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Flashcards in Neuroendocrine Deck (12):
1

Describe the anatomical and physiological basis for hypothalamic control of posterior pituitary (neurohypophysis) function.

Secretion of vasopressin and oxytocin directly into system circulation.
-Synthesized in magnocellular neurons in supraoptic and paraventricular nuclei of hypothalamus
-Transporter via axoplasmic transport to nerve terminals in posterior pituitary
-Stored in vesicles until released by neural activity

2

List the primary stimuli for vasopressin and oxytocin and discuss how target tissue responses
feedback to offset these stimuli.

Vasopressin
-Stimulus: increased blood osmolality, hypovolemia, hypotension
-Response: water resorption by kidney, vasoconstriction

Oxytocin
-Stimulus: suckling, uterine stimulation (stretch)
-Response: milk ejection reflex, uterine contraction

3

Describe the anatomical and physiological basis for hypothalamic control of anterior pituitary
function.

1. Hypothalamic releasing hormones are synthesized in parvocellular neurons in paraventricular nucleus
2. Transported via axons to MEDIAN EMINENCE
3. Released from nerve terminals into hypophyseal PORTAL vein
4. Travel down vein to the pituitary cells in at the secondary plexus where the releasing hormones can excite or inhibit hormones in the anterior pituitary.
5. Hormones secreted into hypophyseal vein/systemic circulation.

4

Explain the etiology of diabetes insipidus and discuss the rationale for current treatments.

No vasopressin, thus high osmolality can't trigger water resorption in kidneys. Major etiology is head trauma i.e. severing of pituitary stalk. 2nd most is auto-immune destruction of magnocellular neurons.
1. Polyuria (frequent urination); real dilute urine.
2. Polydipsia (frequent drinking) because these individuals are constantly thirsty due to high osmolality.

Treatment: Replace vasopressin. Use form that acts only on kidney, thus sparing vasoconstriction. Desamino-VP (ddAVP).

5

Explain the etiology of galactorrhea-amenorrhea and discuss the rationale for current treatments.

Lactation with no period. Due to increase blood prolactin levels, most likely from micro adenoma in pituitary gland. Prolactin causes milk production i.e. lactation; also causes decreased FSH and LH in anterior pituitary, thus the amenorrhea.

Treament:
1. Surgery to remove tumor
2. Pharmaceutical. Dopamine receptor agonist decreases prolactin. Bromocryptine better chance of getting pregnant.

6

Discuss the neural and hormonal basis for preabsorptive satiety signals to control food intake.

-Gastric distention is a satiety factor (increase mechanoreceptive firing, increase vagal afferents, increased activity in Nucleus Tractus Solitarus, decreased food intake)
-Nutrient in intestine is satiety factor (caloric value sensed)

7

Discuss the symptoms and etiology of Prader-Willi syndrome.

-Deletion on chromosome 15. 1/25,000
-Symptoms: fetal hypotonia, mental retardation, hypogonadotropic hypogonadism, obesity, HYPERPHAGIA. Excessive ghrelin secretion.

8

List the primary hypothalamic nuclei that control food intake and the neural circuits that
interconnect them.

See diagram.

9

Provide evidence that leptin is an adiposity signal that acts in the hypothalamus to control food
intake.

Leptin acts in the arcuate nucleus to inhibit neuropeptide Y (NPY) and activate melanocortin (from POMC), thus decreasing food intake.

10

Evaluate potential neuropharmacological approaches to treat hyperphagia-induced obesity.

Goal would be to block NPY and up regulate melanocortin receptors.
Decrease eating: melanocortin, leptin, CRH, CCK
Increase eating: NPY, ghrelin, orexin

11

Activation of lateral hypothalamic area results in what?

Release of anabolic neurotransmitter orexin. Increases eating/growth.

12

Activation of paraventricular nucleus results in what?

Release of catabolic neurotransmitter corticotropin releasing factor. Decreases eating/growth.