The hypothalamic–neurohypophysial system regulates the hypothalamic–pituitary–adrenal axis under stress: An old concept revisited

  title={The hypothalamic–neurohypophysial system regulates the hypothalamic–pituitary–adrenal axis under stress: An old concept revisited},
  author={Mario Engelmann and Rainer Landgraf and Carsten T. Wotjak},
  journal={Frontiers in Neuroendocrinology},

The Hypothalamic-Pituitary-Adrenal Axis : The Actions of the Central Nervous System and Potential Biomarkers

By understanding the pathways that can lead to altered HPA axis activity and by using biomarkers to assess HPA functionality, health care practitioners can make more informed clinical decisions to enhance patient care.

The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress

The role of the HPA axis in the integration of adaptive responses to stress is discussed and the major neuronal and endocrine systems that contribute to the regulation of theHPA axis and the maintenance of homeostasis in the face of aversive stimuli are identified.

The effects of apelin on hypothalamic–pituitary–adrenal axis neuroendocrine function are mediated through corticotrophin-releasing factor- and vasopressin-dependent mechanisms

The data confirm that the in vivo effects of apelin on hypothalamic–pituitary–adrenal neuroendocrine function appear to be mediated through both CRF- and AVP-dependent mechanisms.

Temazepam Triggers the Release of Vasopressin into the Rat Hypothalamic Paraventricular Nucleus: Novel Insight into Benzodiazepine Action on Hypothalamic–Pituitary–Adrenocortical System Activity During Stress

Temazepam modulates the central nervous regulation of the HPA axis by altering intra-PVN AVP release and an increasingly released AVP of magnocellular origin seems to provide a negative tonus on ACTH secretion most probably via inhibiting the release of ACTH secretagogues from the median eminence into hypophyseal portal blood.

Estrogens and neuroendocrine hypothalamic-pituitary-adrenal axis function.

Estrogen treatment of aging rats normalized the response to stress, restored the dexamethasone inhibition of the stress response and increased GR density in defined hippocampal areas, and contributed to stabilize the function of the HPA axis.



Neuroendocrine pharmacology of stress.

The Activity of the Hypothalamo-Neurohypophysial System in Response to Acute Stressor Exposure: Neuroendocrine and Electrophysiological Observations

Observations on stress-induced alterations of the electrical and secretory activity of vasopressin (AVP) and oxytocin (OXT) neurones originating within the supraoptic nucleus (SON) and constituting the hypothalamo-neurohypophysial system (HNS) in the male rat shed new light on the neurone–neurone and glial–neuronone interactions that ensure an appropriate neuroendocrine stress response.

Brain Oxytocin Inhibits Basal and Stress‐Induced Activity of the Hypothalamo‐Pituitary‐Adrenal Axis in Male and Female Rats: Partial Action Within the Paraventricular Nucleus

A novel, gender‐independent physiological function of endogenous brain oxytocin in the regulation of neuroendocrine stress responses is demonstrated in both male and virgin female rats.

Alterations in Central Neuropeptide Expression, Release, and Receptor Binding in Rats Bred for High Anxiety: Critical Role of Vasopressin

The elevated expression and release of AVP within the PVN of HAB rats together with the behavioral effects of the AVP V1-receptor antagonist suggest a critical involvement of this neuropeptide in neuroendocrine and behavioral phenomena associated with trait anxiety/depression.

Increased expression of corticotropin-releasing hormone and vasopressin messenger ribonucleic acid (mRNA) in the hypothalamic paraventricular nucleus during repeated stress: association with reduction in glucocorticoid receptor mRNA levels.

The data indicate that a CORT-mediated decrease in hippocampal and hypothalamic glucocorticoid receptor mRNA levels is not the only mechanism contributing to the maintenance of a robust HPA response after repeated stress and postulates that the relative shift from CRH to AVP in the PVN after repeated Stress is mediated by both a greater sensitivity of AVP to CORT negative feedback and Cort-independent mechanisms.