Neurochemical Systems Regulating the Hypothalamo-Pituitary-Adrenocortical Axis

Herman, James P.; Figueiredo, Helmer F.; Mueller, Nancy K.; Ostrander, Michelle M.; Zhang, R.; Tauchi, Miyuki; Choi, Dennis C.; Furay, Amy R.; Evanson, Nathan K.; Nelson, E. B.; Ulrich‐Lai, Yvonne M.

doi:10.1007/978-0-387-30405-2_13

Cited by 5 publications

(13 citation statements)

References 467 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The PVN is a target for numerous stress-excitatory neuropeptidergic neurons, including angiotensin II (subfornical organ), glucagon-like peptide 1 (from the NTS), alpha-MSH (from the arcuate nucleus) and neuropeptide Y (multiple sources), to name a few (75). Peptidergic innervation largely emanates from viscerosensory relays and may in part underlie HPA axis activation in response to fluid/electrolyte balance (subfornical inputs), cardiovascular challenge (NTS), visceral illness (NTS) and metabolic imbalance (arcuate nucleus).…”

Section: Dynamics Of the Hpa Axis ‘Stress Response’mentioning

confidence: 99%

See 1 more Smart Citation

Regulation of the Hypothalamic‐Pituitary‐Adrenocortical Stress Response

Herman

McKlveen

Ghosal

et al. 2016

Comprehensive Physiology

1,199

946

View full text Add to dashboard Cite

The hypothalamo-pituitary-adrenocortical (HPA axis) is required for stress adaptation. Activation of the HPA axis causes secretion of glucocorticoids, which act on multiple organ systems to redirect energy resources to meet real or anticipated demand. The HPA stress response is driven primarily by neural mechanisms, invoking corticotrophin releasing hormone (CRH) release from hypothalamic paraventricular nucleus (PVN) neurons. Pathways activating CRH release are stressor dependent: reactive responses to homeostatic disruption frequently involve direct noradrenergic or peptidergic drive of PVN neurons by sensory relays, whereas anticipatory responses use oligosynaptic pathways originating in upstream limbic structures. Anticipatory responses are driven largely by disinhibition, mediated by trans-synaptic silencing of tonic PVN inhibition via GABAergic neurons in the amygdala. Stress responses are inhibited by negative feedback mechanisms, whereby glucocorticoids act to diminish drive (brainstem), promote trans-synaptic inhibition by limbic structures (e.g, hippocampus). Glucocorticoids also act at the PVN to rapidly inhibit CRH neuronal activity via membrane glucocorticoid receptors. Chronic stress-induced activation of the HPA axis takes many forms (chronic basal hypersecretion, sensitized stress responses, even adrenal exhaustion), with manifestation dependent upon factors such as stressor chronicity, intensity, frequency and modality. Neural mechanisms driving chronic stress responses can be distinct from those controlling acute reactions, including recruitment of novel limbic, hypothalamic and brainstem circuits. Importantly, an individual’s response to acute or chronic stress is determined by numerous factors, including genetics, early life experience, environmental conditions, sex and age. The context in which stressors occur will determine whether an individual’s acute or chronic stress responses are adaptive or maladaptive (pathological).

show abstract

Section: Dynamics Of the Hpa Axis ‘Stress Response’mentioning

confidence: 99%

“…Some candidates include enkephalin, somatostatin, and melanin concentrating hormone, to name a few (75). Once again, neuropeptides are often (though not always) co-localized with classical transmitters, and may serve the role of augmenting or diminishing the impact of the primary signaling molecule.…”

Section: Dynamics Of the Hpa Axis ‘Stress Response’mentioning

confidence: 99%

Regulation of the Hypothalamic‐Pituitary‐Adrenocortical Stress Response

Herman

McKlveen

Ghosal

et al. 2016

Comprehensive Physiology

1,199

946

View full text Add to dashboard Cite

show abstract

“…Serotonin and noradrenalin are strongly associated with circadian rhythms (see [52] for review), and serotonin is recognized as a mediator of deep sleep [53]. Moreover, a deficient serotonin system is strongly associated with major depression [54].…”

Section: Dysfunctional Transmitter Systems In Fibromyalgiamentioning

confidence: 99%

“…For example, deficient noradrenergic modulatory function is hypothesized to increase the vulnerability to stress-related pathology [58]. In line with this hypothesis, all of the neurotransmitters systems found to be altered in fibromyalgia exert influences on the sympathetic nervous system or the HPA axis stress system (see [52, 59] for review; see Table 1). …”

Section: The Role Of Altered Transmitters In Stress Systemsmentioning

confidence: 99%

“…In addition to increasing pain sensitivity, alterations in serotonin, noradrenalin, and substance P may contribute to disturbances in sleep or mood in fibromyalgia patients. Serotonin and noradrenalin are strongly associated with circadian rhythms (see [ 52 ] for review), and serotonin is recognized as a mediator of deep sleep [ 53 ]. Moreover, a deficient serotonin system is strongly associated with major depression [ 54 ].…”

Section: Dysfunctional Transmitter Systems In Fibromyalgiamentioning

confidence: 99%

See 1 more Smart Citation

Dysfunctional Neurotransmitter Systems in Fibromyalgia, Their Role in Central Stress Circuitry and Pharmacological Actions on These Systems

Becker

Schweinhardt

2012

Pain Research and Treatment

View full text Add to dashboard Cite

Fibromyalgia is considered a stress-related disorder, and hypo- as well as hyperactive stress systems (sympathetic nervous system and hypothalamic-pituitary-adrenal axis) have been found. Some observations raise doubts on the view that alterations in these stress systems are solely responsible for fibromyalgia symptoms. Cumulative evidence points at dysfunctional transmitter systems that may underlie the major symptoms of the condition. In addition, all transmitter systems found to be altered in fibromyalgia influence the body's stress systems. Since both transmitter and stress systems change during chronic stress, it is conceivable that both systems change in parallel, interact, and contribute to the phenotype of fibromyalgia. As we outline in this paper, subgroups of patients might exhibit varying degrees and types of transmitter dysfunction, explaining differences in symptomatoloy and contributing to the heterogeneity of fibromyalgia. The finding that not all fibromyalgia patients respond to the same medications, targeting dysfunctional transmitter systems, further supports this hypothesis.

show abstract

Endocrine Testing in Acute and Critical Illness

Morovat¹

2018

Endocrine and Metabolic Medical Emergencies

View full text Add to dashboard Cite

Neurochemical Systems Regulating the Hypothalamo-Pituitary-Adrenocortical Axis

Cited by 5 publications

References 467 publications

Regulation of the Hypothalamic‐Pituitary‐Adrenocortical Stress Response

Regulation of the Hypothalamic‐Pituitary‐Adrenocortical Stress Response

Dysfunctional Neurotransmitter Systems in Fibromyalgia, Their Role in Central Stress Circuitry and Pharmacological Actions on These Systems

Endocrine Testing in Acute and Critical Illness

Contact Info

Product

Resources

About