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FNS 3: H+H
Neuro Lecture 3: Hypothalamus + Homeostasis
| Question | Answer |
|---|---|
| In the classic view of HT & energy balance, the LH was thought to be the (what?) center | feeding center |
| In the classic view of HT & energy balance, stimulation of the LH was thought to do what? | elicit feeding |
| In the classic view of HT & energy balance, lesions of the LH were thought to do what? | reduce feeding |
| In the classic view of HT & energy balance, the VMH was thought to be the (what?) center | satiety center |
| In the classic view of HT & energy balance, stimulation of the VMH was thought to do what? | reduce feeding |
| In the classic view of HT & energy balance, lesions of the VMH were thought to do what? | increase feeding |
| In certain case studies (Reeves & Plum 1969), what were the effects described to accompany VMH lesions? | hyperphagia, rage, and dementia |
| How is the revised/current view of the HT & energy balance different than the classic view? | the current view is that both the LH and VMH play roles in feeding/metabolism- more important long term for body weight regulation than feeding |
| What is the new (named) hypothesis of HT & energy balance? | Set Point Hypothesis- the HT encodes a set point for body weight and defends against deviations by regulating food intake and/or caloric expenditure |
| What are 3 examples of peripheral hormones that regulate feeding? Where are they secreted from? | ghrelin (from gut), insulin (from pancreas), and leptin (from adipose) |
| When is ghrelin secreted? | to initiate feeding |
| When is insulin secreted? | to terminate feeding |
| When/why is leptin secreted? | for long-term energy balance |
| What does orexigenic mean? | promotes food intake |
| Which neuropeptide systems do leptin activate? Inhibit? | Activates anorexigenic neuropeptide systems and inhibits orexigenic neuropeptide systems |
| In the fat mice example, which neuropeptide was deficient/dysfunctional? | leptin |
| What was the population of O’Rahilly’s pediatric study? What were the results? | obese, leptin-deficient kids that responded well to leptin therapy |
| Does dry mouth play a large or small role in the physiological basis of thirst? | small |
| What are the two factors that must be balanced in fluid homeostasis? | fluid intake and “sodium appetite” |
| What was one fluid injection technique that stimulated drinking in animals? | hypertonic saline was injected into the rostral HT |
| Where are baroreceptors that facilitate autonomic responses for fluid homeostasis? | aortic arch, venous return, and lungs |
| Which structure of the HT is known as the hypothalamic ‘sensor’? What is it sensitive to? | OVLT (organum vasculosum of the lamina terminalis)- osmosensitive |
| Which structure of the HT is known as the hypothalamic ‘effector’? Where does it ‘effect’? | supraoptic nucleus (SON)- magnocellular vasopressin and oxytocin neurons project to posterior pituitary |
| What do OVLT neurons regulate? | activity of magnocellular neurosecretory cells in the supraoptic and paraventricular nuclei |
| What is another name for vasopressin (VP)? | ADH |
| What is diuresis? | urine production |
| What is natriuresis? | sodium excretion |
| What do VP and oxytocin do? | modulate diuresis and natriuresis |
| What is VP’s effect on antidiuresis (anti-urine production)? | decreases urine production |
| What is oxytocin’s effect on natriuresis (Na excretion)? | increases it |
| In a hypotonic state, what are the effects on thirst, vasopressin, oxytocin, and salt appetite? | decrease thirst, VP, OT; increase salt intake |
| In a hypertonic state, what are the effects on thirst, vasopressin, oxytocin, and salt appetite? | increase thirst, VP, OT; decrease salt intake |
| What are the major target organs for the release of ADH in fluid homeostasis? | kidneys (water resorption), vessels (vasoconstriction/dilation for BP) and thirst (behavioral respsonse) |
| Precise detection of small changes in body temperature and ability to enact appropriate regulatory mechanisms to deal with challenges is a function of which structure? | the hypothalamus |
| Which area contains the temperature reduction center? | anterior hypothalamus |
| At what point do changes in blood temperature activate thermosensitive neurons to activate behavioral cooling systems? (how big of a change in temperature) | less than 1 degree |
| Which area contains the heat conservation center? | posterior hypothalamus |
| Name the type of molecules that increase the body temperature “set-point” to induce a fever (and other sick behaviors like sleep, less appetite)? | pro-inflammatory cytokines (eg interleukins) |
| Where do cytokines access the brain? What type of organ is it? | the OVLT (organum vasculosum of the lamina terminalis)- it’s a circumventricular organ |
| Once cytokines access the brain (OVLT), what molecules are sent to the hypothalamus? How are they catalyzed? | prostoglandins (PGE-2) are catalyzed by cyclooxygenase |
| Once prostoglandins are formed, how is the temperature set point centrally regulated? | PGE-2 acts on the anterior hypothalamus/preoptic area to increase the temperature set point |
| Which part of the hypothalamus is important for stress responses? | anterior pituitary |
| What is the prototypical stress hormone? Where is it secreted from and what structure regulates its secretion? | cortisol release from the adrenal glands is regulated by the hypothalamus |
| What is the system that mediates stress interactions between brain and periphery? | HPA axis (hypothalamic-pituitary- adrenal axis) |
| What structure can stimulate the HPA axis? | amygdala |
| What type of receptors are common in the hippocampus? | glucocorticoid receptors |
| How does cortisol affect hippocampus function (memory formation) acutely? Chronically? | facilitates acutely, “deleterious” chronically |
| What did Rush (1996) find about cortisol? | they found non-suppression of cortisol in 27% of major depression subjects and 43% in bipolar individuals |
| What are some signs/symptoms of hypothalamus damage? | thermal dysregulation, eating/metabolic changes, sleep disturbances- they depend on the location/extent of damage |
| What is the condition of widespread damage of the hypothalamus called? | hypothalamic syndrome |
| Name 4 common causes of HT damage | 1)infections along cranial cavity floor, 2) fractures of skull base, 3) Thiamine (B1) deficiency, 4) Pituitary tumors |
| What is Korsakoff’s disease associated with? | alcoholism, memory disturbances (confabulations)- HT degeneration |
| What are pituitary tumors often associated with? | visual disturbances (tunnel vision- bitemporal hemianopsia) and endocrine abnormalities |
| What is the cause of Cushing’s syndrome? | pituitary tumor cells secrete high levels of ACTH |
| What are some symptoms of Cushing’s syndrome? | abdominal obesity, diabetes, HBP, muscle weakness, fatigue, mood swings, decreased libido, menstrual disturbances in women, osteoporosis, ankle edema, excessive thirst, compromised immunity |
Created by:
mbyess
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