We have investigated the changes in the spontaneous firing pattern induced by DHPG ((S)-3,5-dihydroxyphenylglycine) and NMDA (N-methyl-d-aspartic acid) on rat dopaminergic neurons in substantia nigra pars compacta (SNc) using sharp microelectrode recordings in in vitro conditions. Twenty-five out of 33 cells modified the regular single-pacemaker activity in burst firing when exposed to the Group I metabotropic glutamate receptor (mGluR) agonist DHPG (30 muM) and d-tubocurarine (500 muM) (d-TC), whereas they all fired in bursts during NMDA (20 muM) plus d-TC application. The blockade of SK-channels by d-TC and apamin was essential for the production of both types of bursts. Although the two drugs induced a similar number of action potentials per burst, the DHPG-induced bursts had a lower frequency, a longer duration and a longer plateau period without spikes. In addition, the DHPG-induced bursting had a longer wash-out, could be reduced or blocked by the mGluR I selective, non-competitive antagonist CPCCOEt (7-cyclopropan[b]chromen-1a-carboxylic acid ethyl ester) (100 muM) while it was not affected by the mGluR 5 selective antagonist MPEP (2-methyl-6-(phenylethynyl)-pyridine (10 muM). These results suggest that both the activation of glutamate metabotropic type I and NMDA ionotropic receptors induce burst firing in the dopaminergic cells of the ventral midbrain when the activity of the SK-channels is reduced. (C) 2002 Elsevier Science Ltd. All rights reserved.

Prisco, S., Natoli, S., Bernardi, G., Mercuri, N.b. (2002). Group I metabotropic glutamate receptors activate burst firing in rat midbrain dopaminergic neurons. NEUROPHARMACOLOGY, 42(3), 289-296 [10.1016/S0028-3908(01)00192-7].

Group I metabotropic glutamate receptors activate burst firing in rat midbrain dopaminergic neurons

NATOLI, SILVIA;BERNARDI, GIORGIO;MERCURI, NICOLA BIAGIO
2002-01-01

Abstract

We have investigated the changes in the spontaneous firing pattern induced by DHPG ((S)-3,5-dihydroxyphenylglycine) and NMDA (N-methyl-d-aspartic acid) on rat dopaminergic neurons in substantia nigra pars compacta (SNc) using sharp microelectrode recordings in in vitro conditions. Twenty-five out of 33 cells modified the regular single-pacemaker activity in burst firing when exposed to the Group I metabotropic glutamate receptor (mGluR) agonist DHPG (30 muM) and d-tubocurarine (500 muM) (d-TC), whereas they all fired in bursts during NMDA (20 muM) plus d-TC application. The blockade of SK-channels by d-TC and apamin was essential for the production of both types of bursts. Although the two drugs induced a similar number of action potentials per burst, the DHPG-induced bursts had a lower frequency, a longer duration and a longer plateau period without spikes. In addition, the DHPG-induced bursting had a longer wash-out, could be reduced or blocked by the mGluR I selective, non-competitive antagonist CPCCOEt (7-cyclopropan[b]chromen-1a-carboxylic acid ethyl ester) (100 muM) while it was not affected by the mGluR 5 selective antagonist MPEP (2-methyl-6-(phenylethynyl)-pyridine (10 muM). These results suggest that both the activation of glutamate metabotropic type I and NMDA ionotropic receptors induce burst firing in the dopaminergic cells of the ventral midbrain when the activity of the SK-channels is reduced. (C) 2002 Elsevier Science Ltd. All rights reserved.
2002
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/41 - ANESTESIOLOGIA
Settore MED/26 - NEUROLOGIA
English
Con Impact Factor ISI
DHPG; NMDA; d-tubucurarine; apamin; SK-channels; single-spike mode; bursts; dopaminergic neurons
VENTRAL TEGMENTAL AREA; NIGRA ZONA COMPACTA; METHYL-D-ASPARTATE; SUBSTANTIA-NIGRA; INWARD CURRENT; MEMBRANE-PROPERTIES; POTASSIUM CHANNELS; SMALL-CONDUCTANCE; NMDA RECEPTORS; IMPULSE FLOW
Prisco, S., Natoli, S., Bernardi, G., Mercuri, N.b. (2002). Group I metabotropic glutamate receptors activate burst firing in rat midbrain dopaminergic neurons. NEUROPHARMACOLOGY, 42(3), 289-296 [10.1016/S0028-3908(01)00192-7].
Prisco, S; Natoli, S; Bernardi, G; Mercuri, Nb
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/55387
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