Evidence for 5-HT1A binding sites in chick embryo brain and discrimination by 5-methoxytryptamine.

The displacement characteristics of [3H]5-hydroxytryptamine (5-HT1) binding by several serotonergic ligands were studied in the chick embryo brain. Although most of ligands tested displaced [3H]5-HT in a manner suggestive of a single site, displacement curves for (+/-)-8-hydroxy-dipropylaminotetralin (8-OH-DPAT), 5-methoxytryptamine, 5-methyltryptamine and 5-methoxy-N,N-dimethyltryptamine displayed non-unity Hill plots, suggesting multiple site interactions. However, if spiperone (2 microM) was included in the assays, the Hill coefficients of these compounds were all similarly increased toward unity, suggesting that 8-OH-DPAT as well as 5-methoxy and 5-methyl substituted tryptamines, have a high affinity for and can discriminate 5-HT1A binding sites in the chick embryo brain.

Down-regulation of [3H]5-hydroxytryptamine binding sites in chick embryo brain by monoamine oxidase inhibitors or fenfluramine and potentiation by d,l-5-hydroxytryptophan.

Three monoamine oxidase (MAO) inhibitors--pargyline, clorgyline and deprenyl--as well as the serotonin (5-HT, 5-hydroxytryptamine) releasing agent fenfluramine were administered to developing chick embryos and the effects on [3H]5-HT binding parameters and endogenous 5-HT levels were assessed. Multiple, but not acute, pretreatments with any of the three MAO inhibitors significantly increased 5-HT levels (p less than 0.01) and decreased receptor number (Bmax) to a maximum of 20% (p less than 0.01) without affecting the affinity (KD). When d,l-5-hydroxytryptophan (d,l-5-HTP) was similarly administered there were large increases in 5-HT levels (p less than 0.01), but no significant effects on either Bmax or KD. However, if d,l-5-HTP was co-administered with any of the MAO inhibitors there was a significant (p less than 0.01) enhancement of the MAO inhibitor-induced down-regulation to a maximum of about 40%. Multiple pretreatments with fenfluramine resulted in dose-related decreases in 5-HT levels (p less than 0.01) and Bmax (p less than 0.01) without affecting KD. The largest decrease in [3H]5-HT binding sites inducible by fenfluramine treatment alone was also about 40%. When given in combination with d,l-5-HTP, there was a potentiation of the down-regulation capabilities of fenfluramine at several different dosage levels; however, maximal down-regulation was also limited to 40%. Evidence was presented suggesting that these effects were not due to endogenous 5-HT or drugs remaining in the tissue preparation. The overall evidence implies that merely increasing endogenous 5-HT levels, as by precursor administration, does not necessarily induce down-regulation unless the 5-HT is also made available as functional 5-HT.

[Thrombosis of the left popliteal artery from hypertrophy of the gemellus muscle (author's transl)]. / Thrombose de l'artère poplitée gauche par hypertrophie des muscles jumeaux.

The authors report a case of thrombosis of the left popliteal artery in a man aged 20 years, secondary to repeated minimal trauma from contact with a hypertrophied internal gemellus muscle. A bifurcation abnormality was also present. They review the anatomical variations seen at the end of the femoro-popliteal trunk and define the clinical and angiographic characteristics of popliteal thrombosis due to adjoining muscle hypertrophy.