and LSD high affinity binding sites to brain synaptosomal membranes

tryptaminergic nerves, prevented the accumulation of [3H1-5-HT in supra-ependymal nerve terminals. However, desipramine, a known catecholamineuptake blocker, had no effect on this accumulation. The demonstration of a specific uptake mechanism for 5-HT in supra-ependymal nerve terminals confirms the tryptaminergic nature of these nerves (Richards, Lorez & Tranzer, 1973; Lorez & Richards, 1973; Richards & Tranzer, 1974; Lorez & Richards, 1975). The physiological significance of this uptake mechanism is likely to be the removal of the amine from the vicinity of the effector organ (periventricular target cell) in order to terminate the possible neurotransmitter action of 5-HT. The presence of 5-HT in CSF (Holman & Vogt, 1972), probably secreted in part by supra-ependymal nerve terminals, suggests that there may be specific receptors and a physiological role for this amine in periventricular brain regions. This may also be true of the human brain since supra-ependymal nerve terminals have recently been observed in the lateral and fourth ventricles of human postmortem tissue by electron microscopy; it might be expected that these nerves also store and accumulate 5-HT although this has to be demonstrated. Since the hallucinogenic drug DLSD is known to have a high affinity for 5-HT (Bennett & Snyder, 1975) and DA (Creese, Burt & Snyder, 1976) receptors, the localization of binding sites for [3H1DLSD was studied by autoradiography in order to identify 5-HT receptors in periventricular brain regions (presuming the absence of DA receptors in these regions). The results indicate that, 1 h after intraventricular administration of 350 gM [3H1-DLSD, a significant binding of LSD could be observed in the ependymal and subependymal zone of several periventricular brain regions. However, the label did not seem to be selectively bound to any particular structure. Experiments are now in progress to test the ability of DLSD and 2-bromo-LSD, but not LLSD, to displace the [3H1-DLSD visualized by autoradiography and thereby identify specifically bound label and possibly the target sites for the 5-HT.