Group I metabotropic glutamate receptors activate burst firing in rat midbrain dopaminergic neurons.
Neuropharmacology
; 42(3): 289-96, 2002 Mar.
Article
em En
| MEDLINE
| ID: mdl-11897107
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 microM) and d-tubocurarine (500 microM) (d-TC), whereas they all fired in bursts during NMDA (20 microM) 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 1 selective, non-competitive antagonist CPCCOEt (7-cyclopropan[b]chromen-1a-carboxylic acid ethyl ester) (100 microM) while it was not affected by the mGluR 5 selective antagonist MPEP (2-methyl-6-(phenylethynyl)-pyridine (10 microM). These results suggest that both the activation of glutamate metabotropic type 1 and NMDA ionotropic receptors induce burst firing in the dopaminergic cells of the ventral midbrain when the activity of the SK-channels is reduced.
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Base de dados:
MEDLINE
Assunto principal:
Potenciais de Ação
/
Mesencéfalo
/
Dopamina
/
Receptores de Glutamato Metabotrópico
/
Metoxi-Hidroxifenilglicol
/
Neurônios
Limite:
Animals
Idioma:
En
Revista:
Neuropharmacology
Ano de publicação:
2002
Tipo de documento:
Article
País de afiliação:
Itália