engleski

Muscarinic stimulation of ovarian growth and activation of phosphoinositide signalling in the ovary: induction by hemicastration

Autonomic innervation influences growth of the ovary remaining after hemicastration, but the neurotransmitter(s) involved have not been identified. In presented experiments muscarinic antagonist propantheline (ip), cholinergic denervation (botulinum toxin locally) and subdiaphragmal vagotomy inhibited compensatory increase of ovarian weight, protein and total RNA and DNA contents in mature rats, as evidenced on postoperative day 10. Muscarinic agonist bethanecol (ip) reversed the effects of propantheline and botulinum toxin but not the effect of vagotomy. tHis implied cholinergic, seemingly "non-vagal" stimulation of compensatory growth via ovarian muscarinic receptors. In contrast, treatments (up to 24 days) were ineffective in sham-operated or intact animals, which indicated a lack of muscarinic influence on ovarian growth when both organs were in situ. Fifteen minuter after hemicastration 1,2-diacylglycerol (DAG) levels in the remaining ovaries were increased. Atropine (iv) or botulinum toxin pretreatments and vagotomy inhibited DAG accumulation, while carbachol (in vitro) enhanced it. Carbachol was ineffective when atropine injection or vagotomy followed the operation (10 minutes). On posoperative days 2, 10 and 28 ovarian DAG levels were not increased. The carbachol-induced DAG accumulation was inhibited by atropine in vivo or in vitro. Cholinergic/muscarinic agents did not affect DAG levles in control ovaries (intact or sham-operated rats) at all. The results indicated a rapid, hemicastration-induced and muscarinic receptor-mediated activation of phosphoinositide (PI) signalling in the remaining ovary. In contrast to the sitation when both organs were in situ, following hemicastration ovarian PI system was responsive to muscarinic influence. This"switch" occurred shortly after the operation and depended on a "non-muscarinic" vagal information. In conclusion, hemicastration induces muscarinic influence on ovarian growth and enables muscarinic activation of PI signalling in the ovary. Thus, it seems that it changes ovarian muscarinic receptor function.

ovary; compensatory growth; muscarinic receptors; phosphoinositide signalling

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