1 / 14

Stress responses and the HPA axis

Stress responses and the HPA axis. Define stressors Describe chain of events = stress response Autonomic system Endocrine system, specifically: HPA axis 1. Time course of response 2. Balance of 2 receptors 3. Pathologies 4. Gene regulation Individual differences Epigenetics.

davis-witt
Download Presentation

Stress responses and the HPA axis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Stress responses and the HPA axis • Define stressors • Describe chain of events = stress response • Autonomic system • Endocrine system, specifically: • HPA axis • 1. Time course of response • 2. Balance of 2 receptors • 3. Pathologies • 4. Gene regulation • Individual differences • Epigenetics

  2. What is stress? • Stressor: • Stimulus that threatens animal’s physiological homeostasis (Kloets et al., 2005) • Physical vs. Psychological (Environmental vs. Predicted) • Stress Response: • Active maintenance of physiological homeostasis • Autonomic (Fight or Flight) • Hypothalamic-Pituitary-Adrenocortical (HPA) systems

  3. Fight or Flight Response Stressor Sympathetic Nervous System/ Catecholamines ‘Fight or Flight’

  4. Stressor Brain Stem (e.g. LC) Stressor PVN http://www.biology.ucr.edu/people/faculty/Garland/HPA_axis.jpg

  5. Corticosteroid Receptors • Two types – Both respond to corticosteroids • Mineralocorticoid Receptor (MR): • Appraisal, initial stress response • Important in gene transcription activity • More sensitive to corticosteroids (10x) • Glucocorticoid Receptor (GR): • Terminates stress response for recovery (i.e. decrease CRH production) • Increased sensitivity to corticosteroids during stress • High density in PVN, aminergic & Hipp • Promotes stressor-related memory storage

  6. MR x GR

  7. Chronically Stressed Animal • Prolonged and/or repeated exposure to stressor (i.e. prolonged increase in corticosteroids) can have maladaptive consequences • Hypertension, type-II diabetes, ulcers, etc. • Chronic stress  Neuroendocrine change • hippocampal (CA3) atrophy, reduced proliferation (MR) • GRs and MRs downregulated • Diminished Denate Granule cell turnover rate • Reduced 5-HT receptor function • Reduced LTP/Facilitated LTD • Produce a Stress-typology • ‘Coping’ can disrupt maladaptive changes • [What behaviours, Sheng] lead to higher hippocampal GR gene expression and decreased anxiety-related behaviour • Stress experience (stressors and coping) and genetic background cause long-term changes

  8. Summary Stressors activate sympathetic and HPA systems Glucocorticoids regulate stress response through MR and GR interaction Prolonged stress  physiological problems and neuroendocrine functioning Individual differences in genetics and experience important in stress response

  9. STRESS and steroids Cortisol ..is behind it all • Cortisol is a glucocorticoid (a steroid hormone), released from the adrenal glands that are perched ‘on top’ of the kidneys • AFFERENT: Its release is controlled by Adrenocorticotropic hormone(ACTH), a hormone secreted into the blood stream from the anterior pituitary. • ACTH is controlled by Corticotropin-releasing hormone (CRH) a hormone and neurotransmitter released by the hypothalamus. • EFFERENT: Cortisol inhibits CRH release, in a negative-feedback loop. • Beyond the HPA axis (see above), mineralocorticoid and glucocorticoid receptors in the brain respond to adrenal products like cortisol to evoke fast, sympathetic (MR) responses and slow, parasymathetic (GR) recovery. [see also K+S figs 49-12, 13]

  10. STRESSOther Concepts • Binary action: fast response v. slow recovery phases (Box1,3) • Neural effects of MR and GRs (Box 2): • Rapid: not well understood – protein conformational changes, • glutamate release in hippocampus • Longer-lasting: up-regulation of transcription via GREs, • down-regulation of transcription via TFs • Chronic stress can reduce synaptic branching and #s, reduced new cell proliferation in dentate gyrus, reduced DA levels, and positive-feedback CRH-noradrenaline loop. • Box 3 – numerous relations between stress responses and risk factors for depression.

More Related