Biomedical subjects

M J Besson

Publications and source records attributed to M J Besson.

At least 55 records · Page 3Linked to original sources

PubMed1976

Radioautographic study of in vivo incorporation of 3H-monoamines in the cat caudate nucleus: identification of serotoninergic fibers.

The localization of radioactivity was examined in the caudate nucleus of the cat, treated with an MAO inhibitor, following local superfusion of the ventricular surface of the structure with low concentration of 3H-catecholamines or [3H]5-HT. The caudate nucleus was superfused continuously from 30 to 240 min using a cup technique. Light microscope or high resolution radioautographs revealed: (1) a rather diffuse incorporation of 3H-catecholamines under the subependymal region which could be hardly attributed to a specific population of nerve terminals. A loose binding of 3H-catecholamines into dopaminergic terminals could be involved in this effect. (2) An intense and selective uptake of [3H]5-HT in fine scarce varicose nerve fibers localized in the ventricle as in the subependymal layer and in the neuropil of the nucleus. The labeled fibers contained numerous round or elongated large granular vesicles of 80-120 nm and exhibited only very few synaptic contacts suggesting a possible extrasynaptic liberation of 5-HT.

Animals↗

PubMed1976

Nicotinic effect of acetylcholine on the release of newly synthesized (3H)dopamine in rat striatal slices and cat caudate nucleus.

The effect of acetylcholine (ACh), carbachol and nicotinic blocking agents on the release of newly synthesized [3H]dopamine ([3H]DA) was studied in vitro on rat striatal slices and in vivo on the cat caudate nucleus. In the latter case, the animals were anaesthetized with halothane; in some experimetns an 'encéphale isolé' preparation was used to eliminate anaesthesia. Rat striatal slices placed in a superfusion chamber were continuously superfused with L-[3,5-3H]tyrosine. A cup placed on the ventricular surface of the cat caudate nucleus similarly allowed a continuous superfusion of the structure with the 3H amino acid. In both cases the quantities of [3H]DA contained in serial superfusate fractions were estimated; the drugs were always added in superfusing medium. In vitro ACh (10(-5) M) and carbachol (10(-5) M) enhanced the release of [3H]DA (90%). Similar results were obtained in vivo in anaesthetized cats. The effect of ACh (10(-5) M) was more pronounced (125%) in presence of eserine (10(-4) M) than with ACh alone (65%). ACh was also effective in unanaesthetized cats. The ACh effect on [3H]DA release was reproducible within the same experiment both in vitro and in vivo. This allowed to test the effect of anticholinergic agents on the ACh induced release of [3H]DA. In vivo hexamethonium (10(-4) M, 10(-5) M) partially blocked the release of [3H]DA induced by ACh (10(-5) M) alone; the effect was not seen when ACh was added in the presence of eserine (10(-4) M). Both in vivo and in vitro the prior introduction of mecamylamine into the superfusing medium antagonized the stimulating effect of ACh (10(-5) M) on [3H]DA release. The effects of this nicotinic blocking agent were seen with various concentrations (10(-6); (10(-5) 10(-4) in the in vitro experiments.

Acetylcholine↗

PubMed1976

The role of presynaptic receptors in the release and synthesis of 3H-dopamine by slices of rat striatum.

Striatal slices were continuously superfused with L-3,5-(3)H-tyrosine (50 muCi/ml) and 4H-H2O [index of 3H-dopamine (3H-DA) synthesis] and 3H-DA estimated in 0.5 ml (2.5 min) superfusate fractions. Depolarization with 50 mM K+ for 7.5 min induced a marked increase in 3H-DA release and a biphasic effect on synthesis (slight increase in the first fraction followed by a significant decrease in the third and fourth fractions). The decrease in the rate of 4H-H2O formation induced by K+ was not related to modifications of the specific activity of tyrosine in tissues. The possibility that the inhibition of synthesis was due to alterations in DA concentration in the synaptic cleft was examined. Benztropine in a concentration which produced inhibition of DA uptake (10(-6) M) increased the K+ induced overflow of 3H-DA but failed to alter the inhibition of synthesis. On the other hand, when the powerful neuroleptic fluphenazine was added to the superfusion medium in a concentration which only weakly blocked 3H-DA uptake (10(-6) M) it potentiated 3H-DA release and prevented the inhibition of synthesis both in the absence or presence of benztropine. A similar effect was seen following the in vivo treatment of rats with fluphenazine (2 mg/kg; 1 1/2 h before sacrifice). The addition of exogenous DA (0.6 X 10(-6) M) or NA (10(-6) M) to the superfusion medium increased 3H-DA outflow and reduced DA synthesis while isoproterenol (10(-6) M) was without effect. The DA inhibitory effect on synthesis was still observed in the presence of benztropine (10(-6) M) while the NA effect was prevented. This concentration of benztropine blocked both DA and NA uptake. The administration of fluphenazine (10(-6) M) significantly prevented the decrease in 3H-DA synthesis induced by exogenous DA and partially prevented the effect of NA. In addition, the effect of exogenous DA on the inhibition of synthesis was still seen in the presence of 2-amino-4-hydroxy-6,7-dimethyl-5,6,-7,8-tetrahydropteridine hydrochloride (DMPH4) (to protect against end-product inhibition). The present results provide direct support for the concept that activation of presynaptic DA receptors located on DA terminals in the striatum of the rat results in an inhibition of synthesis and release of the transmitter.

Animals↗

PubMed1976