Changes in extracellular LHRH and β-endorphin-like immunoreactivity in the nucleus infundibularis-median eminence of anestrous ewes under stress condition

Tomaszewska, D.; Mateusiak, Krystyna; Przekop, F

doi:10.1007/s007020050156

Cited by 11 publications

(3 citation statements)

References 25 publications

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“…However, because progesterone was not present in our ovariectomized ewes, it would not cause these changes. Finally, we also observed seasonal changes in ␤-EN input to GnRH dendrites (increase) that did not correlate with this response and thus these changes may reflect other actions of opioids in modulating GnRH secretion (89,90).…”

Section: Seasonal Variation In Gnrh Inputsmentioning

confidence: 78%

Seasonal Plasticity within the Gonadotropin-Releasing Hormone (GnRH) System of the Ewe: Changes in Identified GnRH Inputs and Glial Association

et al. 2003

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The annual reproductive cycle in sheep may reflect a functional remodeling within the GnRH system. Specifically, changes in total synaptic input and association with the polysialylated form of neural cell adhesion molecule have been observed. Whether seasonal changes in a specific subset(s) of GnRH inputs occur or whether glial cells specifically play a role in this remodeling is not clear. We therefore examined GnRH neurons of breeding season (BS) and nonbreeding season (anestrus) ewes and tested the hypotheses that specific (i.e. gamma-aminobutyric acid, catecholamine, neuropeptide Y, or beta-endorphin) inputs to GnRH neurons change seasonally, and concomitant with any changes in neural inputs is a change in glial apposition. Using triple-label immunofluorescent visualization of GnRH, glial acidic fibrillary protein and neuromodulator/neural terminal markers combined with confocal microscopy and optical sectioning techniques, we confirmed that total numbers of neural inputs to GnRH neurons vary with season and demonstrated that specific inputs contribute to these overall changes. Specifically, neuropeptide Y and gamma-aminobutyric acid inputs to GnRH neurons increased during BS and beta-endorphin inputs were greater during either anestrus (GnRH somas) or BS (GnRH dendrites). Associated with the changes in GnRH inputs were seasonal changes in glial apposition, glial acidic fibrillary protein density, and the thickness of glial fibrils. These findings are interpreted to suggest an increase in net stimulatory inputs to GnRH neurons during the BS contributes to the seasonal changes in GnRH neurosecretion and that this increased innervation is perhaps stabilized by glial processes.

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Section: Seasonal Variation In Gnrh Inputsmentioning

confidence: 78%

Seasonal Plasticity within the Gonadotropin-Releasing Hormone (GnRH) System of the Ewe: Changes in Identified GnRH Inputs and Glial Association

et al. 2003

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“…The increase in plasma level of this hormone proves the activation of the HPA stress axis, which can suppress the activity of the HPG axis [ 62 – 64 ]. It has been documented that stress causes changes in the activity of the HPG axis, and the nature of these changes depends on the type of stressor, duration of exposure to that stressor and physiological state of the animal [ 65 , 66 ]. Hormones and peptides released during stress response play an important role in modulating the influence of stress on the reproductive functions of the organism.…”

Section: Discussionmentioning

confidence: 99%

Effect of CD14/TLR4 antagonist on GnRH/LH secretion in ewe during central inflammation induced by intracerebroventricular administration of LPS

Haziak

Herman

Wojtulewicz

et al. 2018

J Animal Sci Biotechnol

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BackgroundImmune stress induced by lipopolysaccharide (LPS) influences the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) secretion. Presence of LPS interacting Toll-like receptor (TLR) 4 in the hypothalamus may enable the direct action of LPS on the GnRH/LH secretion. So, the aim of the study was to investigate the influence of intracerebroventricular (icv) injection of TLR4 antagonist on GnRH/LH secretion in anestrous ewes during LPS-induced central inflammation. Animals were divided into three groups icv-treated with: Ringer-Locke solution, LPS and TLR4 antagonist followed by LPS.ResultsIt was demonstrated that TLR4 antagonist reduced LPS-dependent suppression of GnRH gene expression in the preoptic area and in the medial basal hypothalamus, and suppression of receptor for GnRH gene expression in the anterior pituitary gland. It was also shown that TLR4 antagonist reduced suppression of LH release caused by icv injection of LPS. Central administration of LPS stimulated TLR4 gene expression in the medial basal hypothalamus.ConclusionsIt was indicated that blockade of TLR4 prevents the inhibitory effect of centrally acting LPS on the GnRH/LH secretion. This suggests that some negative effects of bacterial infection on the hypothalamic-pituitary-gonadal axis activity at the hypothalamic level may be caused by central action of LPS acting through TLR4.

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“…Two interesting studies that have provided this link determined that treatment with naloxone, an endogenous opioid peptide antagonist, increased the amplitude of GnRH pulses in ovariectomized ewes (34) and castrated rams (21). This is noteworthy because there is evidence that endogenous opioid peptides play an inhibitory role in GnRH pulsatile regulation and are increased in response to stress (21,(35)(36)(37). Clearly, further work is needed to determine whether endogenous opioid peptides, or other inhibitory molecules, mediate the suppression of GnRH pulse amplitude in response to psychosocial stress.…”

Section: Discussionmentioning

confidence: 99%

Psychosocial Stress Inhibits Amplitude of Gonadotropin-Releasing Hormone Pulses Independent of Cortisol Action on the Type II Glucocorticoid Receptor

et al. 2009

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Our laboratory has developed a paradigm of psychosocial stress (sequential layering of isolation, blindfold, and predator cues) that robustly elevates cortisol secretion and decreases LH pulse amplitude in ovariectomized ewes. This decrease in LH pulse amplitude is due, at least in part, to a reduction in pituitary responsiveness to GnRH, caused by cortisol acting via the type II glucocorticoid receptor (GR). The first experiment of the current study aimed to determine whether this layered psychosocial stress also inhibits pulsatile GnRH release into pituitary portal blood. The stress paradigm significantly reduced GnRH pulse amplitude compared with nonstressed ovariectomized ewes. The second experiment tested if this stress-induced decrease in GnRH pulse amplitude is mediated by cortisol action on the type II GR. Ovariectomized ewes were allocated to three groups: nonstress control, stress, and stress plus the type II GR antagonist RU486. The layered psychosocial stress paradigm decreased GnRH and LH pulse amplitude compared with nonstress controls. Importantly, the stress also lowered GnRH pulse amplitude to a comparable extent in ewes in which cortisol action via the type II GR was antagonized. Therefore, we conclude that psychosocial stress reduces the amplitude of GnRH pulses independent of cortisol action on the type II GR. The present findings, combined with our recent observations, suggest that the mechanisms by which psychosocial stress inhibits reproductive neuroendocrine activity at the hypothalamic and pituitary levels are fundamentally different. (Endocrinology 150: 762-769, 2009) V arious types of stress potently stimulate the hypothalamic-pituitary-adrenal axis and simultaneously suppress reproductive neuroendocrine activity. For example, psychosocial stress increases circulating levels of glucocorticoids and inhibits pulsatile LH secretion (1-4). Recent studies in ovariectomized sheep have demonstrated that a stress-like elevation of plasma cortisol decreases pulsatile LH secretion in the absence of stress and that this occurs via suppression of pituitary responsiveness to GnRH (5-7). This effect of cortisol, which reflects a direct action on the pituitary and mediation by the type II glucocorticoid receptor (GR), occurs without concurrent inhibition of pulsatile GnRH secretion (6,8,9). Our laboratory has recently described a paradigm of psychosocial stress that consists of sequential layering of isolation, restraint, blindfold, and predator cues (barking dog sound and odor) (10). This model of psychosocial stress ("layered stress paradigm") causes a robust elevation in circulating cortisol along with a profound decrease in LH pulse amplitude and steroidinduced sexual behavior in ovariectomized ewes (10, 11). The decrease in LH pulse amplitude was observed not only in ovariectomized ewes in which LH pulses were driven by endogenous GnRH pulses, it was also evident in a pituitary-clamp model in which endogenous GnRH pulses were blocked and LH pulses were driven by fixed hourly boluses of exogenous...

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Changes in extracellular LHRH and β-endorphin-like immunoreactivity in the nucleus infundibularis-median eminence of anestrous ewes under stress condition

Cited by 11 publications

References 25 publications

Seasonal Plasticity within the Gonadotropin-Releasing Hormone (GnRH) System of the Ewe: Changes in Identified GnRH Inputs and Glial Association

Seasonal Plasticity within the Gonadotropin-Releasing Hormone (GnRH) System of the Ewe: Changes in Identified GnRH Inputs and Glial Association

Effect of CD14/TLR4 antagonist on GnRH/LH secretion in ewe during central inflammation induced by intracerebroventricular administration of LPS

Psychosocial Stress Inhibits Amplitude of Gonadotropin-Releasing Hormone Pulses Independent of Cortisol Action on the Type II Glucocorticoid Receptor

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