Clark Flashcards

1
Q

define puberty

A

the physiological requirement of the body to develop specific hypothalamic neurons to release adequate quantities of gonadrotropic hormone (GnRH) in order to attain reproductive ability

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2
Q

Functions (3) of GnRH

A

promote gametogenesis, steroidogenesis, & development of reproductive tissues

FSH & LH = steroid hormones

Via upregulating FSH + LH release from anterior pituitary gland (FSH -> folliculuar development; LH -> ovulation)

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3
Q

Average age at puberty for dogs and cats (male versus female)

A

Dogs: 9mo (M), 12mo (F)
Cats: 9mo (M), 8mo (F)

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4
Q

Average age at puberty for large & small ruminants (M vs. F)

A

Bovine: 11mo (M&F)
Ovine/Caprine: 7mo (M&F- spring-born), 12mo (M&F- fall-born)

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5
Q

Describe the PRE-PUBERTAL and POST-PUBERTAL EFFECTS on GnRH secretion in males versus females

A

PRE-PUBERTAL
- Males & Females: hypothalamus’ tonic & surge centers release basal levels of GnRH

POST-PUBERTAL
- Females: tonic center controls post-pubertal basal levels of GnRH; surge controls pre-ovulatory GnRH surge (which initiates LH surge)

  • Males: surge center is absent- only have tonic center

basal = frequent, low amplitude

post-pubertal GnRH basal level = HIGHER than pre-pubertal

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6
Q

What is meant by “de-feminized” surge center in males? How does it “feminized” surge center develop in females?

A

In males, testosterone freely crosses the BBB and aromatizes into estrodial, de-feminizing the surge center in the hypothalamus

The surge center develops in females b/c estradiol (which is released by the fetal ovary) is prevented from entering the BBB via alpha fetoprotein (alpha-FP)

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7
Q

What causes pre-ovulatory LH surges in females?

A

high amounts of estradiol release by the dominant follicle

High levels of E2 -> (+) directly on AP // LH -> -> LH surge

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8
Q

Factors (6) that affect age @ puberty

A

1. Body weight!!! (40-50% of mature weight)
2. Socio-environment (biostimulation = presence of a post-pubertal//more-mature male)
3. Genetics - e.g., sire scrotal circumference (SC)
4. Breed (purebred vs crosses)
5. Birth season (fall-born vs spring-born)
6. Density of housing groups (swine)

need adequate wt gain once reaching puberty to maintain normal cycles

in cattle, the bigger the SC in the sire, the earlier the puberty in their daughters

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9
Q

Describe patterns in puberty in seasonal breeders - ovine/sheep

A

Ovine//sheep - both males & females
- Spring-born: puberty in fall (age of 1st puberty = ~7 months)
- Fall-born: puberty NEXT fall (age of 1st puberty = ~12months)

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10
Q

What prompts onset of puberty in queens?

A

increased photoperiods in jan/feb => LOTS of springtime kitties :)

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11
Q

1º versus 2º follicles

A

: FSH acts on them, stimulating their development//slight increase in size => Granulosa Cells (GCs) proliferate around 1º follicles => become 2º follicles

: GCs produce small amt. of estradiol; FSH causes the GCs to release follicular fluid around the 2º follicle, forming the antral follicle (3º follicle)//antrum; GCs begin to differentiate into 2 cell types

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12
Q

What are the 3 distinct layers of Antral Follicles?

A

1. Theca externa
2. Theca interna (produce androgens under influence of LH)
3. Granulosa Cell Layer (possess FSH receptors; produce estrogen, inhibin & follicular fluid)

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13
Q

Theca cells

A

cells of antral follices (the 3º follicles) that produce enzymes that convert cholesterol into testosterone

(+) feedback from LH; homolog in males = leydig/interstitial cells

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14
Q

GCs

A

Females:
- proliferate around developing follicle, releasing smal amts of E2
- in 2º follicle, increase E2 production + are stimulated (by FSH) to produce follicular fluid -> -> antral/3º follicle. Also, begin to differentiate into 3 distinct layers: theca externa, theca interna, GC layers
- GC layer: FSH-binding stimulates T => E2. Also, secretes inhibin

inhibin (-) feedback on AP -> decr. FSH secretion

in males, T => E2 in sertoli cells

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15
Q

How does the dominant follicle emerge & what are its functions?

A
  • emerges from the continued increase in size of antral follicle development (while other follicles in the cohort undergo atresia=atrophy).
  • produces increasing amts of estrogen & inhibin (via the GCs)
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16
Q

Steroid Hormones
- what are the 3
- what is their base structure
- what is their charge
- where are they produced

A
  • Estrogen, Progesterone, Testosterone
  • Cholesterol-based
  • Neutral charge
  • Gonads, adrenals, placenta
estradiol = 1º form of estrogen
17
Q

Primary action of GNRH

A

Release of FSH + LH (in both males & females)

18
Q

Primary action of LH in males versus females

A

males: stimulate testosterone production (cholesterol => Testosterone in the Leydig Cells)

females: stimulates ovulation, form CL, stimulate luteal cells to secrete P4

19
Q

Primary action of FSH in males versus females

A

males: sertoli cell function (convert T => E2 ; secrete inhibin)
females: follicular development + E2 synthesis

incr. [E2] -> (-) feedback on GnRH; inhibin (-) feedback FSH

20
Q

Describe feedback mechanisms of estrogen & LH

A
  • E2 has (+) feedback on hypothal -> incr. GnRH release. -> (+) feedback on AP -> FSH + LH release.
  • Once [E2] levels peak from dominant follicle, E2 has direct (+) feedback on AP /LH -> pre-ovulatory LH surge -> ovulation.
  • From ovulation, the CL develops -> luteal celsl secrete P4. -> P4 has (-) feedback on hypothal -> decr. GnRH release.
21
Q

Gonadectomy effects

A

disrupts the H-P-G axis & results in very high levels of gonadotropins

22
Q

Primary action of Prostaglandin F2-alpha (a fatty acid)

A

luteolysis of corpus luteum

23
Q

Reproductive hormones originate from:

A

Hypothalamus, pituitary gland, gonads, uterus + placenta