the onset of reproductive activity

heterogenous growth and body ‘fatness’

Reproduction is a ‘luxury’.

Essential tissues prioritised.

Growth (increased mass) is accompanied by a relative decrease in metabolic rate.

More dietary energy ‘left over’ for ‘non- essential’ functions = fat deposition

to breed or not to breed - is there an option?

menarche - starts from first period - human - puberty

reproductive quiescence: pre-pubertal

Anoestrus: seasonal, lactational

infertility

reproductive activity: post-pubertal

Oestrus: seasonal, behavioural

Sub-fertility

reproductive senescence:

the menopause in humans

puberty definitions

Definitions: The ability to accomplish reproduction successfully

Male: Spermatozoa capable of fertilizing in the ejaculate

Female: Pregnancy supported without deleterious effects

A process which occurs over time, and is dependent on body growth and maturation.

Pre-pubertal: Hyperthalamic neurons and Hypothalamic-Pituitary-Gonadal axis established but quiescent

Peri-puberty: Acquire ability to receive information from pre-synaptic neurons to increase frequency and promote GnRH secretion

Puberty: Increased frequency and amplitude of GnRH secretion

hypothalamic-Pituitary-Gonadal axis

This is the hormonal axis that controls sexual development and reproduction. It consists of:

• Hypothalamus → releases GnRH

• Pituitary gland → releases LH and FSH in response to GnRH

• Gonads (ovaries/testes) → produce sex hormones (estrogen, progesterone, testosterone) in response to LH/FSH

GnRH = Gonadotropin-Releasing Hormone

This is the hormone released by the hypothalamus that stimulates the pituitary gland to release gonadotropins (LH and FSH), which then act on the gonads.

gonad

a gonad is a reproductive organ that produces gametes (sex cells) and sex hormones.

There are two types:

In males:

• Testes (testicles)

• Produce sperm (male gametes)

• Produce testosterone (primary male sex hormone)

In females:

• Ovaries

• Produce eggs/ova (female gametes)

• Produce estrogen and progesterone (primary female sex hormones)

timing of puberty

Influenced by:

• Season and photoperiod

• Genetics (breed) e.g.:

• Bitches: Border Collie, 9 months: Whippet, 18 months.

• Heifers: Dairy, 7-9 months; Traditional Beef, 12-13 months

• Bos indicus, 24 months

• Nutrition

• Social cues (presence / absence of opposite sex)

• Housing density (sows)

brain puberty

Independent of gonadal and anterior pituitary status.

• Can induce ovulation in pre-pubertal animals by exogenous GnRH administration

Dependent on ability of hypothalamus to secrete sufficient GnRH to stimulate pituitary gonadotrophin secretion.

for heifers- 2 months for LH pulse frequency is enough to drive gonadal function

before and after brain puberty

Before puberty: Tonic (male) or Tonic and Surge (female) Centres release low frequency, low amplitude GnRH pulses.

Mature neural activity in the surge centre is essential for ovulation- need surge centre to develop:

Tonic GnRH neurones must fire more frequently and release large amounts of GnRH to stimulate the ovary to develop oocytes leading to oestradiol secretion.

Surge GnRH causing the Preovulatory LH surge is dependent on sufficient Tonic GnRH to drive ovarian activity and allow oestradiol (E2) secretion.

male brain pubery

before puberty, the brain is too sensitive to negative feedback, keeping testosterone levels low

puberty happens because brain loses this extreme sensitivity, allowing testosterone levels to surge and allow testicular development

🛑 Before Puberty

• The brain is highly sensitive to negative feedback.

• Even tiny amounts of testosterone/E2 shut down GnRH, LH, and FSH.

• Result: Testosterone stays very low.

🚀 At Puberty

• The brain becomes less sensitive to negative feedback.

• It ignores low-level hormone signals and keeps pumping GnRH, LH, and FSH.

• Result: Testicular development begins and testosterone surges.

🧠 The Role of E2 (Estradiol)

• Testosterone enters the brain and converts to E2 via aromatase in brain, fat tissue, and testes.

• This brain-made E2 provides the actual negative feedback signal.

Even though testosterone is the dominant sex hormone in males, estradiol still plays important roles in male physiology:

• Bone health and closure of growth plates

• Brain function

• Libido

• Feedback regulation of the HPG axis

female brain puberty

More complex: Hypothalamic surge and tonic centres respond differently to oestradiol feedback

This diagram is explaining the female HPG axis and the menstrual cycle regulation.

Here's what it shows:

The HPG Axis (right side):

• Hypothalamus releases GnRH

• Anterior Pituitary Gland releases LH and FSH

• Gonad (ovary) produces estradiol (E2) and other gonadal hormones

• These hormones act on the reproductive tract and create secondary sexual characteristics

Key difference from the male diagram: The feedback is labeled as "+ve & -ve" (positive and negative), which is unique to females:

• Negative feedback: Most of the time, estradiol inhibits GnRH/LH/FSH release (similar to males)

• Positive feedback: At mid-cycle when estradiol levels peak, it actually stimulates a surge of LH and FSH, triggering ovulation

The brain diagram (top left): Shows the "surge centre" and "tonic centre" in the hypothalamus, illustrating how estradiol can have both positive (surge) and negative (tonic) feedback effects depending on timing and estradiol levels during the menstrual cycle.

brain puberty experiment proof

Female: Oestradiol (E2) feedback can be positive (Surge Centre) and negative (Tonic Centre)

Experiment:

• Ovariectomised (no endogenous E2)

• Subcutaneous E2 implant

Conclusion: Surge Centre is highly sensitive to positive E2 feedback from an early age

BUT: Pre-pubertal lambs don’t ovulate because their inactive ovaries fail to produce sufficient E2.

During puberty:

• Tonic centre becomes less sensitive to negative E2 feedback.

• At low [E2] (pre-pubertal), negative feedback is strong

• As negative feedback decreases, increased GnRH pulse frequency stimulates ovarian function

body condition and puberty

Puberty: dependant on body mass and fatness

Puberty occurs exactly at the inflection point of the growth curve, meaning it is triggered when an animal reaches a specific milestone in body mass.

📈 Growth Phases & Puberty

• Self-accelerating phase: Growth rate increases rapidly after birth.

• Inflection point (Puberty): Growth rate reaches its absolute maximum speed.

• Self-decelerating phase: Growth slows down toward mature weight.

🥩 Connection to Body Condition

• Mass threshold: Puberty cannot start without reaching a critical body mass.

• Fatness trigger: Adequate body fat stores signal the brain that energy is sufficient for reproduction.

• Gating mechanism: The inflection point represents this ideal nutritional and physical readiness.

plane of nutrition and puberty

The plane of nutrition dictates the speed of growth, which directly determines the age at which an animal hits the required weight threshold for puberty.

📈 Nutrition Plane Effects

• Maximal Feeding (High Plane): Accelerates growth rate, pushing the animal to hit the puberty mass threshold much earlier in time (advances puberty).

• Restricted Feeding (Low Plane): Delays growth rate, taking the animal much longer to reach the necessary weight milestone (delays puberty).

• Constant Mass Threshold: Note that the horizontal "Puberty" weight line stays at the exact same level; only the time axis shifts based on food availability.

factors influencing the hypothalamic pulse generator

GnRH released into hypophyseal-portal system - neuroendocrine effect on the anterior pituitary - in response to kisspeptin neurons

when an animal has fat cells they have more adipocytes - so more of a hormone called leptin is formed in these adipocytes → triggers our neuropeptide Y neurones → triggers kisspeptin neurones which stimulate GnRH → production of LH and FSH in anterior pituitary

this is how fatness can help puberty process

if animal is skinnier so less of the effect

blood glucose and fatty acid concentrations

blood glucose and fatty acid concentrations can modify GnRH pulse frequency to alter reproductive status

The Experiment: Researchers use ovariectomized ewe lambs (ovaries removed) to isolate the brain. This lets them study exactly how the hypothalamus reacts to nutrition without ovarian hormones getting in the way.

Creating a Synthetic Energy Deficit: Giving them 2-deoxyglucose (2DG) stops the body from metabolizing glucose. This tricks the body into pretending it has zero sugar reserves, simulating an acute starvation situation.

Hypothalamus Response: The hypothalamus detects this low blood sugar phenomenon and drastically decreases both the frequency and amplitude of GnRH pulses.

The Downstream Effect: Because the brain's baseline pulses flatten out, the pituitary cannot release the massive preovulatory LH surge required to trigger ovulation.

Real-World Link: This explains why anorexic individuals or animals in a severe energy deficit stop cycling entirely—the brain actively puts the brakes on GnRH and LH to prevent reproduction during starvation.

flushing - feeding ewes higher plane of nutrition - more follicles recruited - so when ovulated more oocytes/follicles - twin/trippling pregnancy

factors influencing the hypothalamic pulse generator

just a summary so adipocytes(fat), glucose and fatty acids influence it

seasonality

quality of food increases in spring and summer

better to have offspring in spring

breeding seasons

horses-long day breeders

sheep-short day breeders

cows-non-seasonal

Y-axis: Day length (hours)

X-axis: Months of year, December (winter), March (spring), June (summer), September(autumn)

🐴 Horses: Long-Day Breeders

• Breeding Season: Spring and summer (increasing day length).

• Gestation: Lasts 11 months.

• Timing: They conceive in the spring to give birth the following spring.

🐑 Sheep: Short-Day Breeders

• Breeding Season: Autumn and winter (decreasing day length).

• Gestation: Lasts 5 months.

• Timing: They conceive in the autumn to give birth the following spring.

🐮 Cows: Non-Seasonal Breeders

• Breeding Season: Year-round (not dependent on photoperiod).

• Gestation: Lasts 9 months.

• The Question Mark: They can breed at any time of year, but the graph shows a June conception purely to align with a spring birth.

RHT: retino-hypothalamic tract.

SCN: Suprachiasmatic nucleus

P: Pineal gland

NAT: n-acetyl transferase

BSCG: Bilaterl superior cervical ganglia

light comes in through the eye and travels down the neurones

goes down the retinal hypothalamic tract

synapsis at the suprachiasmatic nucleus

synapses then down neck to bilateral superior cervical ganglions

then travels up again to brain to the pineal gland

conversion of tryptophan to serotonin

then seratonin to melatonin (catalysed by n-acetyl transferase) - if theres daylight this second step is inhibited, cos when light is present melatonin levels drop

pineal melatonin secretion

• Daily pattern of melatonin secretion changes throughout the year

• Melatonin is only secreted during the hours of darkness.

• The hypothalamus is sensitive to melatonin during the late afternoon.

• Coincidence of hypothalamic sensitivity and melatonin indicate a short day

breeding seasons

summary pretty much

now on the right

got long and short daylight breeders

start with horse on right - low level of melatonin in summer- short nights and long days - u get stimulation of RFRP neurons - increase in RFRP 3

in horse and some cows species - we want to breed days are longer - increase in GnRH increase in cyclicity - kisspeptins are stimulated

sheep are short day breeder - low melatonin also stimulate RFRP 3 increase - kisspeptins are inhibited

RFRP neurons translate seasonal daylight changes to directly control reproductive cycles via kisspeptin.

In contrast, Neuropeptide Y (NPY) neurons primarily regulate metabolic appetite and energy balance during starvation.

summary