(11) Seasonal Breeding

Question 1

(Rhythms)

classified on periodicty

1. occur at intervals less than one day?
2. around a day?
3. longer than a day - includes those with annual occurence (the circannual rhtyms)

Answer 1

1. ultradian (heartbeat, respiration)
2. circadian (body temp, adrenal activity, sleep)
3. Intradian (estrous, migration, pelage, hibernation)

Question 2

(Circannual Rhtyms)

1. While many species have an annual rhythm - not all match up with seasons

for example, elephants have cycles but they don’t match up seasonally

dog has circannual cycles but they aren’t controlled by photoperiod - in wolf they are

domestication decreaes photoperiod controls (or extends breeding season)

Question 3

read highlighted on 103-106

Question 4

(So How does the GnRH pulse generator really work?)

1. main director of GnRH neurons is what?
2. Do GnRH neurons have receptors for this?

respond by doing what?

disrupting this system does what?

Answer 4

1. peptide called kisspeptin
2. yes (or at least their terminals in the median eminence where the gnRH is secreted from do)

releasing GnRH

blocks GnRH release

Question 5

(Overview ofo the Steps in Photoperiod Control of Reproduction)

(Cyclical histogenesis is going to alter the hypothalamic drive for GnRH secretion by altering inputs on the kisspeptin/GnRH system. How this works and gets entrained to photoperiod follows:)

1. Ambient daylength is perceived by the retina and used to entrain what?
2. The SCN (via nerve relays) controls what?
3. Melatonin circulates and duration of melatonin elevation controls what?
4. Special thyrotropes located in the pars tuberalis of the pituitary have melatonin receptors and respond to short melatonin signals (long days) by secreting what?

Answer 5

1. an endogenous circadian clock in the SCN (suprachiasmiatic nucleus)
2. melatonin production by pineal gland (only occurs at night)
3. activity of target cells (with melatonin receptors)
4. thyroid stimulating hormone (TSH)

Question 6

(Overview ofo the Steps in Photoperiod Control of Reproduction) cont

5. This TSH activates cells in the hypothalamus - tanacytes around third ventricle - to do what?
6. T3 is one of the main controllers in tissue histogenesis… it currently appears that
7. 1 In long-day breeders the histogenesis results in increases in cell types and alterations in connections that do what?
8. 2 In short day breeders the histogenesis results in increases in cell types and connections that do what?

Answer 6

5. increase levels of DIO2 and/or decrease levels of DIO3 causing inactive thyroid hormone (T4 from the circulation) to be converted to active thyroid hormone (T3) locally in the hypothalamus.
6. 1 increase and stimulate KNDy neurons so there is increased kisspeptin and thus increased GnRH frequency (these animals are stimulated to strat cycling)
7. 2 inhibit KNDy neurons and thus keep GnRH pulse frequency low. These short day breeders start cycling when they become refractory to this input

Question 7

(Steps 1 and 2: Measuring the Daylength and SCN Control of Daily Melatonin Secretion)

1. photoreceptor for mammals is what?
2. nerves from the retina project via the what to the what?
3. The SCN directs fibers to what?
4. superior cervical ganglion is the sole innervation of what?

Answer 7

1. the retina
2. retinohypothalamic tract to the SCN
3. superior cervical ganglion
4. pineal gland which secretes melantonin

Question 8

(two mechanisms by which photoperiod gets to pineal gland)

1. in neurons of SCN there are oscillating clock genes which cause circadian rhythms - these do what?
2. if you keep in complete dark - secrete melatonin whole time?
3. Under natural conditions the activity of these SCN clock genes is entrained to light dark cycle. result is that SCN stimulates melanain release. (shown in diagram)
4. During hours of darkness, will enough light exposure cause cessation of melatonin secretion?

Answer 8

1. alter the electrical activity of the SCN - and thus activity of tissues innervated (pineal gland)
2. no (eventually pacemaker in SCN will shut it off)
3. yep (natural at dawn, can be artificial)

Question 9

(How does light exposure stop melatonin secretion?)

1. During the night, adrenergic input onto the pineal gland cells from the SCG is increased or decreased?

what is the NT?

2. Tis input stimulates the activity (by increasing transcription) of what?
3. This is form fo sho in rodents.

how are ungulates and primates different?

Answer 9

1. increased

noradrenalin

2. N-acetyl-transferase (NAT) (the rate limiting enzyme in melatonin synthesis)

(As a result, the activity of NAT is 30 to 70 times higher at night and melatonin synthesis is increased. At dawn, light exposure on the retina transmitted through pathway 2 above, causes cessation of the adrenergic stimulation and levels of NAT, and thus melatonin, decrease.)

3. NAT is constitutively expressed - light exposure breaks down NAT enzyme

(So melatonin release from the pineal gland is basically the SCN’s way of transducing the external photoperiod information into something the body can use. The duration of elevated melatonin level each day (24 hrs) is then interpreted (or transduced) by downstream targets, like the reproductive system.)

Question 10

(Steps 3 and 4: The melatonin signal acts on the Pituitary Pars Tuberalis to cause directed TSH release.)

1. this mech involves 3rd part of pituitary - the what?

contains cells (thyrotrophs) that produce what?

2. how are these thyrotrophs different from reuglar lones of anterior pit gland?
3. so what do they have?

that do what?

Answer 10

1. pars tuberalis (a layer of cells that wrap around the neural stalk but are part of the adenophypophysis)

TSH (thyroid stimulating hormone)

2. regular repsond to TRH by making TSH, subject to inhibitory feedback from T3

these don’t have TRH receptors or T3 receptors - so don’t repsond to stimulatroy input by hypothalamic TRH and aren’t inhibited by T3

3. melatonin (MT1) receptors

secrete TSH in response to short daily melatnonin signals (long-day)

this TSH then goes in retrograde to hypothalamus, to cells around 3rd ventricle

Question 11

(Step 5: Thyroid hormone activation locally within the Hypothalamus)

1. in hypothalamus the TSH binds to receptors on what?
2. In these cells the effect is what?
3. what converts inactive T4 to active T3 at cell surface?
4. what catabolizes T4 to rT3 and T3 to T2 (both inactive)?
5. TSH stimulus (long days) causes up regulation of what?

Answer 11

1. tanacytes and astroglial cells that surround base of thrid ventricle
2. alters activity of diodinase enzymes that control conversion of T4(inaactive) to T3 (active) and catabloism of active hormone to inactive
3. type II diodinase (DIO2)
4. type III diodinase (DIO3)
5. DIO2 (less frequently there is down regulation of DIO3)

(In either case long days stimulate conversion of inactive T4 to active T3, which is now available to affect surrounding cells.)

Question 12

(Step 6: It’s (Seasonal) Histogenesis Time)

(In the ewe two mechanisms appear to be at work to inhibit the frequency of GnRH pulses in the non-breeding season:)

1. What is by far the dominant system?
2. the second?

Answer 12

1. increased sensitivty of GnRH pulse generator to inhibitory gonadal steroid (estrogen) feedback

(This system becomes exquisitely sensitive so that even tiny amounts of estrogen are sufficient to keep GnRH pulses in check.)

2. Secondly, there appears to be a steroid independent mechanism at work because a less severe restriction of GnRH pulse frequency is seen seasonally in ovariectomized animals.

Question 13

(Mech 1: Altered sensitivity to steroid feedback - the Ewe)

(During seasonal anestrus…)

1. there a fewer what in the ARC?
2. A subset of dopaminergic neurons become active and do what?
3. Stimulatory inputs onto dopaminergic neurons from glutaminergic neurons are increased

these glutaminergic neurons have what kind of receptors?

during anestrus the number of these neurons increases as does the number of what?

4. Inhibitory inputs onto the dopmainergic neurons by GABA neurons are inhibted by what?

Answer 13

1. KNDy nerouns (those present have fewer projections to GnRH neurons - so less drive input on GnRH neurons)
2. inhibit GnRH secretion from axon terminals in median eminence

inhibit KnDy neurons

these dopaminergic neurons don’t have estrogen receptors… but….

3. estrogen receptors and are stimulated by estrogen

contacts they make with DA neurons (seasonal plastiity)

4. estrogen (there are no fewer GABA neurons during anestrus but their activity is inhibited by estrogen at this time)

(So the GnRH stimulatory kisspeptin system is down-regulated by being exquisitely sensitive to estrogen feedback in the non-breeding season while the GnRH inhibitory dopamine system is up-regulated at the same time by alterations in the balance of estrogen sensitive glutaminergic and GABA ergic inputs to it.)

Question 14

(Mechanism 2: Steroid-independent inhibition of GnRH release)

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