Sakakibara · Journal of neuroendocrinology 2013 · controlled laboratory animal experiment · n=?

Different critical perinatal periods and hypothalamic sites of oestradiol action in the defeminisation of luteinising hormone surge and lordosis capacity in the rat.

Cited 12 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Non-clinical animal research (design analogy)

PubMed 22994299 · doi:10.1111/j.1365-2826.2012.02389.x · record verified 2026-08-26

What was done

Investigators evaluated the timing and neuroanatomical sites of perinatal oestradiol action required for the defeminisation of the GnRH/LH surge versus lordosis capacity in rats. Perinatal interventions included subcutaneous oestradiol-benzoate injections on embryonic day 21 (E21), day of birth (D0), or postnatal day 5 (D5) in females; perinatal castration on E21, D0, or D5 in males; neonatal local oestradiol implantation into anterior (AVPV/POA), mid, or posterior hypothalamic regions in females; and neonatal NMDA antagonist administration in males. In adulthood, animals were assessed for oestradiol-induced LH surge capability and lordosis behavior.

What was found

The abstract reports directional outcomes without exact numerical values or statistics: - Subcutaneous oestradiol-benzoate on E21, D0, or D5 completely abolished adult oestradiol-induced LH surges in female rats but did not inhibit lordosis. - Perinatal castration on E21 or D0 partially rescued the LH surge in males, whereas castration at E21 through D5 totally rescued lordosis. - Neonatal oestradiol implantation specifically in the anterior hypothalamus (AVPV/POA) abolished the LH surge in females, while mid and posterior hypothalamic implants had no effect; lordosis was unaffected by oestradiol implants in any hypothalamic region tested. - Neonatal NMDA antagonist treatment in males rescued lordosis capacity but not the LH surge.

Why it matters

This study demonstrates that the defeminisation of the neuroendocrine LH surge and female sexual behaviour in rats occur via distinct critical developmental windows, distinct neuroanatomical sites (with anterior hypothalamic AVPV/POA mediating surge defeminisation), and different neurotransmitter pathways.

Limits

The abstract provides no sample sizes ($n$), variance measures, or quantitative values. As an animal laboratory study in rats, the findings cannot be directly applied to human neuroendocrine physiology.

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