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A Pittaluga

Publications and source records attributed to A Pittaluga.

44 records · Page 3Linked to original sources
PubMed1986

Differential pharmacology and function of two 5-HT1 receptors modulating transmitter release in rat cerebellum.

The release of endogenous glutamate (GLU) elicited by depolarization of rat cerebellum synaptosomes was inhibited potently (pEC30 = 9.77) by 5-hydroxytryptamine (5-HT). The 5-HT action was antagonized by methiothepin (pA2 = 10.37); ketanserin, methysergide, cinanserin and spiperone were ineffective. Exogenous 5-HT also inhibited the release of [3H]-5-HT from cerebellar synaptosomes (pEC30 = 8.73). Methiothepin, but not ketanserin, methysergide, cinanserin or spiperone counteracted the inhibition (pA2 = 9.28). The receptors involved (presynaptic 5-HT heteroreceptors and autoreceptors) were activated by the 5-HT1 agonist RU 24969 (5-methoxy-3-[1,2,3,6-tetrahydropyridin-4-yl]-1H-indole) which showed comparable activity at the two receptor systems. (-)-Propranolol, used as a 5-HT1 antagonist, shifted to the right (pA2 = 8.05) the dose-response curve of 5-HT at the autoreceptors, but was ineffective at the receptors regulating GLU release. On the contrary, the 5-HT1A agonist 8-hydroxy-2-di-N-propylamino)tetralin activated the presynaptic heteroreceptors (pEC30 = 7.98), but was ineffective as a 5-HT autoreceptor agonist. The results allow the following major conclusions: 5-HT receptors are located on GLU terminals in rat cerebellum where they may modulate in an inhibitory way the release of GLU; 5-HT autoreceptors possibly involved in a negative feedback regulation of 5-HT release are present on cerebellar 5-HT nerve endings; 5-HT autoreceptors and heteroreceptors can be pharmacologically differentiated and appear to represent subtypes of the 5-HT1 receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1984

Noradrenaline uptake inhibitors do not reduce the presynaptic action of clonidine on 3H-noradrenaline release in superfused synaptosomes.

The interaction between clonidine, as an agonist at the alpha 2-autoreceptors regulating noradrenaline release, and inhibitors of noradrenaline neuronal uptake was investigated in superfused synaptosomes, i.e. in conditions preventing accumulation of the released transmitter in the vicinity of presynaptic autoreceptors. Desipramine or cocaine did not release the inhibitory action of clonidine on the release of 3H-noradrenaline evoked by 15 mM KCl from rat cortex synaptosomes, even when the concentration ratio between uptake inhibitor and clonidine was very high. The present results do not support the hypothesis of an interaction between imidazolines and noradrenaline uptake inhibitors at the level of alpha 2-autoreceptors, or that of a functional coupling between presynaptic alpha 2-autoreceptors and noradrenaline uptake mechanism.

Animals↗
PubMed1983

Differential blockade by (-)mianserin of the alpha 2-adrenoceptors mediating inhibition of noradrenaline and serotonin release from rat brain synaptosomes.

Mianserin and its two enantiomers were studied as antagonists of the alpha 2-adrenoceptors mediating inhibition of noradrenaline and 5-hydroxytryptamine release in rat brain cortex. The inhibitory effect of exogenous noradrenaline on the release of 3H-noradrenaline evoked by 15 mM KCl from superfused cortical synaptosomes was antagonized by racemic mianserin and by (+)mianserin; the (-)enantiomer was ineffective. In contrast, both (+)mianserin and (-)mianserin antagonized the inhibitory effect of noradrenaline on the release of 3H-5-hydroxytryptamine. The results suggest that the alpha 2-autoreceptors on noradrenergic nerve endings differ from the alpha 2-adrenoceptors located on serotoninergic terminals.

Adrenergic alpha-Antagonists↗