Table 1.

Summary of neuroendocrine defects in PNA models and associated mechanistic findings.

Species	Prenatal steroid	↑ LH levels	↑ LH pulse frequency	E +FB defect	E −FB defect	P −FB defect	Associated findings
Rhesus monkey	T (GD 40-80)	Yesa,b	unknown	Noc	Yesc	Yesd
Sheep	T (GD 30-90)	Yese,f,g	Yesh,i	Yesf,j,k	Yesg	Yesl,m	Absence of c-Fos expression in GnRH neurons following OVX+E surge paradigmn Reduced synaptic contacts to GnRH neurons, reduced glial ensheathment (OVX+Eo or intact+prostaglandin f2α injectionp) Reduced cells expressing dynorphin, neurokinin B, PR in arcuate nucleus; loss of neuropeptide coexpression in kisspeptin cells (OVX+standard hormone treatment)q
Rat	T (GD 16-19)	Yes (3 mg dose)r	Yes (1 mg dose)s	Yess	unknown	unknown	Reduced PR expression in MBH and POA on proestrus (OVX+Er or intacts) Impaired estradiol-induced increase in PR expression (OVX)s
Mouse	DHT (GD 16-19)	Yest,u	unknown	Nov	Yesv	unknown	Elevated GnRH neuronal activity (intact)u Increase in GABAergic neurotransmission/GABA release sites on GnRH neurons (intact)t Increased spine density on GnRH neurons in rPOA; failure of E-induced surge to increase spines (OVX+E)v

^aAbbott et al., 2005

^bDumesic et al., 1997

^cSteiner et al., 1976

^dLevine et al., 2005

^eManikkam et al., 2008

^fSharma et al., 2002

^gSarma et al., 2005

^hSavabieasfahani et al., 2005

ⁱSteckler et al., 2009

^jHerbosa et al., 1996

^kUnsworth et al., 2005

^lRobinson et al., 1999

^mVeiga-Lopez et al., 2008

ⁿWood et al., 1996

^oKim et al., 1999

^pJansen et al., 2011

^qCheng et al., 2010

^rWu et al., 2010

^sFoecking et al., 2005

^tSullivan and Moenter, 2004a

^uRoland and Moenter, 2011a

^vMoore et al., 2013

LH, luteinizing hormone; E, estradiol; FB, feedback; T, testosterone; OVX, ovariectomized; PR, progesterone receptor; GD, gestational day; MBH, mediobasal hypothalamus; DHT, dihydrotestosterone; GnRH, gonadotropin releasing hormone; GABA, gamma aminobutyric acid; rPOA, rostral preoptic area