Puberty, anestrus Flashcards

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1
Q

GnRH during late fetal/neonatal periods

A

GnRH neurons are capable of and do secrete GnRH

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2
Q

GnRH during juvenile period

A
  • GnRH secretion decreases and is maintained at very low levels
  • if you stimulate GnRH neurons, they can secrete it
  • if supplied with GnRH, pituitary responds with secretion of FSH/LH
  • if stimulated with FSH/LH, the ovaries will respond
  • tl;dr: the hypothalamo-pituitary-gonadal axis is held in check by suppression of GnRH secretion from the hypothalamus –> puberty is a reactivation
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3
Q

how are GnRH pulses held in check during juvenile period then re-activated in puberty

A
  • developmental clock that times genetic program for puberty and sets a lower age limit on its occurrence
  • clock receives input from permissive signals that may delay puberty if they are limiting
  • cannot advance puberty earlier than genetically preset lowest age
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4
Q

what is the critical change for puberty

A

in the hypothalamus –> increase in frequency of GnRH pulses (reverse the decreased stimulatory inputs on GnRH neurons and increased inhibitory inputs from juvenile period)

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5
Q

direct drive hypothesis

A
  • when alterations do not involve gonadal steroid feedback (steroid independent)
  • puberty is simply the result of an increased drive for GnRH secretion
  • different cell types in hypothalamus provide inhibitory or stimulatory inputs to GnRH neurons
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6
Q

gonadostat hypothesis

A
  • when inputs involved in suppression and reactivation of GnRH neurons include re-setting of sensitivity to gonadal steroid feedback (negative feedback inhibition from gonadal steroids)
  • during puberty, sensitivity to inhibitory steroid feedback decreases
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7
Q

inhibitory and stimulatory influences in direct drive hypothesis

A
  • inhibitory: GABA, NPY

- stimulatory: glutamate

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8
Q

what is the initiation of puberty tied to

A

body growth (somatic development), not necessarily chronologic age

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9
Q

peripheral signals that trigger puberty

A

glucose, insulin, IGF-1, leptin

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10
Q

photoperiod influence on puberty

A
  • seasonal breeders can only attain puberty within the breeding season
  • whether puberty is achieved during the first available breeding season after birth depends on growth rate and their time of birth in the previous spring (how long they have to achieve target and how long it will take)
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11
Q

food supply influence on puberty

A
  • seasonal variations in nutrition influence growth rate

- vital in short-lived species

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12
Q

social factors in attainment of puberty

A
  • pheromonal, perhaps tactile

- pheromone in urine of male mice accelerates puberty in females

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13
Q

sex differences in time of puberty

A

-sexually imprinted differences in controls over GnRH secretion

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14
Q

genetic influences on age at puberty

A
  • alterations in developmental clock

- alterations in the time taken to achieve certain permissive cue goals (somatic development/body composition)

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15
Q

7 types of anestrus

A
  • juvenile: prior to puberty though there will be follicular development (not mature)
  • nutritional: periods of nutritional stress and poor body condition
  • seasonal: in seasonal breeders during the non-breeding season
  • lactational (suckling/milked)
  • behavioral
  • senile
  • pathological
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16
Q

mechanism of suckling anestrus

A
  • suppression of cyclicity relies on daily frequency of suckling
  • suckling acts at hypothalamus to reduce GnRH secretion
  • increased sensitivity to negative feedback inhibition by estrogen
17
Q

hypothalamo-pituitary-ovarian physiology of the pregnant and early post-partum cow

A
  • early/mid pregnancy: follicles emerge and regress due to high progesterone
  • late pregnancy: progesterone and estrogen high –> suppression of FSH (ovary is quiescent)
  • birth: progesterone and estrogen fall, FSH release –> follicular growth
  • post-partum anestrus due to defects in attainment of follicular dominance and final maturation of dominant follicles
18
Q

milked anestrus info

A
  • increase in GH following calving drives nutrient partitioning to support lactation
  • energy balance!
  • GnRH inhibited until cow is past worst negative energy balance (1-2 wks post-partum) and then increases
19
Q

principles of milked anestrus (BCS, etc)

A
  • cows in poor body condition and those with lowest voluntary intake (fattest cows) are in greatest negative energy balance, lose most BCS, take longest time to return to cyclicity
  • cows with low feed intake and/or catabolizing lots of body tissue have high circulating non-esterified fatty acids but low cholesterol, glucose, insulin –> prevents GH receptor formation –> IGF-1 stays low
  • increased feed intake in high producing cows increases clearance of estradiol –> lower circulating levels of estrogen
20
Q

what does low estrogen as a result of continued low LH mean

A
  • reduced expression of estrus

- LH surge not induced, follicle is anovulatory and becomes atretic, new follicle emerges

21
Q

what happens with improved energy balance

A
  • central inhibition of GnRH pulses lifted permitting increased LH pulses
  • increased insulin stimulates receptors for GH
  • dominant follicles can fully mature and secrete sufficient estrogen to give LH surge and ovulation
22
Q

behavioral anestrus

A
  • social: first time breeding, mate preference
  • seasonal: first of breeding season often silent
  • post-partum: presence of offspring
  • juvenile: first ovulation without estrus
23
Q

senile anestrus

A

menopause (humans mostly)

24
Q

pathological anestrus

A
  • systemic disorders suppress hypothalamo-pituitary axis
  • excess cortisol from adrenal in cushings
  • insufficient cortisol in addisons
  • hypothyroidism
  • any disease affecting reproductive organs
  • disorders of sexual differentiation