scholarly journals A conceptual model of the influence of stress on female reproduction

Reproduction ◽  
2003 ◽  
pp. 151-163 ◽  
Author(s):  
H Dobson ◽  
S Ghuman ◽  
S Prabhakar ◽  
R Smith
Keyword(s):  
Neuropeptide Y ◽  
Brain Stem ◽  
Paraventricular Nucleus ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Pulse Frequency ◽  
Medial Preoptic Area ◽  
Aminobenzoic Acid ◽  
Female Reproduction ◽  
Cell Recruitment

Intriguingly, similar neurotransmitters and nuclei within the hypothalamus control stress and reproduction. GnRH neurone recruitment and activity is regulated by a balance between stimulation, suppression and permissiveness controlled by noradrenaline, neuropeptide Y and serotonin from the brain stem, impact from glutamate in the medial preoptic area and neuropeptide Y in the arcuate nucleus, in opposition to the restraining influences of gamma-aminobenzoic acid within the medial preoptic area and opioids from the arcuate nucleus. Stress also activates neuropeptide Y perikarya in the arcuate nucleus and brain stem noradrenaline neurones. The latter project either indirectly, via the medial preoptic area, or directly to the paraventricular nucleus to release corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP). Within the medial preoptic area, GnRH neurones synapse with CRH and AVP axons. Stimulation of CRH neurones in the paraventricular nucleus also activates gamma-aminobenzoic acid and opioid neurones in the medial preoptic area and reduces GnRH cell recruitment, thereby decreasing GnRH pulse frequency. Oestradiol enhances stress-induced noradrenaline suppression of LH pulse frequency but when applied in the paraventricular nucleus or brain stem, and not in the medial preoptic area or arcuate nucleus. The importance of CRH and AVP in the medial preoptic area needs confirming in a species other than the rat, which uses adrenal activation to time the onset of the GnRH surge. Another stress-activated pathway involves the amygdala and bed of the nucleus stria terminalis, which contain CRH neurones and accumulate gamma-aminobenzoic acid during stress.

Neonatal handling reduces angiotensin II receptor density in the medial preoptic area and paraventricular nucleus but not in arcuate nucleus and locus coeruleus of female rats

2006 ◽  
Vol 1067 (1) ◽  
pp. 177-180 ◽  
Author(s):  
Cármen Marilei Gomes ◽  
Márcio Vinícius Fagundes Donadio ◽  
Inélia Franskoviaki ◽  
Janete A. Anselmo-Franci ◽  
Celso Rodrigues Franci ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Locus Coeruleus ◽  
Paraventricular Nucleus ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Female Rats ◽  
Receptor Density ◽  
Angiotensin Ii Receptor ◽  
Neonatal Handling

Interleukin-1 beta-induced anorexia and pyrexia in rat: relationship to hypothalamic neuropeptide Y

1995 ◽  
Vol 269 (5) ◽  
pp. E852-E857 ◽  
Author(s):  
H. D. McCarthy ◽  
S. Dryden ◽  
G. Williams
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Core Temperature ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Interleukin 1 ◽  
Medial Preoptic Area ◽  
Interleukin 1 Beta

We investigated the effect of recombinant human interleukin-1 beta (rhIL-1 beta)-induced anorexia and pyrexia on the hypothalamic neuropeptide Y (NPY)-ergic system, which stimulates feeding and reduces thermogenesis. In meal-fed rats, food intake decreased by 83%, 90 min after IL-1 beta treatment (1.3 micrograms/100 g ip; n - 8) vs. controls. NPY concentrations were significantly higher in the medial preoptic area (MPO), paraventricular (PVN), ventromedial (VMN), and dorsomedial (DMN) nuclei but unchanged in the arcuate nucleus (ARC) in both IL-1 beta-treated and pair-fed groups. Indomethacin (0.25 mg/100 g ip) reduced IL-1 beta-induced anorexia and tended to normalize NPY concentrations. In study 2, IL-1 beta increased core temperature by 1.1 degrees C above preinjection values (P < 0.001) and significantly raised NPY concentrations in the MPO, PVN, VMN, and DMN compared with controls, 60 min postinjection. Indomethacin prevented the pyrexia and normalized hypothalamic NPY levels. As NPY concentrations were not increased in the ARC (the hypothalamic site of synthesis), we suggest that the increased NPY levels may result from blocked release, which would be in accord with the known experimental effects of NPY.

A high level of male sexual activity is necessary for the activation of the medial preoptic area and the arcuate nucleus during the ‘male effect’ in anestrous goats

2016 ◽  
Vol 165 ◽  
pp. 173-178 ◽  
Author(s):  
Marie Bedos ◽  
Wendy Portillo ◽  
Jean-Philippe Dubois ◽  
Gerardo Duarte ◽  
José A. Flores ◽  
...  
Keyword(s):  
Sexual Activity ◽  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Male Effect ◽  
High Level

scholarly journals Arcuate nucleus kisspeptin response to increased nutrition in rams

2019 ◽  
Vol 31 (11) ◽  
pp. 1682 ◽  
Author(s):  
S. E. Rietema ◽  
P. A. R. Hawken ◽  
C. J. Scott ◽  
M. N. Lehman ◽  
G. B. Martin ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Preoptic Area ◽  
Pulse Generator ◽  
Pulse Frequency ◽  
Nutritional Supplementation ◽  
Environmental Cues ◽  
Dorsomedial Hypothalamus ◽  
Gonadotrophin Releasing Hormone ◽  
Kndy Neurons

Rams respond to acute nutritional supplementation by increasing the frequency of gonadotrophin-releasing hormone (GnRH) pulses. Kisspeptin neurons may mediate the effect of environmental cues on GnRH secretion, so we tested whether the ram response to nutrition involves activation of kisspeptin neurons in the arcuate nucleus (ARC), namely kisspeptin, neurokin B, dynorphin (KNDy) neurons. Rams were given extra lupin grain with their normal ration. Blood was sampled before feeding, and continued until animals were killed for collection of brain tissue at 2 or 11h after supplementation. In supplemented rams, LH pulse frequency increased after feeding, whereas control animals showed no change. Within the caudal ARC, there were more kisspeptin neurons in supplemented rams than in controls and a higher proportion of kisspeptin cells coexpressed Fos, regardless of the time the rams were killed. There were more Fos cells in the mid-ARC and mid-dorsomedial hypothalamus of the supplemented compared with control rams. No effect of nutrition was found on kisspeptin expression in the rostral or mid-ARC, or on GnRH expression in the preoptic area. Kisspeptin neurons in the caudal ARC appear to mediate the increase in GnRH and LH production due to acute nutritional supplementation, supporting the hypothesised role of the KNDy neurons as the pulse generator for GnRH.

The role of neuropeptide Y (NPY) in the control of LH secretion in the ewe with respect to season, NPY receptor subtype and the site of action in the hypothalamus

1995 ◽  
Vol 147 (3) ◽  
pp. 565-579 ◽  
Author(s):  
M L Barker-Gibb ◽  
C J Scott ◽  
J H Boublik ◽  
I J Clarke
Keyword(s):  
Neuropeptide Y ◽  
Breeding Season ◽  
Preoptic Area ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Suppressive Effect ◽  
Plasma Prolactin ◽  
Post Injection ◽  
Lh Secretion ◽  
Saline Vehicle

Abstract Neuropeptide Y1–36 (NPY1–36) acts through Y1 and Y2 receptors while the C-terminal NPY fragments NPY18–36 and N-acetyl[Leu28,31]pNPY24–36 act only through the Y2 receptor. We have investigated the effects of intracerebroventricular (i.c.v.) administration of NPY1–36, NPY18–36 and N-acetyl[leu28,31]pNPY24–36 on LH secretion in the ovariectomised (OVX) ewe. These peptides were administered into a lateral ventricle (LV) or the third ventricle (3V) of OVX ewes during the non-breeding and breeding seasons. Microinjections of NPY were also made into the preoptic area (POA) during both seasons to investigate the effects of NPY at the level of the GnRH cell bodies. Tamed sheep were fitted with 19 gauge guide tubes into the LV, 3V or the septo-preoptic area (POA). Jugular venous blood samples were taken every 10 min for 3 h. Sheep were then given NPY1–36 (10 μg), NPY18–36 (100 μg) or saline vehicle into the LV; N-acetyl[Leu28,31]pNPY24–36 (100 μg), NPY1–36 (10 μg or 100 μg), NPY18–36 (10 μg or 100 μg) or saline vehicle into the 3V, or NPY1–36 (1 μg, 5 μg, 10 μg) into the POA. Blood sampling continued for a further 3 h. LH was measured in plasma by radioimmunoassay. LV or 3V injection of 10 μg NPY1–36 caused a small but significant (P<0·025) increase in the interval from the last pre-injection pulse of LH to the first post-injection LH pulse during the breeding season. Other LH pulse parameters were not significantly affected. NPY18–36 did not produce any significant change in LH pulsatility when injected into the LV, and neither peptide had any effect on plasma prolactin or GH levels. There was a significant (P<0·01) reduction in LH pulse frequency after 3V injection of 10 μg and 100 μg NPY and 100 μg NPY18–36. Pulse amplitude was reduced by 3V administration of the Y2 agonist, N-acetyl[Leu28–31]pNPY24–36 and 100 μ NPY18–36. When the amplitude of the first post-injection LH pulse was analysed, 10 μg NPY also had a significant (P<0·05) suppressive effect. During the non-breeding season, 100 μg NPY1–36 (but not 10 μg) decreased (P<0·01) LH pulse frequency. LH pulse amplitude was significantly (P<0·01) decreased by 100 μg NPY18–36. Doses of 10 μg NPY1–36 and 100 μg NPY18–36 had greater inhibitory effects on pulse frequency during the breeding season but the suppressive effect of 100 μg NPY was similar between seasons. Microinjections of NPY into the POA decreased (P<0·01) average plasma LH levels during the non-breeding season at a dose of 10 μg but did not significantly affect pulse frequency or amplitude. We conclude that a substantial component of the inhibitory action of NPY on LH secretion in the absence of steroids is mediated by the Y2 receptor. This inhibition is probably exerted by way of a presynaptic action on GnRH terminals in the median eminence as NPY does not modulate the frequency or amplitude of LH pulses at the level of the GnRH cell bodies in the POA. Journal of Endocrinology (1995) 147, 565–579

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