Effect of secretion of splenocytes after superior ovarian nerve section on the ovarian steroidogenesis.
It is known that ovary and spleen are innervated extensively by afferent and efferent noradrenergic sympathetic nerve fibers from the celiac ganglion. Furthermore, immune cells located in the ovary influence the ovarian physiology. However, the peripheral interaction between the immune and neuroendocrine system is poorly understood. This work was undertaken to study the effect of superior ovarian nerve (SON) transection, in adult rats, on the number of splenocyte beta-adrenergic receptors and their possible relation to ovarian steroidogenesis, measuring the effect of secretions of those splenocytes on progesterone and estradiol release from the ovary. Seven days after SON transection, the splenocytes were isolated and then cultured for 48 h. Their number of beta-adrenergic receptors, measured using [125I]-cyanopindolol as ligand, increased, and their culture media, used to stimulate ovaries from 60-day-old intact (neither SON-transected nor sham-operated) rats in vitro on diestrous day 2 showed a decrease in progesterone release and an increase in estradiol release in relation to splenocyte culture media of control rats (sham-operated; p < 0.001, respectively). The effects of in vivo SON transection were simulated by an in vitro system modulating the splenocyte beta-adrenergic receptor number. The splenocytes from SON-transectioned rats were preincubated with and without norepinephrine (NE) 10(-6) M for 48 h, a low and high number of beta-adrenergic receptors respectively, and then were stimulated with NE 10(-6) M for 24 h. After that, the culture medium from splenocytes with a low number of beta-adrenergic receptors induced progesterone release from the ovaries of intact rats (p < 0. 001), but produced no change in estradiol release. The data suggest that splenocyte secretions, which participate in the ovarian steroidogenic response, particularly in progesterone release, might be controlled by adrenergic influences since the number of splenocyte beta-adrenergic receptors changes through SON-celiac ganglion-noradrenergic postganglionic innervation of the spleen. In estradiol release, probably other neurotransmitters than norepinephrine (NE) are involved when the SON is sectioned. In this paper we also show functional evidence for modulation of immune function by the sympathetic nervous system and its principal neurotransmitter, NE.
Laboratorio de Biología de la Reproducción, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, Argentina.
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Forneris
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Oliveros
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Aguado
D000818:Animals; D002478:Cells, Cultured; D004958:Estradiol / Q000096:biosynthesis / Q000378:metabolism*; D005260:Female; D010053:Ovary / Q000294:innervation / Q000378:metabolism*; D011374:Progesterone / Q000096:biosynthesis / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D013154:Spleen / Q000166:cytology / Q000294:innervation / Q000378:metabolism*
D011943:Receptors, Adrenergic, beta; D011374:Progesterone; D004958:Estradiol