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puberty
physical changes by which the body matures into an adult body capable of sexual reproduction
adolescence
maturation of cognitive, emotional, and social behaviors necessary for independence and successful navigation of the adult world
puberty timing in females
around 8-10 years of age; terminates at around 12-14 years of age
puberty timing in males
around 11-12 years of age; terminates at around age 17
timing of adolescence
extends from puberty to adulthood (independence)
rats pubertal milestones
females: vaginal opening followed by first estrus
males: preputial separation - separation of foreskin from the glans of the penis
human pubertal milestones
females: first menses, breast development, growth spurt, public and underarm hair
males; testicular enlargement, penis growth, growth spurt, deepening of the voice, facial hair growth
james tanner
pediatric endocrinologist that developed a scale which measures the stages of puberty based on external characteristics
GnRH
portal blood system
anterior pituitary
LH
FSH
testes
ovaries
gonadal steriods
hypothalamic - pituitary - gonadal axis
neurosecretory cells secrete BLANK in pulses from terminal in median eminence. GnRH enters the BLANK BLANK BLANK, and travels to the BLANK BLANK to signal synthesis and secretion of BLANK and BLANK from gonadotropes. Bloodborned LH and FSH act on target cells in BLANK and BLANK to direct secretion of BLANK BLANK
gamete development
reproductive brain behavior
promote secondary sex characteristics and physical growth
increase in gonadal steriods at puberty play a role in:
growth hormone
increases during puberty; stimulate the growth of bones and muscles
GHRH
hypothalamus
anterior pituitary
GH
somatotropic cells
BLANK is released from neurosecretory cells in the BLANK in the portal blood system down the BLANK BLANK, which releases BLANK in pulsatile manner from BLANK BLANK
increased pulse frequency
pulsatile pattern of GnRH secretion changes at puberty → required to product pattern of gonadotropin and steriod secretion that supports gonadal function and reproductive behaviors
environmental
social
metabolic
signals that time puberty onset
leptin
protein hormone derived from fat tissue that enters the blood stream; the metabolic signal for puberty
receptors found on GnRH neurons in hypothalamus, regulate or may initiate the onset of GnRH secretion and thus puberty
GPR54
gene required for mammalian puberty
kisspeptin
hypothalamic neuropeptide involved in activating GnRH neurons in mammalian puberty through its actions at its G-protein coupled receptor
gain of function mutation
kisspeptin receptor signaling is enchanced, which lead to increased activation of HPG axis → puberty starts before the normal age
precocious puberty
puberty starts before normal age
loss of function mutation
leads to idiopathuc hypogonadotropic hypogonadism
IHH
failure to undergo puberty; infertile due to failure to produce LH and FSH → problem is with the normal release of GnRH
early puberty effects
short stature
increase risk for metabolic disorders
increased risk for breast cancer
lupron
GnRH agonist; suppresses GnRH and halts precoious puberty via negative feedback
delayed puberty
child does not show physical changes of puberty by age 14 (girls) and age 15 (boys)
treated with hormone therapy
delay puberty effects
short stature
low bone density - osteroporosis
fertility issues
protective against reproductive cancers
steriod hormones
required for the expression of reproductive behavior
organizational effects
irreversible changes in CNS structure and programming of adult behavioral responses to hormones caused by exposure to steriods during sensitive period in early development
activational effects
faciltation of behavior by steriods in adulthood - which is reversible if hormone is removed
2-stage model
gonadal hormones permanently organize the brain and behavior during two critical periods
perinatal period
puberty
2 sensitive periods of the 2-stage model
perinatal period
initial steriod dependent sexual differenitation occurs
puberty period
second wave of steriod neural organization during this time point which builds on and refines neural circuits that were sexually differentiated during early development
syrian hamster
used to understand the effects of pubertal hormones on social behavior
experimental paradigm
remove testes of syrian hamsters after sexual differenitation and before puberty; administer testosterone in adulthood
experimental results
when testicular hormone was absent during adolecent brain development, syrian hamster had disrupted social and sexual behaviors — this was irreversible
consistent with hypothesis that adolescence may be a sensitive period for further steriod-dependent organization of neural circuits mediating reproductively relevant behavior
normal behavior
male rats do not interact with one another in a novel behavior
castrate rats before puberty
male rats interact with one another in a novel environment - do not develop anxiety
reinstate testosterone during puberty
reinstates anxiety/normal behavior in male rats
reinstate testosterone during adulthood
does not reinstate anxiety/normal behavior in male rats
spatial tasks
males tend to do better on these tasks compared to females
spatial task experimental paradigm
Men with IHH that started before puberty - no/low testosterone during puberty
Men who acquired IHH that started in adulthood - had normal levels of testosterone during puberty
Controls - healthy men and women
spatial task experiemental results and conclusion
men that developed IHH before puberty performed worse on spatial tasks than healthy men and men that developed IHH during adulthood
Performed similar to females
Conclusion: spatial cognition may be programmed by testosterone during pubertal development
Morris Water Maze Task
spatial task that males tend to do better on compared to females
Morris Water Maze experiment and results
females with non-classic CAH (mild form; diagnosed in childhood) - they have higher levels of testosterone due to its overproduction from adrenal glands throughout puberty - These females performed better on the Morris Water Maze Task compared to females, and did similar to males
CONCLUSION - cognitive function in humans can be programmed by steroid hormones during puberty
Revised two-stage model
this model includes two periods of elevated hormone secretion within a large post-natal window of decreasing sensitivity to organizing actions of testosterone
The adolescent brain is sensitive to neural organization by hormones; even if there isn’t a distinct critical period of development
Are there actually two stages:
Test by examining whether hormonal exposure is critically necessary only during adolescence or if testosterone has a similar organizing effect if it occurs outside the age-range during which adolescence normally occurs
Hypothesis - if adolescence marks the opening of a unique sensitive period for testosterone dependent behavioral organization, then only those males receiving testosterone during normal time of puberty should display typical male behaviors
Experimental paradigm - castrate syrian hamsters, and then reinstate testosterone during these three time points:
Before puberty (early)
During puberty (on time)
After puberty (late)
Results: both early and on-time puberty groups displayed appropriate male sexual behavior in adulthood; early treatments most effect in organizing mating behavior
Adolescence is not a sensitive period for testosterone-dependent behavioral organization distinct from the neonatal period rather, adolescence if part of a protracted sensitive period that likely begins perinatally and ends in late adolescence
Sensitivity to the organizing actions of testosterone decreases across the post-natal development
Implication: organizing effects of testosterone at puberty may differ if puberty occurs early vs. late - this could lead to individual differences in sex-typical behaviors
pre-frontal cortex
a brain region critical for impulse control, emotional regulation, and executive function - not fully developed in teens
are hormones involved
unknown how much of a causal role pubertal hormones play in the development of the adolescent brain