Abstract
Stress is the physiologic response to adverse stimuli that strain homeostatic mechanisms and elicit changes in behavior. As an energy-expensive function non-essential for the survival of the individual, reproduction is particularly vulnerable to the suppressive effects of stress. The stress response is driven by the hypothalamo-pituitary-adrenal (HPA) axis and crosstalk with the reproductive axis is commonly assumed. GnRH neurons form the apex of the hypothalamo-pituitary-gonadal (HPG) axis, their neuroendocrine activity encoding instructions that maintain reproductive homeostasis. They are under the stringent control of a myriad neural systems that compute the demands of the organism and prevailing environmental stimuli. The function of GnRH neurons is susceptible to the deleterious effects of stress, although the mechanisms involved are not well understood. A number of discrete neural circuits that are activated in response to stress have also been demonstrated to regulate GnRH neurosecretion. Of these, neurons containing the neuropeptides corticotropin-releasing factor (CRF), neurokinin B (NKB), RFamide related peptide 3 (RFRP-3) and calcitonin gene related peptide (CGRP), are of particular interest, as are hypothalamic and amygdalar γ-aminobutyric acid (GABA)-ergic neurons. Further, stress hormones are able to interact with downstream effectors of the HPG axis within the pituitary and gonads, impinging on reproductive function. In this chapter we explore the role of the GnRH neuron in the wider context of stress effects on reproductive function, addressing key discoveries and methodological breakthroughs that aid our understanding of the complex mechanisms by which stress impacts on reproduction.
Original language | English |
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Title of host publication | The GnRH Neuron and its Control |
Publisher | WILEY-BLACKWELL |
Pages | 357-381 |
Number of pages | 25 |
ISBN (Electronic) | 9781119233275 |
ISBN (Print) | 9781119233244 |
DOIs | |
Publication status | Published - 5 Apr 2018 |
Keywords
- GnRH neuronal network
- LH secretion
- Maternal stress response
- Mouse models
- Neuroendocrine mechanisms
- Reproductive function