EFFECTS OF HISTAMINE IMPLANTS IN SEVERAL BRAIN REGIONS ON THE RELEASE OF PROLACTIN IN CONSCIOUS ADULT MALE RATS

1981 ◽  
Vol 88 (3) ◽  
pp. 351-358 ◽  
Author(s):  
E. O. ALVAREZ ◽  
A. O. DONOSO
Keyword(s):  
Plasma Levels ◽  
Anterior Part ◽  
Central Area ◽  
Brain Regions ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Amygdaloid Nucleus ◽  
Acute Administration ◽  
Hypothalamic Area

The levels of prolactin in the plasma of conscious male rats were determined at various times after an acute administration of histamine or a histamine releasing agent, compound 48/80, in three brain regions. The brain structures that were examined were, the caudal part of the preoptic area and anterior part of the anterior hypothalamic area (POA–AHA), the arcuate nucleus–ventromedial nucleus region (ARC–VMN) and the medial–basal amygdaloid nucleus of the limbic system (AME). A marked increase in plasma levels of prolactin was observed when implants of histamine were in the POA–AHA region. A more consistent increase was found when 1 μg histamine was injected in the same region; values of prolactin were about 3·6 times greater than in their controls injected with 0·9% saline. Such increased hormone levels lasted up to 2 h. A similar rise in prolactin level was found when the implants of histamine were located in the ARC–VMN region. When compound 48/80 or empty cannulae were placed in those brain regions that were examined, no changes in plasma levels of prolactin were induced. Both histamine and compound 48/80 elicited a delayed and long-lasting decrease of the high plasma level of prolactin present in rats bearing cannulae in the AME region. The results suggest that in the male rat, histaminergic sites, located in rostral and mediobasal hypothalamus and in the central area of the amygdala, are involved in the mechanisms controlling prolactin secretion.

Refining the Effects Observed in a Developmental Neurobehavioral Study of Ammonium Perchlorate Administered Orally in Drinking Water to Rats. II. Behavioral and Neurodevelopment Effects

2005 ◽  
Vol 24 (6) ◽  
pp. 451-467 ◽  
Author(s):  
Raymond G. York ◽  
John Barnett ◽  
Michael F. Girard ◽  
David R. Mattie ◽  
Marni V. K. Bekkedal ◽  
...  
Keyword(s):  
Drinking Water ◽  
Ammonium Perchlorate ◽  
Brain Regions ◽  
Male Rats ◽  
Male Rat ◽  
Sprague Dawley ◽  
Continuous Access ◽  
Brain Morphometry ◽  
The Central Nervous System ◽  
The Right

A developmental neurotoxicity study was conducted to generate additional data on the potential functional and morphological hazard to the central nervous system caused by ammonium perchlorate in offspring from in utero and lactation exposure. Female Sprague-Dawley rats (23 to 25/group) were given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 10.0 mg/kg-day perchlorate in the drinking water beginning 2 weeks prior to mating and continuing through day 10 of lactation for the behavioral function assessment or given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 30.0 mg/kg-day beginning on gestation day 0 and continuing through day 10 of lactation for neurodevelopment assessments. Motor activity was conducted on postpartum days 14, 18, and 22 and juvenile brain weights, neurohistopathological examinations, and regional brain morphometry were conducted on postpartum days 10 and 22. This research revealed a sexually dimorphic response, with some brain regions being larger in perchlorate-treated male rats than in comparable controls. Even so, there was no evidence of any obvious exposure-related effects on male rat brain weights or neuropathology. The most consistent exposure-related effect in the male pups was on the thickness of the corpus callosum, with both the right- and left-sided measures of the thickness of this white matter tract being significantly greater for the male pups in the 0.1 and 1.0 mg/kg-day exposure groups. The behavioral testing suggests prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups.

Somatostatin Inhibits prolactin secretion in the estradiol primed male rat

1981 ◽  
Vol 59 (10) ◽  
pp. 1082-1088 ◽  
Author(s):  
G. R. Cooper ◽  
S. H. Shin
Keyword(s):  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Blocking Agent ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Dependent Manner ◽  
Intact Male ◽  
Plasma Prl

Somatostatin inhibits not only growth hormone secretion, but also the secretion of several other hormones. The role of somatostatin in prolactin (PRL) secretion has not been clearly demonstrated. The present study was undertaken to examine the effects of somatostatin on rat PRL secretion in several different circumstances where the circulating PRL level is elevated: (1) the estradiol primed intact male rat, (2) normal and (3) estradiol primed rats pretreated with pimozide, (4) normal and (5) estradiol primed hypophysectomized male rats with adenohypophyses grafted under the kidney capsule (HAG rat). Blood samples (70 μL) were taken every 2 min via an indwelling atrial cannula from conscious, unrestrained animals. In the estradiol primed intact rats, a bolus injection of somatostatin (10, 100, and 1000 μg/kg) lowered PRL levels in a dose-dependent manner. When the PRL concentration was elevated by the administration of pimozide (3 mg/kg), a dopaminergic receptor blocking agent, somatostatin was ineffective in decreasing plasma PRL concentration but the PRL concentration was lowered by somatostatin when the rat had been primed with estradiol. Somatostatin had no effect on the normal HAG rats, but lowered the plasma PRL concentration in the estradiol primed HAG rats. Since somatostatin inhibits PRL secretion only in the estradiol primed rats, it is suggested that estradiol priming creates a new environment, presumably via new or altered receptors, which can be inhibited by somatostatin.

EARLY EFFECTS OF STILBOESTROL ON GROWTH HORMONE AND PROLACTIN SECRETION AND ON PITUITARY MITOTIC ACTIVITY IN THE MALE RAT

1973 ◽  
Vol 58 (2) ◽  
pp. 227-231 ◽  
Author(s):  
H. M. LLOYD ◽  
J. D. MEARES ◽  
JOAN JACOBI
Keyword(s):  
Growth Hormone ◽  
Mitotic Activity ◽  
Single Injection ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Serum Prolactin ◽  
Serum Growth Hormone ◽  
Total Period ◽  
Early Effects

SUMMARY The effects of a single injection of 1 mg diethylstilboestrol dipropionate on pituitary mitotic activity and on secretion of growth hormone and prolactin were investigated in male rats on each of the first 15 days following the single dose and then at intervals for a total period of 63 days. Mitotic activity increased to a maximum on day 4 and then gradually diminished. Serum growth hormone was moderately increased during the 2nd week and serum prolactin showed a gradual rise with a return to normal on day 63. In the pituitary gland, growth hormone concentration diminished until day 28, whereas prolactin rose quickly at first, maintained a raised level and increased further on day 43. During the first 12 days, pituitary weight was significantly correlated with serum growth hormone and prolactin concentration. During days 13–28, serum prolactin, but not growth hormone, was significantly correlated with the pituitary mitotic index.

Effect of ergocristine on prolactin secretion in the male rat with pituitaries grafted beneath the kidney capsule

1979 ◽  
Vol 57 (11) ◽  
pp. 1313-1316 ◽  
Author(s):  
S. H. Shin
Keyword(s):  
Bolus Injection ◽  
Decay Curve ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Plasma Prolactin ◽  
Elevated Plasma ◽  
Kidney Capsule ◽  
Fourfold Increase ◽  
Single Bolus Injection

Male rats in which three pituitaries were grafted beneath the kidney capsule showed approximately a fourfold increase in circulating plasma prolactin concentration. The elevated plasma prolactin concentration did not remain at a constant level but fluctuated with time. The elevated prolactin concentration declined immediately after a single bolus injection of ergocristine (30 μg/kg). The slope of the prolactin decay curve, determined by sequential blood sampling, was parallel to a theoretical slope having a 7-min half-life. This result indicates that ergocristine blocked prolactin secretion immediately and completely as the decay curve (T1/2 = 6.5 min, confidence interval 4.5–11.3) resulting from the administration of ergocristine is the same as the endogenous prolactin decay curve (T1/2 = 7 min).

Long-Term Decreases in the Expression of Calcineurin and GABAA Receptors Induced by Early Maternal Separation Are Associated with Increased Anxiety-Like Behavior in Adult Male Rats

2020 ◽  
pp. 1-10
Author(s):  
Maryam Mahmoodkhani ◽  
Maedeh Ghasemi ◽  
Leila Derafshpour ◽  
Mohammad Amini ◽  
Nasrin Mehranfard
Keyword(s):  
Anxiety Disorders ◽  
Glutamate Receptors ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Central Area ◽  
Early Life Stress ◽  
Brain Regions ◽  
Male Rats ◽  
Lower Percentage

<b><i>Introduction:</i></b> Early life stress is a well-described risk factor of anxiety disorders in adulthood. Dysfunction in GABA/glutamate receptors and their functional regulator, calcineurin, is linked to anxiety disorders. Here, we investigated the effect of early life stress, such as repeated maternal separation (MS; 3 h per day from postnatal day [P] 2 to 11), on changes in the expression of calcineurin as well as the ionotropic glutamatergic and GABAergic receptors including α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl-D-aspartate (NMDA) and GABA<sub>A</sub> receptors in the hippocampus and prefrontal cortex (PFC) of adolescent (P35) and adult (P62) male Wistar rats and their correlations with anxiety-like behavior in adulthood. <b><i>Methods:</i></b> The protein levels were assessed by Western blot analysis. Anxiety-like behavior was measured in the elevated plus maze (EPM) and open field (OF) tests. <b><i>Results:</i></b> MS induced a regional transient decrease of glutamate receptors expression at P35, with decreased NMDA and AMPA receptor levels, respectively, in the hippocampus and PFC, suggesting a possible decrease in excitatory synaptic strength. In contrast to glutamate receptors, MS had long-lasting influence on GABA<sub>A</sub> receptor and calcineurin levels, with reduced expression of GABA<sub>A</sub> receptor and calcineurin in both brain regions at P35 that continued into adulthood. These results were accompanied by increased anxiety behavior in adulthood, shown by lower percentage of number of total entries and time spent in the open arms of the EPM, and by lower time spent and number of entries in the OF central area. <b><i>Conclusions:</i></b> Together, our study suggests that GABA<sub>A</sub> receptors via calcineurin-dependent signaling pathways may play an important role in the expression of stress-induced anxiety-like behavior.

scholarly journals Possible Mechanisms of Circulating PYY-Induced Satiation in Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 193-204 ◽  
Author(s):  
Ulrike Stadlbauer ◽  
Myrtha Arnold ◽  
Elisabeth Weber ◽  
Wolfgang Langhans
Keyword(s):  
Plasma Levels ◽  
Jugular Vein ◽  
Area Postrema ◽  
Central Area ◽  
Male Rats ◽  
Acute Effects ◽  
Paraventricular Nuclei ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
The Brain

Peptide tyrosine-tyrosine (PYY) is implicated in eating control, but the site(s) and mechanism(s) of its action remain uncertain. We tested acute effects of intrameal hepatic portal vein (HPV) PYY3-36 infusions on eating in adult, male rats and measured HPV and jugular vein (JV) plasma levels of PYY in response to a solid, mixed-nutrient meal. We also examined the effects of HPV PYY3-36 infusions on JV plasma levels, flavor acceptance, and neuronal activation. Intrameal HPV PYY3-36 infusions [1 and 3 nmol/kg body weight (BW)] selectively reduced (P &lt; 0.05) ongoing meal size. HPV PYY levels increased (P &lt; 0.05) during a chow (12.5 kcal) or an isocaloric high-fat meal. JV PYY levels were generally lower than HPV levels but also increased in response to the chow meal. HPV PYY3-36 infusion (1 nmol/kg BW) caused a greater increase in JV PYY than a meal, but neither 1 nor 3 nmol/kg BW PYY3-36 caused conditioned flavor avoidance. HPV PYY3-36 (1 nmol/kg BW) increased the number of c-Fos-expressing cells in the nucleus tractus solitarii, the hypothalamic arcuate and paraventricular nuclei, the central area of the amygdala, and the nucleus accumbens but not in the area postrema and parabrachial nucleus. These data show that HPV infusions of PYY3-36 inhibit eating in rats without causing avoidance, and they identify some brain areas that might be involved. Endogenous PYY may induce satiation by acting directly in the brain, but further studies should examine whether PYY3–36 administrations that mimic the meal-induced increase in plasma PYY are sufficient to inhibit eating.

Diurnal variation and left-right distribution of pyroglutamyl peptidase I activity in the rat brain and retina

1991 ◽  
Vol 125 (5) ◽  
pp. 570-573 ◽  
Author(s):  
M. Ramirez ◽  
B. Sanchez ◽  
G. Arechaga ◽  
S. Garcia ◽  
P. Lardelli ◽  
...  
Keyword(s):  
Rat Brain ◽  
Brain Regions ◽  
Male Rats ◽  
Hypothalamic Area ◽  
Time Points ◽  
Asymmetrical Distribution ◽  
Cervical Ganglia ◽  
Endogenous Substrates ◽  
The Right ◽  
Light:Dark Cycle

Abstract. The thyroliberin and luliberin contents exhibit a diurnal rhythm within the brain and an asymmetrical distribution of both neuropeptides has been demonstrated in the hypothalamus. Since they have been described as substrates of pyroglutamyl peptidase I, this activity was analysed in several rat brain regions and other structures, in order to investigate its putative diurnal variations and changes in relation to the distribution of these neuropeptides and/or other susceptible substrates. Fluorometric activity was assayed in the retina, pituitary gland, superior cervical ganglia, pineal gland, some selected brain regions, and serum of adult male rats at six different time points of a 12:12 h light:dark cycle, using pyroglutamyl-β-naphthylamide as substrate. A significant circadian rhythm was demonstrated in the retina, the hypothalamus, and the intermediate-posterior pituitary lobe. In addition, a small but significant asymmetrical distribution of this activity, at certain time points, was disclosed: The activity was higher in the left than in the right retina at 10 h of the light period, whereas it was predominant in the right side at 01 h of the dark period. Furthermore, the activity was higher in the left anterior than in the right hypothalamic area at 13 and 01 h. These results could be indicative of a role of this enzymatic activity in the control of the functional status of its endogenous substrates.

DNA SYNTHESIS AND DEPLETION OF PROLACTIN IN THE PITUITARY GLAND OF THE MALE RAT

1978 ◽  
Vol 77 (1) ◽  
pp. 129-136 ◽  
Author(s):  
H. M. LLOYD ◽  
J. M. JACOBI ◽  
J. D. MEARES
Keyword(s):  
Growth Hormone ◽  
Dna Synthesis ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Male Rat ◽  
Serum Prolactin ◽  
Inhibitory Effects ◽  
Pituitary Prolactin

Haloperidol, bromocriptine and diethylstilboestrol dipropionate were given in various régimes to male rats to determine their effects on pituitary DNA synthesis, prolactin secretion and growth hormone secretion. Haloperidol increased serum prolactin but did not stimulate pituitary DNA synthesis or reduce pituitary prolactin concentrations. Haloperidol potentiated the effects of oestrogen on serum prolactin and on pituitary DNA synthesis; pituitary prolactin concentrations were greatly reduced, and growth hormone secretion was slightly inhibited. The inhibitory effects of bromocriptine in oestrogen-stimulated rats were demonstrated by smaller pituitary weights and decreased DNA synthesis; serum prolactin levels were lowered and pituitary prolactin concentrations were increased. Haloperidol, given to rats treated with oestrogen and bromocriptine, reversed the inhibitory effects of bromocriptine on DNA synthesis and serum prolactin; pituitary prolactin concentrations fell to well below normal. The results suggest that the haloperidol potentiation of oestrogeninduced pituitary DNA synthesis may depend upon stimulation of prolactin secretion together with reduction of intracellular prolactin levels.

scholarly journals Mode of GH administration and gene expression in the female rat brain

2017 ◽  
Vol 233 (2) ◽  
pp. 187-196 ◽  
Author(s):  
Marion Walser ◽  
Linus Schiöler ◽  
Jan Oscarsson ◽  
Maria A I Åberg ◽  
Ruth Wickelgren ◽  
...  
Keyword(s):  
Mixed Model ◽  
Brain Regions ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Sexually Dimorphic ◽  
Female Rat ◽  
Expression Levels ◽  
Mixed Model Analysis ◽  
Significant Difference

The endogenous secretion of growth hormone (GH) is sexually dimorphic in rats with females having a more even and males a more pulsatile secretion and low trough levels. The mode of GH administration, mimicking the sexually dimorphic secretion, has different systemic effects. In the brains of male rats, we have previously found that the mode of GH administration differently affects neuron–haemoglobin beta (Hbb) expression whereas effects on other transcripts were moderate. The different modes of GH administration could have different effects on brain transcripts in female rats. Hypophysectomised female rats were given GH either as injections twice daily or as continuous infusion and GH-responsive transcripts were assessed by quantitative reverse transcription polymerase chain reaction in the hippocampus and parietal cortex (cortex). The different modes of GH-administration markedly increased Hbb and 5′-aminolevulinate synthase 2 (Alas2) in both brain regions. As other effects were relatively moderate, a mixed model analysis (MMA) was used to investigate general effects of the treatments. In the hippocampus, MMA showed that GH-infusion suppressed glia- and neuron-related transcript expression levels, whereas GH-injections increased expression levels. In the cortex, GH-infusion instead increased neuron-related transcripts, whereas GH-injections had no significant effect. Interestingly, this contrasts to previous results obtained from male rat cortex where GH-infusion generally decreased expression levels. In conclusion, the results indicate that there is a small but significant difference in response to mode of GH administration in the hippocampus as compared to the cortex. For both modes of GH administration, there was a robust effect on Hbb and Alas2.

scholarly journals Urocortin 3 Modulates the Neuroendocrine Stress Response and Is Regulated in Rat Amygdala and Hypothalamus by Stress and Glucocorticoids

Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4578-4588 ◽  
Author(s):  
Pauline M. Jamieson ◽  
Chien Li ◽  
Christina Kukura ◽  
Joan Vaughan ◽  
Wylie Vale
Keyword(s):  
Stress Response ◽  
Mrna Expression ◽  
Stress Responses ◽  
Restraint Stress ◽  
Brain Regions ◽  
Lateral Septum ◽  
Male Rats ◽  
Hypothalamic Area ◽  
Selective Ligand ◽  
Urocortin 3

The endogenous corticotropin-releasing factor (CRF) type 2 receptor (CRFR2)-selective ligand urocortin 3 is expressed in discrete subcortical brain regions with fibers distributed mainly to hypothalamic and limbic structures. Close anatomical association between major urocortin 3 terminal fields and CRFR2 in hypothalamus, lateral septum, and medial amygdala (MEA) suggest it is well placed to modulate behavioral and hormonal responses to stress. Urocortin 3 was administered intracerebroventricularly to male rats under basal conditions or before a restraint stress, and circulating ACTH, corticosterone, glucose, and insulin were measured. Urocortin 3 activated the hypothalamic-pituitary-adrenal axis under basal conditions and augmented ACTH responses to restraint stress. Elevated blood glucose with lowered insulin to glucose ratios in both groups suggested increased sympathetic activity. Circulating catecholamines were also increased by urocortin 3, providing additional evidence for sympathoadrenomedullary stimulation. Intracerebroventricular urocortin 3 increased vasopressin mRNA expression in the parvocellular division of the hypothalamic paraventricular nucleus, whereas CRF expression was unchanged, providing a possible mechanism by which urocortin 3 mediates its actions. Urocortin 3 mRNA expression was examined after exposure to stress-related paradigms. Restraint increased levels in MEA with a trend to increased expression in the rostral perifornical hypothalamic area, whereas hemorrhage and food deprivation decreased expression in MEA. Adrenalectomy markedly increased expression in the rostral perifornical hypothalamic area, and high-level corticosterone replacement restored this to control levels. The evidence that urocortin 3 has the potential to influence hormonal components of the stress response and the changes in its expression levels after stressors is consistent with a potential function for the endogenous peptide in modulating stress responses.

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