The LH surge that triggers ovulation is caused by positive feedback of estradiol on the hypothalamic-pituitary axis. This positive feedback mechanism is unusual because it requires estradiol concentration to exceed a threshold for a sustained duration. Which cellular mechanism in pituitary gonadotrophs underlies the sensitisation required for the LH surge?

• A Estradiol inhibits somatostatin release from the hypothalamus, removing suppression of gonadotrophs
• B Progesterone acting through progesterone receptors on kisspeptin neurons amplifies GnRH pulse frequency
• C High estradiol upregulates GnRH receptors on gonadotrophs, self-sensitises the GnRH signalling pathway, and increases LH beta-subunit synthesis, enabling a massive LH pulse ✓
• D Rising estradiol converts FSH receptor signalling from Gi to Gs on granulosa cells, redirecting signalling to LH synthesis

Explanation

The LH surge involves two levels of estradiol-driven sensitisation. First, high estradiol stimulates kisspeptin/neurokinin B/dynorphin (KNDy) neurons in the hypothalamic anteroventral periventricular nucleus (AVPV) to increase GnRH pulse frequency and amplitude. Second, prolonged high estradiol (>200 pg/mL for >36–48 hours) upregulates GnRH receptors on gonadotrophs, increases their responsiveness to GnRH (self-priming effect), and increases pre-formed LH beta-subunit — all enabling the explosive LH surge. This positive feedback is unique to the preovulatory follicular phase; before this threshold, estradiol exerts negative feedback.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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