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Titolo:
IONIC BASIS FOR SEROTONIN-INDUCED BISTABLE MEMBRANE-PROPERTIES IN GUINEA-PIG TRIGEMINAL MOTONEURONS
Autore:
HSIAO CF; DELNEGRO CA; TRUEBLOOD PR; CHANDLER SH;
Indirizzi:
UNIV CALIF LOS ANGELES,DEPT PHYSIOL SCI,2851 SLICHTER HALL LOS ANGELES CA 90095 UNIV CALIF LOS ANGELES,DEPT PHYSIOL SCI LOS ANGELES CA 90095 CALIF STATE UNIV FRESNO,DEPT PHYS THERAPY FRESNO CA 93740
Titolo Testata:
Journal of neurophysiology
fascicolo: 6, volume: 79, anno: 1998,
pagine: 2847 - 2856
SICI:
0022-3077(1998)79:6<2847:IBFSBM>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-VITRO; NEURONS INVITRO; ELECTROPHYSIOLOGICAL PROPERTIES; LUMBAR MOTONEURONS; ALPHA-MOTONEURONES; MASTICATORY RHYTHM; FICTIVE LOCOMOTION; FIRING PROPERTIES; NEONATAL RAT; NA CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
63
Recensione:
Indirizzi per estratti:
Citazione:
C.F. Hsiao et al., "IONIC BASIS FOR SEROTONIN-INDUCED BISTABLE MEMBRANE-PROPERTIES IN GUINEA-PIG TRIGEMINAL MOTONEURONS", Journal of neurophysiology, 79(6), 1998, pp. 2847-2856

Abstract

Intracellular recordings and pharmacological manipulations were employed to investigate the ionic basis for serotonin-induced bistable membrane behaviors in guinea pig trigeminal motoneurons (TMNs). In voltageclamp, 10 mu M serotonin (5-HT) induced a region of negative slope resistance (NSR) in the steady-state current-voltage (I-V) relationship at potentials less negative than -58 mV, creating the necessary conditions for membrane bistability. The contributions of sustained Na+ and Ca2+ currents to the generation of the NSR were investigated using specific ion channel antagonists and agonists. The NSR was eliminated by the L-type Ca2+ channel antagonist nifedipine (5-10 mu M), indicating the contribution of L channels. In nifedipine, inward rectification was present in the I-V relationship in a similar voltage range (greater than -58 mV). This region was subsequently linearized by tetrodotoxin (TTX),indicating the presence of a persistent Na+ current. When the 5-HT-induced NSR was eliminated by perfusion in low Ca2+ solution (0.4 mM), it was restored by the Na+ channel agonist veratridine (10 mu M). Commensurate with bistability, in current clamp during bath application of 5-HT, plateau potentials were elicited by transient depolarizing or hyperpolarizing stimuli. Plateau potentials evoked by depolarization were observed under control and TTX conditions, but were blocked by nifedipine, suggesting the participation of an L-type Ca2+ current. Plateau potentials initiated after release from hyperpolarization (anodebreak) were blocked by 300 mu M Ni2+, suggesting the responses reliedon deinactivation of a T-type Ca2+ current. Conditional bursting was also observed in 5-HT. Nifedipine or low Ca2+ solutions blocked bursting, and the L-channel agonist Bay K 8644 (10 mu M) extended the duration of individual bursts, demonstrating the role of L-type Ca2+ currents. Interestingly, when bursting was blocked by nifedipine or low Ca2+,it could be restored by veratridine application via enhancement of the persistent Na+ current. We conclude that bistable membrane behaviorsin TMNs are mediated by L-type Ca2+ and persistent Na+ currents. 5-HTis associated with enhancement of TMN activity during oral-motor activity; the induction of bistable membrane properties by 5-HT representsa cellular mechanism for this enhancement.

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Documento generato il 25/11/20 alle ore 18:53:19