolar stimulating electrode was implanted chronically one week prior to the electrical stimulation. Ninety min before the electrical stimulation, the rats were anaesthetized by ip injection of pentobarbital and a silastic cannula was inserted into the right atrium for blood sampling. Blood samples were withdrawn five times (0, 10, 20, 30 and 60 min) during the experiment. Electrical stimulation was delivered for 10 min just after the first blood sampling. One min after the onset of the stimulation, human GH‐releasing hormone was injected iv to induce GH secretion. Electrical stimulation of several brainstem nuclei, i.e. the locus coeruleus, the rostral portion of the nucleus tractus solitarius and the lateral reticular nucleus suppressed GH secretion and the central gray of the pons showed a tendency for the suppression of GH secretion. On the other hand, electrical stimulation of the parabrachial nucleus and the caudal portion of the nucleus tractus solitarius did not suppress GH secretion. These suppressions were nullified by prior electrolytic lesioning of the hypothalamic periventricular nucleus where the major cell bodies of somatostatin immunoreactive fibres in the median eminence originate. These results indicate that electrical stimulation of several brainstem nuclei excites somatostatin neurons in the periventricular nucleus which are responsible for the suppression of GH secretion.
The Effects of a Growth Hormone‐Releasing Peptide and Growth Hormone‐Releasing Factor in Conscious and Anaesthetized Rats
Authors: Clark R. G. , Carlsson L. M. S. , Trojnar J. , Robinson I. C. A. F. 
Published: September 2006

AbstractThe growth hormone (GH) releasing ability of GH‐releasing factor (GRF) and a GH‐releasing hexapeptide, CHRP, have been studied in anaesthetized and conscious male and female rats. The GH responses to GHRP in anaesthetized rats were inconsistent, and this peptide was much less potent than GRF. Continuous iv infusions of GRF or GHRP both caused an initial GH release which was not maintained, and further GH release could be elicited by injection of GRF during an infusion of GHRP and vice versa. In contrast, conscious rats were much more sensitive to GHRP. Infusions of GHRP or GRF both caused an initial GH release. With GRF infusions, GH release continued in the normal episodic pattern whereas with GHRP infusion, GH secretion remained elevated over baseline and the normal pulsatile rhythm was disrupted. Plasma GH levels fell after stopping GHRP infusion, without an immediate resumption of normal GH pulsatility. Conscious male rats responded intermittently to injections of GRF given iv every 45 min, but when such serial injections of GRF were given during a continuous iv infusion of GHRP, the GH responses to GRF became regular and more uniform. These results suggest that GHRP prevents the normal cyclic refractoriness to GRF in male rats by disrupting cyclic somatostatin release. The greater potency of GHRP in conscious rats may also depend on the release of endogenous GRF since passive immunization with an anti‐GRF serum reduced the plasma GH response to GHRP infusion. Thus in the conscious animal, GHRP may release GH by complex actions at both a hypothalamic and pituitary level.
Estrogen Alters Oxytocin mRNA Levels in the Preoptic Area
Authors: Caldwell J. D. , Brooks P. J. , Jirikowski G. F. , Barakat A. S. , Lund P. K. , Pedersen C. A. 
Published: September 2006

AbstractEstrogen has numerous effects on immunoreactive levels of oxytocin (OXT) centrally, particularly in the preoptic lateral subcommissural nucleus (LSN). In this study in situ hybridization of a 38‐base oligodeoxyribonucleotide (38mer) complementary to OXT mRNA revealed that estrogen treatment altered the pattern of OXT production in the rostral LSN and the more caudal anterior commissural nucleus. Rats were injected with 20 ng estradiol benzoate or sesame oil vehicle im 4 and 5 days after ovariectomy. On the sixth day all animals were perfused with paraformaldehyde‐glutaraldehyde and their brains sectioned to 10 μm thickness in a −10 °C cryostat. Coronal brain sections were taken from four parallel levels of the preoptic‐anterior hypothalamic area. These sections were mounted and hybridized in situ to a [l125]‐labeled 38mer for 16 h at 37 °C. Washed and dried slides were processed for autoradiography and analyzed with a light microscope. The effect of estrogen on OXT production differed between the rostral and caudal sections in both the LSN and periventricular (PeV) areas. Estrogen significantly increased OXT mRNA levels in LSN cells while decreasing hybridization in the anterior commissural nucleus cells. Changes in frequency patterns in the PeV paralleled those in the LSN with a significant drop of hybridization in the caudal PeV. Neurons hybridizing 38mer probe were also found in several other areas including the ventral medial preoptic area, lateral hypothalamus, bed nucleus of the stria terminalis and the nucleus triangularis septi. OXT mRNA levels were affected by estrogen treatments and this effect differed between the preoptic area and anterior hypothalamus. The sensitivity of LSN oxytocinergic cells to estrogen has implications for estrogen‐sensitive OXT‐enhanced reproductive behaviors.
Effects of Orchidectomy on Nigro‐Striatal Dopaminergic Function: Behavioral and Physiological Evidence
Authors: Dluzen Dean E. , Ramirez Victor D. 
Published: September 2006

AbstractIn the present experiments, we examined the effect of castration upon two indices of nigro‐striatal dopaminergic function in the male rat. In Experiment I, differences in spontaneous locomotor behavioral activity between intact and castrated male rats were examined. The total distance traveled, horizontal activity and mean revolutions of castrated male rats were significantly greater than that of intact males. No significant differences between intact and castrated males were obtained for vertical activity. In Experiment II, the spontaneous in vitro dopamine release from the corpus striatum of intact and castrated rats as sampled during the light‐phase (1500 h) and dark‐phase (2400 h) of the photoperiod was examined. At both time periods, the spontaneous in vitro dopamine release of castrated males was significantly greater than that of intact males. Both intact and castrated males showed statistically significant increases in dopamine release at the 2400 h compared to the 1500 h time period. To examine if testicular hormones were responsible for these castration induced changes in dopamine release, in Experiment III we treated castrated male rats with testosterone propionate. Administration of testosterone propionate (0.1 mg/day × 5 days) significantly reduced in vitro dopamine release compared to untreated or castrated male rats receiving vehicle treatment. These results demonstrate that testicular hormones, most likely testosterone, have a markedly suppressive effect upon the nigro‐striatal dopaminergic system as evidenced from changes in spontaneous behavioral activity and in vitro dopamine release.
Oestrogen‐Insensitive Progestin Receptors in the Central Nervous System: Physicochemical and Immunoreactive Characteristics
Authors: Cerbón Marco A. , Martineíz Maryam , Pérez‐Palacios Gregorio 
Published: September 2006

AbstractThe intracellular effects of progesterone in the central nervous system are exerted via two distinct receptors: The classical oestrogen‐regulated progestin receptor and the non‐oestrogen‐inducible progestin receptor. To assess whether the oestrogen‐insensitive receptor is related to the oestrogen‐dependent receptor or whether it is a different binding macromolecule, its physicochemical and immunoreactive characteristics (immunoprecipitation with polyclonal anti‐uterine progesterone receptor antisera) were studied in neural tissues of the female rat. The results disclosed that the dissociation constant (Kd, 0.4–0.5 ± 10−9 M), stereospecificity and sedimentation coefficient (7–8 S) in linear sucrose gradients of the oestrogen‐insensitive progestin receptor were identical to those reported for the oestrogen‐regulated progestin receptor, although its saturation binding capacity was significantly lower. Results of in vitro nuclear acceptor assays revealed that the progestin receptor complexes from cerebellum and cerebral cortex, were able to specifically bind to cell nuclei preparations in a fashion similar to that observed with the uterine progestin receptor, although to a lesser extent. Interestingly, a similar nuclear uptake of receptor complexes was noticed when standardized cerebellum and uterus cytosol preparations with a similar receptor content were used. The anti‐uterine progesterone receptor immunoglobulins used in the immunoprecipitation studies were able to specifically recognize the progestin receptor populations of the anterior pituitary and hypothalamus (oestrogen‐regulated receptors) as well as those of the cerebellum and cerebral cortex (oestrogen‐insensitive receptors). The results presented show that both the oestrogen‐sensitive and the oestrogen‐insensitive cytosol progestin receptors in brain bind the same progesterone‐like molecules used as radioligands and also react with the same antibody when tested in an immunoprecipitation radioassay. The striking similarities found in binding kinetics, physicochemical characteristics and immunoreactive behaviour in the two progestin receptors studied demonstrated that both macromolecules belong to the same family of proteins in spite of their different sensitivity to oestrogens. The overall data seem to suggest a common origin of the two progestin receptor populations in brain but with different mechanisms of hormonal regulation.
Regulation of Anterior Pituitary Gonadotrophin Subunit mRNA Levels by Gonadotrophin‐Releasing Hormone in the Ewe
Authors: Mercer Julie E. , Clarke Lain J. 
Published: September 2006

AbstractLevels of mRNA for the common a subunit and for the β subunits of luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) were measured in the pituitary glands of ovariectomized hypothalamo‐pituitary disconnected ewes. A control group (n = 7) received 250 ng pulses of gonadotrophin‐releasing hormone (GnRH) each hour for one week. To examine the effects of changing GnRH pulse amplitude four sheep were given 250 ng pulses of GnRH for one week and then 25 ng pulses for one week. Plasma LH and FSH concentrations were lowered by reducing the GnRH pulse amplitude but pituitary levels of mRNA for a subunit were increased. Levels of mRNA for FSHβ and LHβ were similar with 25 ng and 250 ng pulses of GnRH. To examine the importance of pulsatile versus continuous GnRH inputs, a group of sheep was given a constant infusion of 250 ng/h GnRH for one week. Compared to sheep given 250 ng pulses of GnRH the mRNA levels for LHβ and FSHβ were lower in sheep given a constant infusion of GnRH; levels of a subunit mRNA were similar in the two groups. To examine the short‐term effects of removing GnRH inputs, ovariectomized, hypothalamo‐pituitary disconnected ewes that had been receiving 250 ng pulses of GnRH each hour were deprived of GnRH for 6 h (n = 4) or 30 h prior to slaughter; levels of mRNA for the three subunits were similar to control values in both of these groups.These studies show that wide variation in GnRH pulse amplitude has little effect on mRNA levels for the gonadotrophin subunits but message levels are affected by the mode of GnRH input (constant versus pulsatile). The maintenance of gonadotrophin subunit mRNA levels for at least 30 h after GnRH deprivation suggests that these mRNA species have a long half‐life or that transcription continues after GnRH withdrawal.
Immunoreactive Prolactin in the Cerebrospinal Fluid of Estrogen‐Treated and Lactating Rats as Determined by Push‐pull Perfusion of the Lateral Ventricles
Authors: Rubin Beverly S. , Bridges Robert S. 
Published: September 2006

AbstractImmunoreactive (ir) prolactin levels in the cerebrospinal fluid were measured in push‐pull perfusion samples collected from the lateral cerebral ventricles in freely‐moving ovariectomized rats prior to and after estrogen treatment, and in rats during pregnancy and lactation. Ir‐prolactin levels in cerebrospinal fluid were elevated throughout the perfusion period in ovariectomized animals given estrogen and in Day 8 lactating females following the onset of nursing by their young. Cerebrospinal fluid perfusates collected from ovariectomized animals prior to estradiol treatment and from females on Days 18 and 22 of gestation contained levels of ir‐prolactin that were below the limit of detectability of the prolactin radioimmunoassay. Data from previous studies in our laboratory suggest that pituitary prolactin is involved in the mediation of maternal responsiveness. Where and how prolactin exerts its actions in this regard remains to be determined. Results of the present study indicate that detectable levels of ir‐prolactin are present in the cerebrospinal fluid of nulliparous females after exposure to an estradiol regimen known to shorten their latency to display maternal responsiveness and in lactating females actively exhibiting maternal behavior. Once in the cerebrospinal fluid, prolactin should have access to neural target sites behind the blood‐brain barrier. The presence of ir‐prolactin in the cerebrospinal fluid of females in the present study is consistent with a role for this protein hormone, acting at the level of the central nervous system, in the facilitation of maternal responsiveness as well as in the regulation of other neural and neuroendocrine processes.
Relationship of Substance P‐lmmunoreactive Nerve Fibers with Somatotropes of the Anterior Pituitary in the Monkey
Authors: Ju Gong , Liu Shaojun 
Published: September 2006

AbstractIn a previous study, substance P‐immunoreactive nerve fibers were demonstrated in the pars distalis of the anterior pituitary in the monkey. The present work investigated their relationship with somatotropes. Pituitaries of Macaca mulatta monkeys were frozen, sectioned and double immunostained with antisera against substance P and human growth hormone. Substance P‐immunoreactive nerve fibers, with many varicosities, were found in close proximity to somatotropes. It is suggested that a direct neural factor may be involved in the regulation of growth hormone secretion.
The Effect on Vasopressin Release of Microinjection of Cholinergic Agonists into the Paraventricular Nucleus of Conscious Rats
Authors: Shoji Masaru , Share Leonard , Crofton Joan T. , Brooks David P. 
Published: September 2006

AbstractWe have studied in conscious unrestrained rats under basal conditions the effect of activation of muscarinic and nicotinic receptors in the paraventricular nucleus on vasopressin secretion and mean arterial blood pressure. The microinjection of oxotremorine (0.2, 2 or 20 ng), a specific muscarinic agonist, produced a substantial, dose‐dependent, transient increase in the plasma vasopressin concentration. There was also a rise in mean arterial blood pressure and a bradycardia that followed the same time‐course as the change in plasma vasopressin levels. The microinjection of nicotine (0.1, 1 or 10 HQ) into the paraventricular nucleus had only questionable effects on vasopressin release and mean arterial blood pressure; heart rate was unaffected. These findings suggest that muscarinic receptors may be of primary importance in the paraventricular nucleus in the Cholinergic stimulation of vasopressin release.
Effects of Glucose on Thyrotrophin‐Releasing Hormone, Growth Hormone‐Releasing Hormone, Somatostatin and Luteinizing Hormone‐Releasing Hormone Release from Rat Hypothalamus in vitro
Authors: Lewis B. M. , Dieguez C. , Ham J. , Page M. D. , Creagh F. M. , Peters J. R. , Scanlon M. F. 
Published: September 2006

AbstractIncreasing concentrations of D‐glucose (1 to 25 mM) inhibited somatostatin, thyrotrophin‐releasing hormone (TRH) and growth hormone‐releasing hormone (GHRH) release from incubated adult rat hypothalami in a stereospecific manner. In contrast, the effects of D‐ and L‐glucose on luteinizing hormone‐releasing hormone release were virtually identical. Increasing concentrations of D‐glucose also inhibited somatostatin release following depolarization with high K+, but had no obvious effect on depolarization‐induced TRH or GHRH release when compared with L‐glucose.In conclusion, D‐glucose exerts a potent, dose‐related modulatory action on the release of rat hypothalamic TRH and GHRH as well as somatostatin in vitro. Further studies are required to establish any physiological relevance of glucose in the modulation of these hypothalamic neuropeptides.
Arcuate Nucleus and Preoptic Area Involvement in Beta‐Endorphin‐lnduced Release of Prolactin in Conscious Ovariectomized Rats†
Authors: Voogt James L. , Reseh Garth , Turkington Susan 
Published: September 2006

AbstractThe ability of ß‐endorphin (ß‐END) to release prolactin and the ability of naloxone to block prolactin's release when delivered to specific hypothalamic areas via push‐pull perfusion was studied in unrestrained, conscious, Ovariectomized rats. Perfusion of either the arcuate nucleus or the preoptic area with ß‐END for 15 to 30 min caused a large, brief increase in plasma prolactin levels. Perfusion for a longer time period (120 min) resulted in peak prolactin levels at 60 min, with a return to baseline by 120 min, suggesting that ß‐END primarily acts to induce a sequence of events that culminates in prolactin release, but other factors are needed to maintain this release over long periods of time. Perfusion of the arcuate nucleus for two 15‐min periods 90 min apart resulted in two surges of prolactin. When naloxone, the opiate receptor antagonist, was added to the perfusate, ß‐END was not capable of stimulating prolactin release. These results provide a model to answer whether endogenous ß‐END has a role in the neuroendocrine regulation of prolactin surges and what the location is of the opiate neurons involved in this neuronal pathway.