Role of the blood-brain barrier in the anticholinergic differential effects on LH and prolactin release in proestrous rats.

The effects of homatropine and atropine on plasma LH and prolactin (PRL) levels during the afternoon of pro-oestrus were investigated. Homatropine methylbromide was unable to block the spontaneous increase of LH but prevented the prolactin surge in pro-oestrous rats at doses of 450 and 700 mg/kg s.c. Atropine sulphate blocked both LH and PRL at doses of 450 and 700 mg/kg s.c. These two anticholinergics when injected into the 3rd ventricle (250 mug/rat) blocked the pro-oestrus increase of LH and inhibited PRL. Pharmacological experiments were performed in parallel and the injection of either homatropine or atropine (450 mg/kg s.c.) resulted in the abolishment of peripheral toxic signs induced by pilocarpine (50 mg/kg s.c.) whereas its central toxic signs were prevented by atropine but not by homatropine. Our findings suggest that the difference in action of systemic injections of atropine and homatropine on LH and PRL release is explained by a relatively low permeability of homatropine to the brain. Therefore, cholinergic LH-controlling mechanisms may be situated above the median eminence and those related to PRL placed outside the blood-brain barrier.