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HPA
Uni of Notts, Neurobiology of Disease, year 2, topic 10
| Term | Definition |
|---|---|
| HPA axis | A neuroendocrine system linking hypothalamus, pituitary, & adrenal gland to regulate stress responses |
| HPA pathway | Hypothalamus releases Corticotropin-releasing hormone (CRH) stimulating the anterior pituitary to release ACTH (Adrenocorticotropic Hormone) stimulating the adrenal cortex to release glucocorticoids (i.e., cortisol or corticosterone) |
| General structure of adrenal gland & three zones of the adrenal cortex & what they produce | Middle medulla, layer of cortex (zona layer) & capped by capsule. Zona glomerulosa (mineralocorticoids), zona fasciculata (glucocorticoids), & zona reticularis (androgens) |
| Neurotransmitters produced in the adrenal medulla | Catecholamines (e.g. adrenaline) from chromaffin cells for release into the blood |
| How hormonal (endocrine) & neurotransmitter (sympathetic systems) differ in adrenal activation | HPA → cortisol, longterm stress activation; SNS → stimulation of medulla by intermediolateral horn of the spinal cord rapid catecholamine release, short term fight-or-flight |
| Metabolic effects of cortisol | Increases gluconeogenesis, lipolysis, proteolysis; suppresses immunity |
| stress hormones differences between humans & rodents | Rodents mainly use corticosterone (not cortisone), with shorter half-life & circadian patterns |
| Suprachiasmatic Nucleus (SCN) | Master circadian clock regulating HPA axis via clock gene transcription (e.g., N-acetyltransferase) |
| Consequences of CLOCK gene alterations | Alters timing & amplitude of cortisol rhythms, disrupting circadian regulation instead of cortisol peaking just before wakeup like normal |
| Difference between acute & chronic stress | Acute stress is adaptive; chronic stress causes maladaptive physiological & psychological effects by progressively causing a more extreme stress phenotype |
| Long-term effects of chronic stress | Cardiovascular disease, hyperglycaemia, insulin resistance, immune suppression as well as gastrointestinal ulcers & dysfunction |
| Mineralocorticoid receptors (MR) | High-affinity receptors in limbic system, active at basal cortisol levels |
| Glucocorticoid receptors (GR) | Low-affinity receptors activated during stress or circadian peaks |
| CNS localisation of GRs | Hypothalamus (stress feedback), hippocampus (memory), brainstem (stress signalling) |
| Locus coeruleus | brainstem noradrenergic nucleus, coordinating arousal & stress responses as the pacemaker system |
| Why the locus coeruleus vulnerable to stress | High firing increases metabolic demand → burdens axonal maintainance & increases risk of catecholamine & glucocorticoid buildup |
| How glucocorticoids affect tau | Promotes tau hyperphosphorylation, disrupting axonal transport; |
| How catecholamines & neuromelanin contribute to oxidative stress | They bind metals & generate reactive oxygen species |
| c-Fos in stress studies | Marker of neuronal activation; increased expression indicates heightened stress response |
| How anxiety is measured in stressed mice | Less time spent in open arms of elevated plus maze |
| chronic cortisol in the hippocampus | Causes excitotoxicity & memory impairment |
| Correlation between depression & HPA abnormalities | 50% of patients with depression have HPA abnormalities |
| How Locus Coerulus stress affects Alzheimer's | Increases amyloid-β & neuroinflammation. c-Fos upregulation allows greater discharge of stress response circuits to baseline stimuli |
Created by:
Denny12