Muscarinic mobilization of choline in rat cerebral cortex does not involve alterations of blood-brain barrier.

Efflux of choline from the rat cerebral cortex in vivo was investigated using the cup technique. After removal of the dura mater, the cup was placed on the cortex. Transmission and scanning electron microscopy revealed that the cortex was separated from the cup solution (100-300 microliter) by basal lamina, pia mater, arachnoid (with discrete defects) and remainders of the subdural neurothelium. Two kinds of experiments were carried out to determine: efflux of unlabelled choline into the cup solution; and translocation of radioactivity from the plasma into the cup solution (via blood-brain barrier and leptomeningeal layers) during i.v. infusion of [3H]choline or [14C]inulin. The former process was highly temperature-sensitive in contrast to the latter. Penicillin-G-sodium, which is known to damage the blood-brain barrier, was added to the cup solution, enhanced efflux of unlabelled choline, and caused a 5-fold increase in the rates of translocation of radioactivity during infusion of either labelled choline or inulin. In contrast, physostigmine (3 X 10(-4) M, added to cup solution) failed to enhance 3H-translocation, but markedly facilitated the efflux of unlabelled choline; this effect was highly temperature-sensitive and was blocked by atropine. It is concluded that activation of muscarinic receptors enhanced the choline efflux from cortical tissue. This effect was caused by cellular mobilization of choline presumably through an action on the metabolism of phosphatidylcholine. The effect was not due to alterations in the translocation of choline from the plasma to the cup solution, i.e. through permeability changes in the blood-brain barrier and in the leptomeningeal 'barrier'.(ABSTRACT TRUNCATED AT 250 WORDS)