TY - JOUR
T1 - Transforming growth factor-α gene expression in the hypothalamus is developmentally regulated and linked to sexual maturation
AU - Jun Ma, Ying
AU - Junier, Marie Pierre
AU - Costa, Maria E.
AU - Ojeda, Sergio R.
N1 - Funding Information:
We wish to thank Janie Gliessman and Diane Hill for their editorial assistance. This work was supported by grants HD25123 and RR00163 from the National Institutes of Health. This is publication no. 1856 of the Oregon Regional Primate Research Center.
PY - 1992/10
Y1 - 1992/10
N2 - Hypothalamic injury causes female sexual precocity by activating luteinizing hormone-releasing hormone (LHRH) neurons, which control sexual development. Transforming growth factor-α (TGF-α) has been implicated in this process, but its involvement in normal sexual maturation is unknown. The present study addresses this issue. TGF-α mRNA and protein were found mostly in astroglia, in regions of the hypothalamus concerned with LHRH control. Hypothalamic TGF-α mRNA levels increased at times when secretion of pituitary gonadotropins-an LHRH-dependent event-was elevated, particularly at the time of puberty. Gonadal steroids involved in the control of LHRH secretion increased TGF-α mRNA levels. Blockade of TGF-α action in the median eminence, a site of glial-LHRH nerve terminal association, delayed puberty. These results suggest that TGF-α of glial origin is a component of the developmental program by which the brain controls mammalian sexual maturation.
AB - Hypothalamic injury causes female sexual precocity by activating luteinizing hormone-releasing hormone (LHRH) neurons, which control sexual development. Transforming growth factor-α (TGF-α) has been implicated in this process, but its involvement in normal sexual maturation is unknown. The present study addresses this issue. TGF-α mRNA and protein were found mostly in astroglia, in regions of the hypothalamus concerned with LHRH control. Hypothalamic TGF-α mRNA levels increased at times when secretion of pituitary gonadotropins-an LHRH-dependent event-was elevated, particularly at the time of puberty. Gonadal steroids involved in the control of LHRH secretion increased TGF-α mRNA levels. Blockade of TGF-α action in the median eminence, a site of glial-LHRH nerve terminal association, delayed puberty. These results suggest that TGF-α of glial origin is a component of the developmental program by which the brain controls mammalian sexual maturation.
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U2 - 10.1016/0896-6273(92)90029-D
DO - 10.1016/0896-6273(92)90029-D
M3 - Article
C2 - 1327011
AN - SCOPUS:0026778806
SN - 0896-6273
VL - 9
SP - 657
EP - 670
JO - Neuron
JF - Neuron
IS - 4
ER -