Puberty and Hormones

Hormones and Puberty

The HPG axis is crucial for the regulation of reproductive hormones.
It involves the interaction between the hypothalamus, pituitary gland, and gonads (ovaries/testes).

Mechanisms of Regulation
- Positive Feedback:
  - Involves hormones inducing hypothalamic neurons to secrete GnRH (Gonadotropin-releasing hormone).
  - High levels of GnRH lead to increased secretion of gonadotropins (LH and FSH).
- Negative Feedback:
  - Hormones can inhibit hypothalamic neurons, resulting in very low levels of GnRH.
Impact During Puberty:
- Ontogenetic shift from negative to positive feedback mechanisms takes place, allowing for reproductive function maturation.

The HPG axis controls various reproductive physiological processes:
- Regulation of menstrual cycles in females.
- Control of spermatogenesis in males.
- Ovulation triggers in females.

Positive Feedback:
- Rise in Estradiol stimulates the surge center of the hypothalamus, increasing GnRH, leading to an LH surge and subsequent ovulation.
Negative Feedback:
- Progesterone inhibits GnRH and in turn decreases LH and FSH, which can lead to incomplete follicular development due to lower FSH.
Neurons from the SURGE CENTER primarily affect the positive feedback mechanism while those from the TONIC CENTER influence negative feedback.

Midcycle: High levels of estradiol trigger ovulation through an LH surge.
Luteal Phase: Progesterone elevation leads to reduced GnRH and gonadotropin levels.

Negative Feedback Example:
- Increased testosterone leads to decreased GnRH, which reduces LH and FSH levels.

Key Indicators of Puberty:
- Age of first estrous and ovulation.
- Age capable of supporting pregnancy without issues.
- Behavioral traits' expression age.
- Male indicators include age of first ejaculation and quality of ejaculate (spermatozoa presence).
External Factors: External environmental and physiological factors can influence the timing of puberty.

Tonic Center & Surge Center:
- Testosterone affects the differentiation of these centers during embryogenesis, impacting reproductive capabilities.
- Testosterone converts to estradiol, which defeminizes the hypothalamus, with the default condition being female.

Fetal estradiol does not defeminize the hypothalamus in females because:
- Alpha-fetoprotein (⍺FP) binds estradiol, preventing it from crossing the blood-brain barrier.
- ⍺FP does not bind testosterone, enabling its influence on male brain differentiation.

Types of Hormonal Secretion Patterns:
- Episodic: Rapid bursts of hormone secretion.
- Basal: Low, consistent background levels.
- Sustained: Steady hormone levels over time.
- Pulsatile patterns organization into predictable rhythms.

After puberty, hormone levels become more pulsatile, with a pronounced surge in estrogen generating a well-organized LH surge during the ovulation cycle.

The full neural activity of hypothalamic centers must be reached for effective regulation post-puberty:
- Tonic and surge centers manage different patterns of GnRH secretion.
- Tonic center maintains basal levels, while surge center handles pulsatile stimulation.

In males, feedback primarily involves simple negative feedback:
- As puberty approaches, GnRH neurons become less sensitive to negative feedback from testosterone and estradiol, leading to increased LH and FSH secretion from the pituitary.

Metabolic signals can also influence GnRH neuron activity:
- Various factors such as blood glucose, leptin, and fatty acids may modulate signaling pathways involving GnRH.
- Interaction between kisspeptin and GnRH neurons may play a role in reproductive endocrine regulation.