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Reproduction > Puberty > Flashcards

Puberty Flashcards

1
Q

How do the GnRH secreting cells form and get to the hypothalamus?

A

GnRH secreting cells differentiate in the medial olfactory placed and migrate along the olfactory tract to the hypothalamus in the medial arcuate nucleus.

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2
Q

What gene is involved in migration of GnRH secreting cells and olfactory cells?

A

KAL1

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3
Q

What is the gonadostat?

A

the hypothalamic neurons in the medial arcuate nucleus that are involved in the release of GnRH.

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4
Q

What is the negative feedback loop in infant and early juvenile development?

A

In the infant there is a surge of GnRH. Then in the early juvenile stage an intense negative feedback loop is made that prevents the gonads from maturing. In the hypothalamus there are GABA secreting cells. When stimulated by increasing levels of FSH, LH, estradiole and testosterone the GABA cells synapse on GnRH secreting cells and have an inhibitory effect on release of GnRH by increasing the inward gCl- therefore hyper polarizing the cell. Therefore, no GnRH release resulting in no FSH/LH release and immature gonads result

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5
Q

What happens to GnRH levels in later juvenile period?

A

GnRH pulses and rate of pulses slowly increases around age 6 and there are very low releases of sex hormones. There is also a small decrease in sensitivity to the negative feedback loop and the gonadostat becomes a little more sensitive to leptin and IGF-1.

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6
Q

What causes GnRH’s pulsatile nature?

A

pulsatile release is an intrinsic property of GnRH secreting cells and is due to integration of stimulatory and inhibitory input on the GnRH secreting nerves (EPSP’s and IPSP’s)

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7
Q

What happens if there is continual GnRH release opposed to pulsatile?

A

continuous GnRH release causes inhibition of FSH/LH because GnRH acts as an autocrine substance and can inhibit itself

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8
Q

Is adrenarche the triggering event for puberty?

A

NO! it is also GnRH independent

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9
Q

What age does adrenarche occur?

A

girls 6-7 and boys 8-9

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10
Q

What initiates adrenarche?

A

Maturation of the zona reticularis due to HGH, IGF-1, insulin and leptin. As reticularis matures, it secretes DHEA and DHEAS and 2 years later there is more androstenedione released.

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11
Q

What happens to DHEA and DHEAS at the target tissue?

A

at target tissues DHEA and DHEAS are converted to testosterone and DHT (intracrinology). This stimulate axillary and pubic hair growth, development of apocrine glands, and increased secretion from sebaceous glands. Can lead to bacterial invasion of glands resulting in body odor and acne.

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12
Q

What results from poor nutrition in 3rd trimester in females?

A

Female babies that are a result from poor 3rd trimester nutrition will end up going through puberty early and will be overweight. As an overcompensation, females will eat more food resulting in more weight gain after birth. This causes an overexpresson of leptin from the fat pads. Leptin has the effect of inhibiting the satiety center in the hypothalamus. Leptin also increases GnRH release by stimulating other hypothalamic factors that stimulate GnRH release, leading to early onset puberty.

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13
Q

Whate results from poor nutrition in 3rd trimester in males?

A

Low BMI at birth can lead to impaired testicular function and prolongs male puberty. Low BMI decreases IGF-1 which plays a role in reproductive performance. If they have a high BMI this can also delay puberty. Testosterone is converted to estradiole (E2) at fat pads so therefore they have less testosterone delaying the onset of puberty

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14
Q

What does a diet high in protein do to the age of onset of puberty in males and females?

A

lowers the age of onset of puberty

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15
Q

What are the 3 processes needed to reset the gonadostat?

A
  1. general nutrition
  2. gene expression
  3. maturation of the limbic system-hypothalamic axis
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16
Q

What leads to gene expression of KiSS-1 gene?

A
  1. general nutrition has a stimulatory effect on leptin which activates the KiSS-1 gene of Kisspeptin-10 secreting nerves that reside in the amygdala and synapse on the GnRH secreting cells.
  2. general nutrition also stimulates expression of frowht facts like IGF-1 sand insulin which activate mTORC1 which increases metabolism in the hypothalamus, therefore increasing activity of the GnRH and Kisspeptin-10 secreting nerves
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17
Q

What 2 events in gene expression help reset the gonadostat?

A
  1. slight increase in GnRH during puberty leads to stimulation of the GPR-54 gene and expression of the GPR-54 receptor on GnRH secreting cells bodies and axons who’s cells bodies are in the arcuate nucleus and axons in the median eminence
  2. leptin activates expression of KiSS-1 leading to secretion of Kisspeptin-10 from the cell bodies in the amygdala and synapse on the GnRH releasing nerves interacting with the newly formed GPR-54 receptors. This interaction stimulates GnRH-1 genes in the nucleus leading to synthesis and secretion of A LOT of GnRH which activates the AP to release large amounts of FSH/LH.
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18
Q

What inhibits Kisspeptin-10 release?

A

estradiol and testosterone

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19
Q

What processes take place during maturation of the limbic system-hypothalamic axis that help to resent the gonadostat?

A

2 events happen at the same time to aid in this process.

  1. amygdala matures resulting in more glial cells and dendritic branching, therefore decreasing the threshold for GnRH release. THE NEG FEEDBACK LOOP IS LESS INTENSE. So the amygdala neurons are more sensitive to Kisspeptin-10, leptin, glutamine, NE and other factors that increase GnRH secretion. Also, kisspeptin-10 secreting nerves increase their rate of secretion which helps in more GnRH secretion and essentially more FSH/LH secretion from AP. (don’t forget that amygdala neurons secrete Kisspeptin-10 aka Kiss-1)
  2. GABA inhibition via GABA receptors in the GnRH secreting cells is lessened. There is increased expression of Cl- transporter KCC-22 that allows Cl- to leave the cell, thus preventing hyper polarization and favoring depolarization and release of GnRH (more sensitive to stimuli now.)
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20
Q

What is the main even that marks the onset of puberty?

A

resetting of the gonadostate negative feedback loops to be less sensitive

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21
Q

What is the role of melatonin?

A

inhibits GnRH secretion

22
Q

If melatonin is high at night, how do we maintain high levels of GnRH at night during puberty?

A
  1. GnRH secretions are very robust
  2. norcturnal melatonin secretion decreases in early puberty
  3. there is a phase lag in which melatonin is secreted at night but it takes 8-12 hours for its inhibitory effects to take place via GnRH-mRNA suppression. This cyclic process allows GnRH to be high at night and low during the day
23
Q

What happens to hormone concentrations as adulthood is reached?

A
  1. GnRH secretions continue to increase and melatonin continues to decrease, allow GnRH levels to maintained during the day in males and during ovulation in females.
  2. Increasing GnRH allows the release of LH followed by FSH. Once FSH levels reach physiologically effective concentrations, the LH concentration can also increase significantly (about one year later in females).
24
Q

What is the Brake Hypothesis?

A

Tires to explain why girls undergo puberty before males. Says that girls start out with higher levels of GnRH in juvenile period, thus the have less negative feedback inhibition and are able to more easily reach adult levels of GnRH than males

25
Q

What causes the growth spurt?

A

increased synergism between GH, IGF-1, and sex hormones leads to accelerated growing at the later stages of puberty. Long bones grow faster than the rest, resulting in the lanky, gawky look (big hands and feet etc)

26
Q

Why do female growth spurts last shorter in duration than males, although they start earlier than males?

A

Because of the increased plasma estradiole in females which also initiates epiphyseal plate closure earlier in girls than boys

27
Q

What causes development of secondary sex characteristics in females?

A

estradiol from the ovaries. Also causes development of the endometrial proliferation

28
Q

What is menarche?

A

first menstrual period

29
Q

When does progesterone increase?

A

after first ovulation which sometimes doesn’t occur until 6-9 months post menarche. Estradiol secretion from the granulosa cells eventually reaches a level where it can finally stimulate LH surge leading to ovulation.

30
Q

What does FSH stimulate in male puberty?

A

testicular growth including increased spermatogenesis and synthesis of inhibin by Sertoli Cells (this provides negative feedback at AP preventing FSH release)

31
Q

What does LH stimulate in male puberty?

A

differentiation of interstitial cells to leydig cells resulting in increased testosterone (provides negative feedback at the hypothalamus preventing Kiss-1 release and at the AP as estradiol preventing LH release)

32
Q

What causes spermatogenesis?

A

FSH, LH and Testosterone release

33
Q

What causes descent of testes?

A

IGF-3 controlled by HOXA10 gene.

34
Q

Compare neuronal development in early and later puberty?

A

Early: high synaptic density and learn very quickly. But diffuse stimulation pattern of the cortex
Late: pruning of nerves, dendrites and receptors. More focal stimulation of cortex. Slower learning curve

35
Q

How is pubertal neural thought process different from adult?

A

Puberty has very direct pathways but uses very diffuse cortex regions. Adults have a more complex thought pattern that involves many area and thought process is actually even more directed

36
Q

What is precocious puberty?

A

premature development of genital organs and secondary sex characteristics

37
Q

What causes precocious puberty in males?

A
  • adrenal hyperplasia: defect in CYP21 which can lead to salt wasting due to lack of cortisol and aldosterone. If less severe can only causes precocious development of pubic hair and phallus and increased linear bone growth. Hypotension may still present
  • leydig cell adenoma
  • virilizing adrenal neoplasm
38
Q

What causes precocious puberty in females?

A
  • estrogen secreting ovarian tumor
  • adrenal hyperplasia: defect in CPY21 or 11B hydroxylase causing androgenital syndromes resulting in masculinization in girls
39
Q

What occurs with CYP21 or 11B hydroxylase mutations?

A

CYP21: hypotension due to not enough aldosterone and cortisol
11B hydroxylase: increased cortisol leading to hypertension

40
Q

What causes delayed puberty?

A
  • not enough GnRH secretion (hypogonadism)
  • due to CNS tumors or idiopathic gonadotropin deficieyce
  • defective GPR-54 or kisspeptin-10 gene expression
41
Q

What is Kallman’s Syndrome?

A

When fetus has defective KAL-1 gene so GnRH and olfactory neurons do not migrate from the olfactory placode to the medial acute nucleus.

42
Q

What is the difference between hypogonadic/hypogonadotropic and hypogandism?

A

Hypogonadic/hypogonadotropic: low GnRH concentrations

Hypogonadism: underdeveloped gonads

43
Q

What is hypergonadic hypogonadism?

A

too much GnRH and FSH/LH due to impaired secretion of gonadal steroids leading to decreased or absent negative feedback

44
Q

Klinefelter syndrome?

A

seminiferous tubular dysgenesis where onset of puberty is not delayed but is impaired

45
Q

LH resistance?

A

occurs in males and is when leydig cells are LH resistant

46
Q

Cryptorchidism?

A

failure of testicular descent into scrotum due to defect or lack of IGF-3 (INSL-3) under control of HO=XA10

47
Q

Congenital adrenal hyperplasia in males?

A

defective CYP17 leading to a lack in adrenal androgens estrogen and testosterone so sexually ambiguous genitalia or female like genitalia. Also have too much corticoids and low aldosterone so hypertension?

48
Q

What is the main cause of female development problems?

A

ovarian mal-development

49
Q

Turner’s Syndrome?

A

gonadal dysgenesis

50
Q

CYP17 defect in females?

A

severe lack of estrogen and no development of secondary female characteristics and vascular hypertension in later life

Reproduction (11 decks)

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