Review: Central non-glucocorticoid inhibitors of the hypothalamo-pituitary-adrenal axis

Jessop, DS

doi:10.1677/joe.0.1600169

Cited by 84 publications

(54 citation statements)

References 133 publications

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“…40 Exposure to stress activates the HPA axis, which is modulated by inhibitory tone imposed by GABAergic neurons on PVN CRH neurons. 12,10 Thus, greater inhibition might induce the blunted ACTH and cortisol responses observed in our study in subjects homozygous for the C allele compared to subjects heterozygous or homozygous for the T allele. Our findings are in concordance with those of a previous study that suggested a role for the GABRA6 polymorphism in the predisposition to hypercortisolism, showing the same direction of association, with higher postprandial salivary cortisol in homozygotes for the T allele in comparison to heterozygotes.…”

Section: Discussionmentioning

confidence: 62%

“…8,10 Modulation of the stress response includes glucocorticoid (GC) feedback at the hippocampal and hypothalamic levels 11 and regulation by neuronal pathways, including the GABAergic inhibitory system. 12 The neurotransmitter GABA, which is the main inhibitory neurotransmitter in the mammalian central nervous system (CNS), inhibits the HPA axis through its actions on GABA receptors expressed by corticotrophin-releasing hormone (CRH) neurons within the paraventricular nucleus (PVN) of the hypothalamus.…”

mentioning

confidence: 99%

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GABRA6 gene polymorphism and an attenuated stress response

et al. 2004

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The glucocorticoid component of the stress response has been the subject of intense scientific scrutiny because of the wide ranging pathological consequences resulting from excess glucocorticoid exposure, including mood and anxiety disorders, and cognitive impairment. Exposure to stress activates the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic adrenomedullary system, which are regulated by neuronal pathways, including the inhibitory GABAergic (c-aminobutyric acid) system. Approximately 60% of the variance in glucocorticod levels may be attributable to genetic individual differences. In the present study, 56 healthy subjects underwent genotyping to determine the influence of the T1521C single nucleotide polymorphism (SNP) in the GABA A a6 receptor subunit gene (GABRA6) on the hormonal and autonomic responses to psychological stress induced by the Trier Social Stress Test (TSST). Adrenocorticotropin (ACTH), cortisol, diastolic blood pressure, and mean blood pressure responses to the TSST were significantly greater in subjects homozygous for the T allele or heterozygous compared to subjects homozygous for the C allele. Behavioral data was collected employing the Revised NEO Personality Inventory (NEO PI-R); subjects homozygous for the C allele scored significantly lower on the Extraversion factor compared to subjects homozygous for the T allele or heterozygous. These results suggest that the T1521C polymorphism in the GABRA6 gene is associated with specific personality characteristics as well as a marked attenuation in hormonal and blood pressure responses to psychological stress.

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Section: Discussionmentioning

confidence: 62%

mentioning

confidence: 99%

GABRA6 gene polymorphism and an attenuated stress response

et al. 2004

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“…This is in agreement with what has been observed in other species. Human and animal studies have established that endogenous opioids can inhibit the hypothalamus-pituitaryadrenal (HPA) axis, and naloxone administration can stimulate ACTH and glucocorticoids secretion (Jessop 1999). On the other hand, acute opioid blockade failed to induce a DHEA-S response in humans, although it was associated with cortisol release (Ceballos et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone secretion in dairy cattle is episodic and unaffected by ACTH stimulation

Marinelli

Trevisi

Dalt

et al. 2007

Journal of Endocrinology

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This paper describes the episodic release and response to adrenal stimulation of cortisol and dehydroepiandrosterone (DHEA) in cows. Observations made in samples taken every 10 min for 8 h (experiment 1) showed that plasma DHEA was significantly greater (P!0 . 001) than DHEA-S, and release of these steroids was episodic and variable between animals (P!0 . 01). No relationship was found between DHEA and cortisol. Significant (P!0 . 001) DHEA-sulphate (DHEA-S) versus cortisol (RZK0 . 264) and DHEA-S versus DHEA (RZ0 . 200) correlations were found. DHEA and DHEA-S were not affected by a single ACTH challenge (experiment 2). In experiment 3, cortisol and DHEA secretions in response to prolonged ACTH administration (every 12 h for 6 days) were studied. On day 7, the episodic cortisol and DHEA release and response to the opioid antagonist naloxone were studied in blood samples taken every 10 min for 8 h. Animals were injected with naloxone after 4 h. A significant increase (P!0 . 05) in mean circulating DHEA and DHEA pulse amplitude was observed during frequent sampling following ACTH treatment. DHEA and DHEA-S plasma concentrations were not affected following luteal regression (experiment 4). The effect of milk secretion around parturition on DHEA secretion was studied in dry and continuously milked cows (experiment 5). Plasma DHEA was significantly lower (P!0 . 05) in milked cows. In the cow, ACTH is not an important DHEA secretagogue. Adrenal contribution to plasma DHEA is scarce. Likely, the placenta is the most important source of DHEA, and the lactating mammary gland can affect circulating DHEA levels. Investigation about the DHEA biological role in cows should be focused around parturition.

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“…It is stimulated by a wide variety of neurotransmitters such as serotonin, norepinephrine and glutamate and is inhibited by γ-aminobutyric acid (GABA), vasopressin, glucocorticoids and other neuropeptides (e.g. opioids, neurotensin, substance P) (Goldstein 1990;Clark et al 1997;Jessop 1999). Discharge of CRF into the hypophyseal-portal system initiates production of adrenocorticotrophic hormone (ACTH) by cells in the anterior pituitary.…”

Section: Stress Responsementioning

confidence: 99%

Factors affecting beef palatability — farmgate to chilled carcass

Ferguson¹,

Bruce²,

Thompson³

et al. 2001

Aust. J. Exp. Agric.

116

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Abstract. The potential eating quality of beef is set by the intrinsic structural and compositional characteristics of muscle. However, the extrinsic factors that prevail during the production of the animal, slaughter and processing of its carcass and finally, cooking can produce changes in these structural and compositional characteristics that ultimately manifest as large variations in beef palatability. The conditions that apply in the 24-48 h immediately before and after slaughter are recognised as having the largest influence on beef palatability. This review specifically examines the critical pre-and post-slaughter factors and discusses their putative effects on biochemical and physical changes in muscle and the consequences to beef palatability. Areas for future research within this domain are also discussed.

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Review: Central non-glucocorticoid inhibitors of the hypothalamo-pituitary-adrenal axis

Cited by 84 publications

References 133 publications

GABRA6 gene polymorphism and an attenuated stress response

GABRA6 gene polymorphism and an attenuated stress response

Dehydroepiandrosterone secretion in dairy cattle is episodic and unaffected by ACTH stimulation

Factors affecting beef palatability — farmgate to chilled carcass

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Review: Central non-glucocorticoid inhibitors of the hypothalamo-pituitary-adrenal axis

Cited by 84 publications

References 133 publications

GABRA6 gene polymorphism and an attenuated stress response

GABRA6 gene polymorphism and an attenuated stress response

Dehydroepiandrosterone secretion in dairy cattle is episodic and unaffected by ACTH stimulation

Factors affecting beef palatability &mdash; farmgate to chilled carcass

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Factors affecting beef palatability — farmgate to chilled carcass