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Titolo:
The modulation of calcium current by GABA metabotropic receptors in a sub-population of pallidal neurons
Autore:
Stefani, A; Spadoni, F; Giacomini, P; Lavaroni, F; Bernardi, G;
Indirizzi:
Univ Roma Tor Vergata, Dipartimento Neurosci, I-00133 Rome, Italy Univ Roma Tor Vergata Rome Italy I-00133 o Neurosci, I-00133 Rome, Italy IRCCS Osped S Lucia, I-00179 Rome, Italy IRCCS Osped S Lucia Rome Italy I-00179 sped S Lucia, I-00179 Rome, Italy Univ Rome La Sapienza, Neurol Clin, Rome, Italy Univ Rome La Sapienza Rome Italy La Sapienza, Neurol Clin, Rome, Italy
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 11, volume: 11, anno: 1999,
pagine: 3995 - 4005
SICI:
0953-816X(199911)11:11<3995:TMOCCB>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT GLOBUS-PALLIDUS; MEDIATED SYNAPTIC POTENTIALS; PRIMATE SUBTHALAMIC NUCLEUS; MPTP-INDUCED PARKINSONISM; BASAL GANGLIA; FUNCTIONAL-ANATOMY; SUBSTANTIA NIGRA; ENTOPEDUNCULAR NUCLEUS; GLUTAMATE RECEPTORS; MOVEMENT-DISORDERS;
Keywords:
baclofen; basal ganglia; movement disorders; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Stefani, A Univ Roma Tor Vergata, Dipartimento Neurosci, Via Di Tor Vergata 135, I-00133 Rome, Italy Univ Roma Tor Vergata Via Di Tor Vergata 135 Rome Italy I-00133
Citazione:
A. Stefani et al., "The modulation of calcium current by GABA metabotropic receptors in a sub-population of pallidal neurons", EUR J NEURO, 11(11), 1999, pp. 3995-4005

Abstract

Globus pallidus (GP) receives an abundant GABAergic (gamma-aminobutyric acid) pathway from the corpus striatum. Several evidences suggested that alterations of this pathway might underlie the development of movement disorders. Classical models on Parkinsonism are centred on the increased excitability of GABAergic striatofugal neurons impinging GP and, therefore, on the presumed hypoactivity of GP neurons, but very few electrophysiological studies have addressed the activation of GABA receptors in mammalian GP. We have isolated calcium currents in GP neurons dissociated from the adult rat brain and analysed GABA-mediated responses. In the presence of bicuculline, thefast, chloride-mediated, ionotropic responses were obscured and GABA produced a large (greater than or equal to 35%) inhibition of calcium currents. The GABA-induced inhibition of calcium currents strongly desensitized was mimicked by baclofen and prevented by hydroxy-saclofen, supporting the involvement of GABA(B) receptors. The baclofen-mediated modulation was: (i) associated with slowing of activation kinetics; (ii) relieved by prepulse facilitation; and (iii) G-protein-mediated. The response was slow in onset, requiring the mobilization of intracellular cAMP, and was abolished by the combination of N-type and P-type calcium channel blockers. The GABA(B)-mediatedeffect, however, was confined to a particular subtype of GP neurons, identified by relatively small to medium soma. Differently, in cells characterized by larger somata and capacitance, the baclofen response was negligible. Intriguingly, these baclofen-resistant, larger neurons manifested a consistent low-voltage-activated (LVA) calcium current, not detected in baclofen-sensitive cells, at least when recorded in whole-cell mode. This study demonstrates that GP neurons express functional GABA(A) and GABA(B) receptors. In a subset of GP neurons, the activation of GABA(B) receptors induces a large modulation of high-voltage-activated (HVA) calcium currents, which may strongly influence basal ganglia circuitry and partially explain some discrepancies of classical models of extrapyramidal disorders.

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Documento generato il 15/07/20 alle ore 08:39:07