Nb. Mercuri et al., ELECTROPHYSIOLOGICAL EFFECTS OF MONOAMINE-OXIDASE INHIBITION ON RAT MIDBRAIN DOPAMINERGIC-NEURONS - AN IN-VITRO STUDY, British Journal of Pharmacology, 117(3), 1996, pp. 528-532
1 The effects of the inhibition of monoamine oxidase (MAO) type A and
B have been evaluated on the spontaneous firing activity of the dopami
nergic (principal) neurones of the rat midbrain intracellularly record
ed from a slice preparation. 2 The non-specific MAO inhibitor, pargyli
ne, superfused at a concentration of 10-100 mu M, decreased or abolish
ed the spontaneous firing discharge of the principal neurones in the s
ubtantia nigra pars compacta and ventral tegmental area. This effect h
ad a slow onset and appeared to be sustained. 3 The administration of
the dopamine D-2/3 receptor antagonist, sulpiride (100-300 nM), antago
nized the pargyline-induced effect, while the superfusion of the dopam
ine D-1 receptor antagonist, SCH 23390 (1-3 mu M) did not counteract t
he induced inhibition of the firing rate. 4 The inhibitor for the MAO
A, clorgyline (30-100 mu M), reduced the firing rate of the dopaminerg
ic neurones. A similar depressant effect was also observed when a MAO
B inhibitor, deprenyl (30-100 mu M), was applied. Lower concentrations
of both drugs (300 nM-10 mu M) did not produce consistent effects on
neuronal discharge. 5 Our data suggest that only the blockade of both
types of MAO enzymes favours the inhibitory action of endogenous dopam
ine on somato-dendritic D-2/3 autoreceptors.