Sm. Celuch, POSSIBLE PARTICIPATION OF HISTAMINE H-3 RECEPTORS IN THE MODULATION OF NORADRENALINE RELEASE FROM RAT SPINAL-CORD SLICES, European journal of pharmacology, 287(2), 1995, pp. 127-133
Rat spinal cord slices prelabelled with [H-3]noradrenaline were superf
used with a medium containing 1 mu M desipramine plus 0.3 mu M phentol
amine. Histamine (0.01-10 mu M) and the selective histamine H-3 recept
or agonist R-(-)-alpha-methylhistamine (0.001-10 mu M) caused a concen
tration-dependent decrease in the release of radioactivity evoked by e
lectrical field stimulation (0.8 Hz, 20 mA, 2 min). The inhibitory eff
ect of histamine was not modified by either pyrilamine (1 mu M) or ran
itidine (10 mu M), but it was antagonized by burimamide (1 mu M). The
inhibitory action of histamine (1 mu M) was attenuated by pertussis to
xin (3 mu g/ml) and was abolished by N-ethylmaleimide (30 mu M). Neith
er forskolin (10 mu M) nor rolipram (100 mu M), nor the combination of
both drugs, modified the inhibitory effect of histamine. Histamine (1
mu M) did not modify the overflow of tritium induced by electrical st
imulation in the absence of phentolamine. The present results suggest
that in the rat spinal cord the release of noradrenaline elicited by e
lectrical stimulation is negatively modulated by histamine, probably t
hrough the activation of histamine H-3 receptors. This modulatory mech
anism is likely to involve the participation of regulatory G(0)/G(1) p
roteins.