TY - JOUR
T1 - Direct hypothalamic control of vasoactive intestinal peptide (VIP) levels in the developing rat ovary
AU - Advis, Juan P.
AU - Ahmed, Carol E.
AU - Ojeda, Sergio R.
N1 - Funding Information:
‘This publication was supported by grants from the NSF (BNS-8318017). the NIH @ID-24870 and RR-O0163), and Tbe Harold Wetterberg Foundation. Part of this research was performed in the ~p~ent of Physiology, University of Texas Health Science Center at Dallas before Dr. Ahmed and Dr. Ojeda relocated. This is publication No. OGQOfr om the Oregon Regional Primate Research Center, Beaverton, OR. *Postdoctoral research fellow supported by NIH Training Grant NIH 5 T32-HDO7062. 3Requests for reprints should be addressed to S. R. Ojeda, Division of Neuroscience, Oregon Regional Primate Research Center, 505 N.W. 185th Avenue, Beaverton, OR 97006.
PY - 1989/4
Y1 - 1989/4
N2 - We have previously identified the neurotransmitter vasoactive intestinal peptide (VIP) in nerve fibers of the immature rat ovary and showed that it stimulates steroid release by a mechanism involving increased synthesis of the components of the cholesterol side-chain cleavage enzyme complex. The present experiments were undertaken to study the ontogeny of ovarian VIP levels and to determine if they change in relation to the initiation of puberty. VIP was already detected in 2-day-old ovaries; levels remained constant at approximately 4.5 pg/mg ovary until the end of juvenile development (day 30). Thereafter, and preceding the peripubertal activation of the ovary, VIP levels increased two-fold, decreased gradually towards the first proestrus, and returned to juvenile values after the first ovulation. Transection of the ovarian nerves eliminated radioimmunoassayable VIP levels in both intact and hypophysectomized rats, indicating that ovarian VIP derives mostly from the extrinsic innervation of the gland. Treatment of hypophysectomized immature female rats with human chorionic gonadotropin (hCG), follicle stimulating hormone (FSH), growth hormone (GH), prolactin (Prl), estradiol, or their combination, failed to reproduce the peripubertal increase in VIP. In contrast, unilateral direct anodal current lesions of the left preoptic-anterior hypothalamic area (POA-AHA) of hypophysectomized juvenile rats led to a significant increase in VIP in the ipsilateral ovary. Surprisingly, both bilateral lesions and lesions of the right POA-AHA also increased VIP levels in the left ovary suggesting the existence of a marked asymmetry in the hypothalamic control of ovarian VIP. Lesions of the ventromedial nucleus, dorsal AHA or small lesions of the AHA were ineffective. The results suggest that: a) in prepubertal rats ovarian VIP levels are controlled by a pituitary-independent, neurally-mediated, mechanism which involves the POA-AHA region of the hypothalamus; b) this control is markedly asymmetric; and c) the lesion-induced increase in ovarian VIP levels may not result from the loss of a discrete inhibitory center, but rather may be the consequence of compensatory reactivity of the areas surrounding the lesion.
AB - We have previously identified the neurotransmitter vasoactive intestinal peptide (VIP) in nerve fibers of the immature rat ovary and showed that it stimulates steroid release by a mechanism involving increased synthesis of the components of the cholesterol side-chain cleavage enzyme complex. The present experiments were undertaken to study the ontogeny of ovarian VIP levels and to determine if they change in relation to the initiation of puberty. VIP was already detected in 2-day-old ovaries; levels remained constant at approximately 4.5 pg/mg ovary until the end of juvenile development (day 30). Thereafter, and preceding the peripubertal activation of the ovary, VIP levels increased two-fold, decreased gradually towards the first proestrus, and returned to juvenile values after the first ovulation. Transection of the ovarian nerves eliminated radioimmunoassayable VIP levels in both intact and hypophysectomized rats, indicating that ovarian VIP derives mostly from the extrinsic innervation of the gland. Treatment of hypophysectomized immature female rats with human chorionic gonadotropin (hCG), follicle stimulating hormone (FSH), growth hormone (GH), prolactin (Prl), estradiol, or their combination, failed to reproduce the peripubertal increase in VIP. In contrast, unilateral direct anodal current lesions of the left preoptic-anterior hypothalamic area (POA-AHA) of hypophysectomized juvenile rats led to a significant increase in VIP in the ipsilateral ovary. Surprisingly, both bilateral lesions and lesions of the right POA-AHA also increased VIP levels in the left ovary suggesting the existence of a marked asymmetry in the hypothalamic control of ovarian VIP. Lesions of the ventromedial nucleus, dorsal AHA or small lesions of the AHA were ineffective. The results suggest that: a) in prepubertal rats ovarian VIP levels are controlled by a pituitary-independent, neurally-mediated, mechanism which involves the POA-AHA region of the hypothalamus; b) this control is markedly asymmetric; and c) the lesion-induced increase in ovarian VIP levels may not result from the loss of a discrete inhibitory center, but rather may be the consequence of compensatory reactivity of the areas surrounding the lesion.
KW - Female puberty
KW - Hypothalamic lesions
KW - Hypothalamus
KW - Ovarian innervation
KW - Vasoactive intestinal peptide
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U2 - 10.1016/0361-9230(89)90077-4
DO - 10.1016/0361-9230(89)90077-4
M3 - Article
C2 - 2736390
AN - SCOPUS:0024654637
SN - 0361-9230
VL - 22
SP - 605
EP - 610
JO - Brain Research Bulletin
JF - Brain Research Bulletin
IS - 4
ER -