Biomedical subjects

C R Barb

Publications and source records attributed to C R Barb.

At least 55 records · Page 3Linked to original sources

PubMed1997

Metabolic changes during the transition from the fed to the acute feed-deprived state in prepuberal and mature gilts.

The present study compared the metabolic response to acute feed deprivation in ovariectomized prepuberal (P; n = 6), 62 +/- 2 kg BW, and mature (M; n = 6) gilts, 124 +/- 4 kg BW. Blood was collected at 1, 2, 3, 4, 6, 8, 12, 16, 20, 24, 28, 32, 40, and 48 h after initiation of feeding. Samples were quantified for glucose, insulin, free fatty acids (FFA), beta-hydroxybutyrate (HBA), IGF-I, IGF binding proteins (BP)-1 to -4, cortisol, and amino acids (AA). At 24 h, blood samples were collected every 15 min for 8 h and an additional 1 h after i.v. injection of GnRH (.2 microgram/kg BW) and growth hormone-releasing factor (GRF; 1 microgram/kg BW). Samples were assayed for growth hormone (GH) and LH. Serum insulin concentrations were lower (P < .05) in P gilts. Plasma glucose concentrations were similar. Serum FFA concentrations were greater (P < .05) in P gilts. Serum concentrations of HBA were greater (P < .001) in P gilts at 48 h. Serum IGF-I concentrations were lower (P < .05) in P gilts by 16 h. Serum IGFBP-1-4 levels were similar. Serum cortisol concentrations were similar. Serum concentrations of the essential AA, isoleucine, lysine, threonine, valine, and phenylalanine were greater (P < .05) in P gilts at 40 h. Serum LH concentrations and response to GnRH were similar. Basal serum GH concentrations and peak response to GRF were greater (P < .05) in P than in M gilts. The transition from fed to unfed state occurs more rapidly in P than in M gilts.

3-Hydroxybutyric Acid↗

PubMed1997

Role of neuropeptides and amino acids in controlling secretion of hormones from the anterior pituitary gland in pigs.

All reproductive processes involve one or more of the protein hormones secreted from the anterior pituitary gland: LH, FSH, prolactin, growth hormone, ACTH and thyroid-stimulating hormone (TSH). Primary hormones of reproduction, such as LH and FSH, directly regulate a reproductive activity. For example, LH and FSH stimulate follicular growth and the associated secretion of oestradiol in sows. In contrast, secondary hormones of reproduction such as TSH are permissive and regulate other physiological systems that indirectly, but profoundly, influence reproduction. Reproduction in pigs can be enhanced by developing strategies to alter and control secretion of hormones from the anterior pituitary gland. However, the successful manipulation of adenohypophysial hormone secretion will require a sound understanding of the mechanisms controlling the function of the hypothalamic-pituitary axis. Hypothalamic hormones including GnRH, dopamine, growth hormone-releasing hormone (GHRH), somatostatin, corticotrophin-releasing hormone (CRH) and thyrotrophin-releasing hormone (TRH) are synthesized in perikarya that possess axons that terminate at the median eminence. These hormones are released into the hypothalamo-hypophysial portal vasculature, travel to the anterior pituitary gland and stimulate or inhibit secretion of adenohypophysial hormones. Secretion of hypothalamic hormones is ultimately controlled by a variety of neurotransmitters and neuropeptides, the most studied in swine being the endogenous opioid peptides (EOP) and more recently, the excitatory amino acids (ExAA). In general, EOP inhibit GnRH and hence LH secretion, and this effect involves the central catecholaminergic system. A definitive role for EOP in the modulation of FSH release remains to be determined. EOP stimulate secretion of GHRH and thus growth hormone release, and depending on the animal model studied, EOP exert either stimulatory or inhibitory influences on prolactin secretion. ExAA, working via N-methyl-D-aspartate (NMDA) receptors at the central nervous system, stimulate secretion of LH, FSH, growth hormone and prolactin in appropriate animal models. However, in certain situations, an inhibitory effect of ExAA on LH secretion has been demonstrated. The modulation of growth hormone and prolactin secretion by ExAA involves EOP. Research investigating the function of ExAA and EOP in the physiological control of swine reproduction warrants further scrutiny.

Animals↗

PubMed1996

Immunocytochemical distribution of catecholamine-synthesizing neurons in the hypothalamus and pituitary gland of pigs: tyrosine hydroxylase and dopamine-beta-hydroxylase.

This study describes the distribution of catecholaminergic neurons in the hypothalamus and the pituitary gland of the domestic pig, Sus scrofa, an animal that is widely used as an experimental model of human physiology in addition to its worldwide agricultural importance. Hypothalamic catecholamine neurons were identified by immunocytochemical staining for the presence of the catecholamine synthesizing enzymes, tyrosine hydroxylase and dopamine-beta-hydroxylase. Tyrosine hydroxylase-immunoreactive perikarya were observed in the periventricular region throughout the extent of the third ventricle, the anterior and retrochiasmatic divisions of the supraoptic nucleus, the suprachiasmatic nucleus, the ventral and dorsolateral regions of the paraventricular nucleus and adjacent dorsal hypothalamus, the ventrolateral arcuate nucleus, and the posterior hypothalamus. Perikarya ranged from parvicellular (10-15 microns) to magnocellular (25-50 microns) and were of multiple shapes (rounded, fusiform, triangular, or multipolar) and generally had two to five processes with branched arborization. No dopamine-beta-hydroxylase immunoreactive perikarya were observed within the hypothalamus or in the adjacent basal forebrain structures. Both tyrosine hydroxylase- and dopamine-beta-hydroxylase-immunoreactive fibers and punctate varicosities were observed throughout areas containing tyrosine hydroxylase perikarya, but dopamine-beta-hydroxylase immunoreactivity was very sparse within the median eminence. Within the pituitary gland, only tyrosine hydroxylase fibers, and not dopamine-beta-hydroxylase immunoreactive fibers, were located throughout the neurohypophyseal tract and within the posterior pituitary in both pars intermedia and pars nervosa regions. Generally, the location and patterns of both catecholamine-synthesizing enzymes were similar to those reported for other mammalian species except for the absence of the A15 dorsal group and the very sparse dopamine-beta-hydroxylase immunoreactive fibers and varicosities in the median eminence in the pig. These findings provide an initial framework for elucidating behavioral and neuroendocrine species differences with regard to catecholamine neurotransmitters.

Animals↗

PubMed1996

Aspartate and glutamate modulation of growth hormone secretion in the pig: possible site of action.

The influence of excitatory amino acids (EAA) on growth hormone (GH) secretion and the possible site of action was investigated in the pig. In Experiment (Exp) I three replicates were conducted with 30 prepuberal gilts, 130 d of age and averaging 70.6 +/- 1.3 kg body weight (BW). Six gilts each received intravenously (i.v.) 0, 50, 100, or 150 mg/kg BW of aspartate (ASP) or glutamate (GLU) in saline. Blood samples were collected every 15 min for 2 hr before and 3 hr after treatment. In Exp II, mature ovariectomized gilts (163 +/- 10 kg BW) that had been immunized against growth hormone releasing factor (GRF) conjugated to human serum albumin (GRFi; n = 4) or against human serum albumin alone (HSAi; n = 5) received 150 mg/kg BW ASP or GLU i.v. in a 2 x 2 factorial arrangement of treatments, which was then repeated in a crossover design. One week later, all animals received 10 mg/kg N-methyl-D,L-aspartate (NMA; EAA agonist) in saline i.v. Blood samples were collected as described above. In Exp III, cultures of anterior pituitary cells from market-weight (averaging 105 kg BW) gilts were studied. On Day 4 of culture, cells (10(5) seeded/well) were challenged with 10(-8), 10(-6), or 10(-4) M ASP or GLU, 10(-6) M [Ala15]-human GRF (1-29)-NH2, or the EAA antagonist, 2-amino-5-phosphonopentanoic acid (10(-4) M; AP5), alone or in combination with ASP or GLU. In Exp I, all doses of ASP and the 100- and 150-mg doses of GLU increased (P < 0.05) GH secretion when compared with Time 0. However, serum GH concentrations were higher (P < 0.01) after 150 mg/kg of ASP when compared with those after 150 mg/kg of GLU. In Exp II, serum GH concentrations increased (P < 0.05) in HSAi but not in GRFi pigs (averaging 1.2 +/- 0.2 ng/ml before and 8.2 +/- 0.7, 6.3 +/- 0.5, and 9.2 +/- 0.5 ng/ml by 15 min after ASP, GLU, and NMA, respectively). In Exp III, relative to controls (40 +/- 6 ng/ml), GH increased (P < 0.05)1.6-, 1.9-, and 1.9-fold and 1.7-, 1.8-, and 2.0-fold after 10(-8), 10(-6), and 10(-4) M ASP and GLU, respectively. The EAA receptor antagonist AP5 failed to prevent the GH response to ASP or GLU, except for 10(-8) M ASP. In summary, ASP is a more potent secretagogue of GH secretion than is GLU in vivo, whereas each is equipotent in vitro. Because no stimulation of GH by EAA was observed in GRFi pigs and no specific dose-response effect of EAA was found in vitro, it may be concluded that modulation by EAA is mediated primarily at the level of the hypothalamus or higher brain centers.

2-Amino-5-phosphonovalerate↗

PubMed1996

Depressed luteinizing hormone response to estradiol in vivo and gonadotropin-releasing hormone in vitro in experimentally diabetic swine.

The influence of the acute withdrawal of insulin therapy in streptozocin-diabetic female swine was examined for changes in 1) the in vivo pulsatile secretion of luteinizing hormone (LH), 2) the preovulatory-like gonadotropin patterns after exogenous estradiol, and 3) the in vitro LH secretion by cultured pituitary cells. In Experiment 1, ovariectomized diabetic pigs (n = 4) were maintained with insulin therapy until 4 d before estradiol benzoate (EB; 7 micrograms/kg body weight; subcutaneous) was administered. Four normal ovariectomized pigs, matched for age and weight, served as controls. The diabetic state was confirmed by the measurement of glucose and insulin concentrations during a glucose tolerance test. Pulsatile LH secretion was not influenced by experimental diabetes mellitus. However, the expected surge in LH was not induced by EB in diabetic gilts. In contrast, three of four normal gilts had a preovulatory-type surge in LH. Concentrations of follicle-stimulating hormone in serum were not affected by diabetes mellitus. Estradiol concentrations in serum after ER were influenced by diabetes mellitus (treatment by time interaction; P < 0.001). In individual estradiol profiles, maximum concentrations were similar (104 +/- 10.4 and 91 +/- 12.0 ng/ml for normal and diabetic pigs, respectively), but the interval to maximum concentration was delayed in diabetic pigs (27.5 vs. 9.0 h; SE = 3.0; P < 0.05). However, the duration of standing estrus (2.2 +/- .3 d) and the interval from EB to estrus (3.6 +/- 0.3 d) were not influenced by diabetes mellitus. In Experiment 2, LH secretion by cultured cells and residual cellular LH content were greater in the pituitaries of normal than diabetic pigs (P < 0.05), and only cells from normal pigs responded to gonadotropin-releasing hormone (GnRH), with increased production of LH (P < 0.05). In conclusion, diabetes mellitus did not affect pulsatile LH secretion but did lower the ability of exogenous estradiol to stimulate a surge in vivo and of GnRH to increase LH in vitro, suggesting that the pituitary response to estradiol and GnRH is more severely affected by diabetes than is the GnRH pulse generator.

Animals↗

PubMed1996

N-methyl-D,L-aspartate-induced growth hormone secretion in barrows: possible mechanisms of action.

Four experiments were conducted to determine mechanisms by which n-methyl-d,l-aspartate (NMA) increases serum concentrations of growth hormone (GH). Blood samples were collected from barrows every 15 min for 2 h (Exp. 1, 2, and 3) or 3 h (Exp. 4) immediately before and immediately after i.v. treatments. In Exp. 1, barrows (n = 4/treatment) received either .9% saline or 1.25, 2.5, or 5 mg of NMA/kg of BW. The change in circulating GH concentrations was greater (P < .05) for barrows receiving 2.5 mg (by 883%) or 5.0 mg of NMA/kg of BW (by 1,095%) than for those injected with saline. In Exp. 2, barrows (n = 4/treatment) received NMA (2.5 mg/kg of BW) or injections of 1.25 mg of the pure d or pure 1 isomers of NMA/kg of BW. Growth hormone concentrations increased by 177% (P < .025) after NMA treatment and by 245% (P < .01) after injection of the pure d isomer of NMA. The pure 1 isomer of NMA had no effect (P > .1) on GH concentrations. In Exp. 3, barrows received NMA (2.5 mg/kg of BW) 10 min after i.m. injection of saline (n = 7) or ketamine hydrochloride ( n = 8; 19.9 mg/kg of BW), an n-methyl-d-aspartate (NMDA) receptor antagonist. The NMA increased (P < .01) GH concentrations by 289% in saline-pretreated barrows but had no effect (P > .1) on barrows pretreated with ketamine hydrochloride. In Exp. 4, barrows (n = 4/treatment) received NMA 3 h after i.v. pretreatment with antisera to GH-releasing factor (GRF; 154 mL) or no pretreatment. Serum GH concentrations increased by 166% (P < .05) after injection of NMA in barrows receiving no pretreatment. The NMA had no effect (P > .1) on GH concentrations in barrows receiving antisera to GRF. Our results support the concept that NMDA stimulates GRF, and hence GH secretion, by activating an NMDA receptor.

Animals↗

PubMed1996

The role of excitatory amino acids in pulsatile secretion of luteinizing hormone in gilts and barrows.

The relationship of excitatory amino acid (EAA) activity to LH secretion was investigated in ovariectomized crossbred prepuberal gilts (93 +/- 1 kg BW) and Yorkshire barrows (94 +/- 2 kg BW) in two experiments. In Exp. 1, eight gilts received, i.m., saline (S) or 20 mg of Ketamine (K)/kg BW, a noncompetitive EAA receptor antagonist. Within these groups, four then received 10 mg of N-methyl-DL-aspartate (NMA)/kg BW, an EAA agonist, or S i.v. Mean serum LH concentrations were similar among groups before treatment, did not change after S+S, but decreased (P < .05) by 1 h after S+NMA, 3 h after K+S, and 2 h after K+NMA. Serum cortisol concentrations did not change after S+S, but were increased (P < .05) from 30 to 90 min after S+NMA, at 120 min after K+S, and from 30 to 120 min after K+NMA. In Exp. 2, barrows received 2.5 mg of NMA/kg BW i.v. immediately after i.m. injection of S (n = 7) or 19.9 mg of K/kg BW (n = 8). Mean serum LH concentrations for the 2 h before treatment were similar among barrows, but decreased (P < .05) by 2 h after K+NMA and was not altered after S+NMA. Serum cortisol concentrations were increased at 30 min after S+NMA and from 60 to 90 min after K+NMA. We suggest that EAA both inhibit and stimulate LH secretion, with the inhibitory effects lying within the basal hypothalamus and the stimulatory effects lying within higher brain centers.

Animals↗

PubMed1995

Catecholaminergic region A15 in the bovine and porcine hypothalamus.

Magnocellular perikarya within the retrochiasmatic division of the supraoptic nucleus of bovine and porcine hypothalami were immunoreactive (ir) with antiserum against tyrosine hydroxylase (TH), but not dopamine-beta-hydroxylase (DBH). Few cells in this region were also immunoreactive for vasopressin (VP) or oxytocin (OT). In contrast, the main division of the supraoptic nucleus contained numerous perikarya immunoreactive for VP and OT, but not TH nor DBH. Both the retrochiasmatic and principal divisions of the supraoptic nuclei contained TH- and DBH-ir fibers and varicosities. This region in bovine and porcine hypothalami corresponds to the ventral A15 catecholaminergic (dopamine-producing) cell group.

Animals↗

PubMed1995

Luteinizing hormone and growth hormone concentrations in serum of prepubertal gilts treated with N-methyl-D,L-aspartate.

Prepubertal Yorkshire gilts, 189 d of age and 96 kg body weight (BW), were used to determine the effects of intravenous injections of N-methyl-D,L-aspartate (NMA) on circulating concentrations of luteinizing hormone (LH) and growth hormone (GH). In Experiment 1, blood was sampled from four gilts every 15 min for 2 hr on four consecutive days. One hour after the initiation of sampling on each day, gilts received either vehicle (0.9% saline solution) or 1.25, 2.5, or 5 mg of NMA/kg BW as per a 4 x 4 latin square arrangement of treatments. There was no effect of treatment (P > 0.1) on concentrations of LH in serum. However, relative to vehicle-treated animals, gilts administered 2.5 mg of NMA/kg BW had elevated (1,120%; P < 0.05) circulating levels of GH. In Experiment 2, samples were collected from 15 gilts at 15-min intervals for 1 hr before and 1 hr after NMA (10 mg/kg BW; n = 8) or vehicle (n = 7). NMA increased serum concentrations of both LH (by 80%; P < 0.05) and GH (by 700%; P < 0.01). We suggest that LH and GH secretion in gilts was enhanced by treatment with NMA.

Animals↗

PubMed1995

Influence of stage of the estrous cycle on insulin-like growth factor-I modulation of luteinizing hormone secretion in the gilt.

Follicular phase (FOL; Days 17-19; n = 8), luteal phase (LUT; Days 7-9; n = 6), and ovariectomized (OVX; n = 5) crossbred gilts were used (Day 0 = onset of estrus). Blood samples were collected via jugular vein cannula every 15 min for 2 h the day before pituitary collection. Serum was assayed for insulin-like growth factor (IGF)-I, IGF-I binding proteins (IGFBP), LH, estradiol (E2), and progesterone (P4). Anterior pituitary cells were dispersed, cultured, and challenged on Day 4 of culture (Day 0 = day of seeding) with 10(-7) M GnRH or IGF-I (10(-11), 10(-10), 10(-9), 10(-8), or 3 x 10(-8) M) individually or in combination. Serum E2 and P4 concentrations indicated that the animals were in the appropriate stage of the estrous cycle. Mean serum LH concentrations were greater (p < 0.0004) for OVX animals compared to FOL and LUT animals. Mean serum IGF-I concentrations were lower (p < 0.05) for OVX compared to FOL and LUT animals, while serum IGFBP were not different among animals. Basal LH secretion (control) was greater (p < 0.04) in OVX than in FOL or LUT cultures. Relative to control, 10(-11) M IGF-I increased (p < 0.02) LH secretion in FOL, LUT, and OVX cultures, and this response was greater (p < 0.05) in FOL and OVX than in LUT cultures. Only the 10(-11) M IGF-I enhanced basal LH secretion in LUT cultures. In addition, 10(-10) M IGF-I increased (p < 0.05) LH secretion in OVX cultures, and 10(-10) and 10(-9) M IGF-I stimulated (p < 0.05) LH secretion in FOL cultures, whereas basal LH secretion in all groups was unaffected (p > 0.05) by 10(-8) or 3 x 10(-8) M IGF-I. The GnRH-induced LH secretion was unaltered by IGF-I treatment. Results indicate that in vitro IGF-I treatment increased basal LH secretion, with reproductive status modulating LH response to IGF-I.

Animals↗

PubMed1995

Biogenic amines in the hypothalamus of rats after diethyldithiocarbamate or AIMAX treatment, an alternative for norepinephrine depletion.

The objective of this study was to determine whether AIMAX (a dithiocarbamoylhydrazine derivative) is suitable for determining the effects of norepinephrine (NE) depletion on reproduction in domestic animals. Therefore, the effect of AIMAX (n = 6) on concentrations of biogenic amines in the medial basal hypothalamus (MBH) and anterior hypothalamic area (AHA) of ovariectomized (OVX) rats primed with ovarian steroids was compared to that of diethyldithiocarbamate (DDC; n = 5), a potent dopamine-beta-hydroxylase (DBH) inhibitor, which is chemically similar to AIMAX. Rats that received only ovarian steroids and saline injections served as controls (n = 6). Treatment with DDC resulted in sedation and reduced body temperature. In contrast, rats behaved normally after AIMAX treatment. AI-MAX reduced (P < .05) NE but increased (P < .05) dopamine (DA) concentrations in MBH and AHA compared with controls. Similar changes in NE and DA concentrations were observed in DDC-treated rats. However, elevated epinephrine (EPI) levels were measured in MBH and AHA of only DDC-treated rats. Serum LH concentrations were suppressed (P < .005) in both AIMAX- and DDC-treated rats compared with control animals. Because AIMAX, like DDC, suppressed hypothalamic NE content and LH secretion, AIMAX should be useful in studying effects of NE depletion on gonadotropin secretion in domestic animals.

Animals↗

PubMed1995

Glucose and free fatty acid modulation of growth hormone and luteinizing hormone secretion by cultured porcine pituitary cells.

The influence of glucose and free fatty acids (FFA) on LH and GH secretion from porcine pituitary cells was examined in culture. Cells were challenged with 10(-9), 10(-8), or 10(-7) M GnRH; 10(-9), 10(-8), or 10(-7) M [Ala15]-h growth hormone-releasing factor-(1-29)NH2 (GRF); 10(-3) or 10(-5) M forskolin; glucose (100, 300, or 600 mg/dL); and oleic or linoleic acid (10(-11) to 10(-5) M) individually or in combinations of glucose, oleic, and linoleic acid with GnRH, GRF, or forskolin. Relative to control (medium alone), GnRH increased (P < .003) LH secretion. Glucose at 100 mg/dL enhanced (P < .05) basal LH release, whereas the 600-mg/dL dose suppressed (P < .05) LH response to GnRH. Except for 10(-7) M, all doses of linoleic acid increased (P < .05) basal LH release, whereas only 10(-5) M linoleic acid suppressed (P < .02) LH response to GnRH. All doses of oleic acid enhanced (P < .05) basal LH release and suppressed (P < .03) the LH response to GnRH. In contrast, neither FFA suppressed the forskolin-induced LH secretion compared to forskolin alone. Growth hormone-releasing factor stimulated (P < .02) GH release in a dose-dependent manner. Glucose did not alter basal GH release but suppressed (P < .01) GRF-induced GH release. Only 300 mg/dL of glucose suppressed (P < .05) forskolin-induced GH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Prolactin secretion after bromocriptine in the hypophysial stalk-transfected gilt.

Blood samples were collected by jugular vein cannula from 6 hypophysial stalk-transected (HST) and 4 intact (INTACT) crossbred gilts at 0800, 0830 and 0900 h. Immediately after the 0900 h sample, thyrotropin releasing hormone (TRH) was injected i.v. to determine anterior pituitary gland response via release of prolactin (PRL). Blood was collected every 15 min for 1 h and every 30 min for an additional 2 h. All gilts received the dopamine (DA) agonist, bromocriptine (CB-154), s.c. at 1600 h and blood sampling and TRH challenge was repeated beginning at 0800 h the next day. Mean serum PRL concentration at 0800, 0830 and 0900 h was termed basal PRL for each day. Before CB-154, basal PRL for HST gilts was greater (P < .01) than for INTACT gilts, whereas, after CB-154, basal PRL were similar among HST and INTACT gilts. Before CB-154, TRH caused peak secretion of PRL of similar magnitude within 15 minutes in both HST and INTACT gilts; PRL decreased to basal concentration by 120 min after TRH in both groups. However, after CB-154, PRL response to TRH was blunted similarly in all gilts. These results indicate that suppression of DA pathways is an antecedent to the physiological mechanism by which a secretagogue, such as TRH, stimulates PRL secretion in the intact pig.

Animals↗

PubMed1994

Opioid modulation of gonadotropin releasing hormone release from the hypothalamic preoptic area in the pig.

Two experiments (Exp) were conducted to examine in vitro the release of gonadotropin releasing hormone (GnRH) from the hypothalamus after treatment with naloxone (NAL) or morphine (MOR). In Exp 1, hypothalamic-preoptic area (HYP-POA) collected from 3 market weight gilts at sacrifice and sagittally halved were perifused for 90 min prior to a 10 min pulse of morphine (MOR; 4.5 x 10(-6) M) followed by NAL (3.1 x 10(-5) M) during the last 5 min of MOR (MOR + NAL; n = 3). The other half of the explants (n = 3) were exposed to NAL for 5 min. Fragments were exposed to KCl (60 mM) at 175 min to assess residual GnRH releasability. In Exp 2, nine gilts were ovariectomized and received either oil vehicle im (V; n = 3); 10 micrograms estradiol-17 beta/kg BW in 42 hr before sacrifice (E; n = 3); .85 mg progesterone/kg BW in twice daily for 6 d prior to sacrifice (P4; n = 3). Blood was collected to assess pituitary sensitivity to GnRH (.2 microgram/kg BW) on the day prior to sacrifice. On the day of sacrifice HYP-POA explants were collected and treated as described in Exp 1 except tissue received only NAL. In Exp 1, NAL increased (P < .05) GnRH release. This response to NAL was attenuated (P < .05) by coadministration of MOR. Cumulative GnRH release after NAL was greater (P < .05) than after MOR + NAL. All tissues responded similarly to KCl with an increase (P < .05) in GnRH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Growth hormone-releasing hormone and somatostatin neurons within the porcine and bovine hypothalamus.

Hypothalamic growth hormone-releasing hormone (GHRH) and somatotropin release-inhibiting factor or somatostatin (SS) immunoreactive (ir) neurons were localized in pigs (n = 8) and cattle (n = 7) to identify neuroanatomical sites involved in the regulation of growth hormone secretion. Coronal and sagittal frozen sections (30-60 microns) of Zamboni's fixed hypothalamic tissue, without prior colchicine treatment were incubated with GHRH or SS primary antisera for 48 h, then visualized by peroxidase-diaminobenzidine immunocytochemistry. Fusiform, bipolar SS-ir perikarya were located about the third ventricle in the periventricular nucleus, extending from rostral aspects of preoptic periventricular nucleus to a level approximate with caudal regions of the paraventricular nucleus. Rounded or fusiform, bipolar GHRH-ir perikarya were mostly located in ventrolateral portions of the arcuate nucleus in pigs and cattle, and within ventral aspects of the ventromedial nucleus in pigs but rarely in cattle. In both pigs and cattle, SS-ir and GHRH-ir fibers projected ventrally into the median eminence with dense and overlapping innervation of the external layer, especially dense in lateral regions. In pigs, but not as distinguishable in cattle, SS-ir fibers also densely innervated the ventromedial and arcuate hypothalamic nuclei. Double immunostained sections revealed close apposition of SS-ir fibers and varicosities with GHRH-ir perikarya in arcuate and ventromedial nuclei, and apposition of SS-ir and GHRH-ir varicosities in the median eminence.

Animals↗

PubMed1993

N-methyl-D,L-aspartate modulation of luteinizing hormone and growth hormone secretion from pig pituitary cells in culture.

Administration of n-methyl-d, l-aspartate (NMA) to pigs in vivo increased GH and suppressed LH secretion. Cultures of anterior pituitary cells from pigs in the follicular phase (FOL; n = 3) and luteal phase (LUT; n = 3) of the estrous cycle, and ovariectomized (OVX; n = 10) pigs were treated with NMA (10(-4), 10(-6) or 10(-8) M) or the NMA antagonist, 2-amino-5-phosphonopentanoic acid (AP5; 10(-4), 10(-6) or 10(-8) M), to determine if NMA affects the pituitary directly. Secreted LH and GH were measured at 4 h after treatment. Basal LH and GH secretion (control; C) were 1.1 +/- 0.6, 4.4 +/- 2.1 and 5.6 +/- 1.3 ng/well and 5.2 +/- 1.2, 7.5 +/- 1.2 and 5.2 +/- 1.7 ng/well for FOL, LUT and OVX, respectively. Relative to C, 10(-4) M NMA increased (P < 0.001) LH secretion 2.4-, 2.2- and 5.1-fold in FOL, LUT and OVX cultures, respectively. The effect of 10(-4) M NMA was inhibited by 10(-4) M AP5 (P < 0.05) in FOL cultures, but not in OVX cultures. GnRH increased (P < 0.001) LH levels 3.1-, 2.3- and 3.8-fold in FOL, LUT and OVX cultures, respectively. Relative to C, 10(-4), 10(-6) and 10(-8) M NMA increased (P < 0.03) GH secretion 1.5-, 1.5- and 2.3-fold in LUT and 1.7-, 2.3- 2.0-fold in OVX cultures, respectively. AP5 alone or in combination with NMA failed to alter basal GH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

N-methyl-d,l-aspartate modulation of pituitary hormone secretion in the pig: role of opioid peptides.

Sixteen ovariectomized (OVX) mature gilts, averaging 139.6 +/- 3.1 kg body weight (BW) were assigned randomly to receive either progesterone (P, 0.85 mg/kg BW, n = 8), or corn oil vehicle (OIL, n = 8) injections im twice daily for 10 d. On the day of experiment, all gilts received either the EAA agonist, N-methyl-d,l-aspartate (NMA; 10 mg/kg BW, iv) alone or NMA plus the EOP antagonist, naloxone (NAL, 1 mg/kg BW, iv), resulting in the following groups of 4 gilts each: OIL-NMA, OIL-NMA-NAL, P-NMA and P-NMA-NAL. Blood samples were collected via jugular cannula every 15 min for 6 hr. All pigs received NMA 5 min following pretreatment with either 0.9% saline or NAL 2 hr after blood collection began and a GnRH challenge 3 hr after NMA. Administration of NMA suppressed (P < 0.03) LH secretion in OIL-NMA gilts and treatment with NAL failed to reverse the suppressive effect of NMA on LH secretion in OIL-NMA-NAL gilts. Similar to OIL-NMA gilts, NMA decreased (P < 0.03) mean serum LH concentrations in P-NMA gilts. However, in P-NMA-NAL gilts, serum LH concentrations were not changed following treatment. All gilts responded to GnRH with increased (P < 0.01) LH secretion. Additionally, administration of NMA increased (P < 0.01) growth hormone (GH) and prolactin (PRL) secretion in both OIL-NMA and P-NMA gilts, but this increase in GH and PRL secretion was attenuated (P < 0.01) by pretreatment with NAL in OIL-NMA-NAL and P-NMA-NAL gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1993

Involvement of the central noradrenergic system in opioid modulation of luteinizing hormone and prolactin secretion in the pig.

The role of norepinephrine (NE) in the progesterone (P)-dependent endogenous opioid peptide (EOP) suppression of LH and prolactin (PRL) secretion in the pig was studied. Fifteen ovariectomized gilts treated with P (0.85 mg/kg b.w. i.m.) twice daily for 10 days were assigned, 5 gilts each, to the following treatment groups: 1) control, 2) AIMAX (N-methyl-N1[1-methyl-2-propenyl]1,2 hydrazinedicarbothioamide), and 3) anti-GnRH serum. On day 4 of P treatment, AIMAX (125 mg per 1.8 kg feed/day), previously shown to be an NE synthesis inhibitor, was fed daily for 7 days to group 2. On the last day of P treatment, group 3 gilts received an i.v. injection of anti-GnRH serum at 0800 h while Group 1 animals received an i.v. injection of serum collected from hypophysectomized gilts. Jugular blood samples were collected every 15 min for 9 h starting at 1000 h. All gilts received two injections of naloxone (NAL; 1 mg/kg b.w., i.v.) at 1400 h and 1600 h and an injection of a GnRH analogue (D-[Ala6-desGly-NH10]-ethylamide; 5 micrograms/pig, i.v.) at 1800 h. Pretreatment serum LH concentrations were lower (p < 0.05) in AIMAX-treated gilts (0.19 +/- 0.09 ng/ml) than in controls (0.53 +/- 0.09 ng/ml), but were similar to those in GnRH antiserum-treated gilts (0.32 +/- 0.09 ng/ml). NAL increased (p < 0.001) serum LH concentrations in control animals and averaged 1.6 +/- 0.2 ng/ml the first h. AIMAX and anti-GnRH serum blocked the NAL-induced LH secretion. Serum PRL concentrations averaged 6.0 +/- 0.1 ng/ml for all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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