TY - JOUR
T1 - Intracellular studies on the dopamine-induced firing inhibition of neostriatal neurons in vitro
T2 - Evidence for D1 receptor involvement
AU - Calabresi, P.
AU - Mercuri, N.
AU - Stanzione, P.
AU - Stefani, A.
AU - Bernardi, G.
PY - 1987
Y1 - 1987
N2 - Intracellular recordings were obtained from rat neostriatal slices. Bath-applied dopamine (1-10 μM) produced a reversible inhibition of the action potentials evoked by direct stimulation and a decrease in the amplitude of the intrastriatally evoked depolarizing postsynaptic potentials. No change in membrane potential was detected during the application of 1-10 μM dopamine. Dopamine application also produced a decrease in anomalous rectification in the depolarizing direction. This subthreshold inward rectification was abolished by tetrodotoxin, but not by calcium-free and cadmium (0.1-1 mM)-containing solutions. The dopamine-induced decrease in excitatory postsynaptic potential amplitude was evident at resting membrane potential or at more positive levels, but was absent at hyperpolarized values of the membrane potential. Addition of bicuculline (50-500 μM) to the medium did not affect the inhibitory action of dopamine. The inhibitory action of dopamina also persisted in calcium-free and cadmium-containing solutions. The adenosine 3′,5′-cyclic monophosphate analogue, 8-bromo-adenosine 3′,5′-cyclic monophosphate (0.1-1 mM), mimicked the effects produced by D1 receptor activation. Bath application of 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393) (1-10 μM), a selective D1 dopaminergic agonist, mimicked the effects of micromolar concentrations of dopamine. The D2 dopaminergic agonists, 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline (LY 171555) and bromocriptine (both at 10 nM-10 μM), had no effects on neostriatal cells. The inhibition induced by micromolar doses of dopamine or SKF 38393 was antagonized by bath applications of R-( + )-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol (SCH 23390; 0.1-10 μM), a D1-selective antagonist, but not by sulpiride (10nM-10μM), a D2 antagonist. We conclude that the inhibitory effect of dopamine on rat striatal neurons is postsynaptically mediated by the activation of D1 dopaminergic receptors via the reduction of a voltage-dependent tetrodotoxin sensitive inward conductance.
AB - Intracellular recordings were obtained from rat neostriatal slices. Bath-applied dopamine (1-10 μM) produced a reversible inhibition of the action potentials evoked by direct stimulation and a decrease in the amplitude of the intrastriatally evoked depolarizing postsynaptic potentials. No change in membrane potential was detected during the application of 1-10 μM dopamine. Dopamine application also produced a decrease in anomalous rectification in the depolarizing direction. This subthreshold inward rectification was abolished by tetrodotoxin, but not by calcium-free and cadmium (0.1-1 mM)-containing solutions. The dopamine-induced decrease in excitatory postsynaptic potential amplitude was evident at resting membrane potential or at more positive levels, but was absent at hyperpolarized values of the membrane potential. Addition of bicuculline (50-500 μM) to the medium did not affect the inhibitory action of dopamine. The inhibitory action of dopamina also persisted in calcium-free and cadmium-containing solutions. The adenosine 3′,5′-cyclic monophosphate analogue, 8-bromo-adenosine 3′,5′-cyclic monophosphate (0.1-1 mM), mimicked the effects produced by D1 receptor activation. Bath application of 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393) (1-10 μM), a selective D1 dopaminergic agonist, mimicked the effects of micromolar concentrations of dopamine. The D2 dopaminergic agonists, 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline (LY 171555) and bromocriptine (both at 10 nM-10 μM), had no effects on neostriatal cells. The inhibition induced by micromolar doses of dopamine or SKF 38393 was antagonized by bath applications of R-( + )-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol (SCH 23390; 0.1-10 μM), a D1-selective antagonist, but not by sulpiride (10nM-10μM), a D2 antagonist. We conclude that the inhibitory effect of dopamine on rat striatal neurons is postsynaptically mediated by the activation of D1 dopaminergic receptors via the reduction of a voltage-dependent tetrodotoxin sensitive inward conductance.
UR - http://www.scopus.com/inward/record.url?scp=0023263479&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023263479&partnerID=8YFLogxK
U2 - 10.1016/0306-4522(87)90239-9
DO - 10.1016/0306-4522(87)90239-9
M3 - Article
C2 - 2955246
AN - SCOPUS:0023263479
VL - 20
SP - 757
EP - 771
JO - Neuroscience
JF - Neuroscience
SN - 0306-4522
IS - 3
ER -