Abstract
Intracellular recordings were obtained from rat trigeminal motoneurons in slice preparations to investigate the role of calcium conductances in the depolarizing and hyperpolarizing spike afterpotential (ADP and mAHP, respectively). The mAHP was suppressed by bath application of 1 μM apamin, 2 mM Mn2+, and 2 mM Co2+, and also by intracellular injection of ethylene glycol-bis(b-aminoethylenether)-N,N,N',N'-tetraacetic acid (EGTA), suggesting that the potassium conductance generating the mAHP is activated by Ca2+ influx. Mn2+ (2 mM) or Cd2+ (500 μM) reduced the ADP, whereas the ADP amplitude was increased by raising extracellular Ca2+ concentration from 2 to 8 mM by bath application of Ba2+ (0.5-5 mM) and by intracellular injection of EGTA. This would suggest that Ca2+ itself is likely to be the charge carrier generating the ADP. Focal application of ω-conotoxin GVIA (10-30 μM) suppressed the mAHP and enhanced the ADP, whereas focal application of ω-agatoxin IVA (10-100 μM) reduced the ADP amplitude without apparent effects on the mAHP. We conclude that Ca2+ influx through ω- agatoxin IVA-sensitive calcium channels is at least in part responsible for the generation of the ADP and that Ca2+ influx through ω-conotoxin GVIA- sensitive calcium channels contributes to the generation of the mAHP. Because of the selective suppression of the ADP and mAHP by ω-agatoxin IVA and ω- conotoxin GVIA, respectively, it is suggested that both calcium channels are separated geometrically in rat trigeminal motoneurons.
| Original language | English |
|---|---|
| Pages (from-to) | 3273-3283 |
| Number of pages | 11 |
| Journal | Journal of Neurophysiology |
| Volume | 77 |
| Issue number | 6 |
| Publication status | Published - 1997 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Physiology
- Neuroscience(all)
Cite this
Role of calcium conductances on spike afterpotentials in rat trigeminal motoneurons. / Kobayashi, Masayuki; Inoue, Tomio; Matsuo, Ryuji; Masuda, Yuji; Hidaka, Osamu; Kang, Youngnam; Morimoto, Toshifumi.
In: Journal of Neurophysiology, Vol. 77, No. 6, 1997, p. 3273-3283.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of calcium conductances on spike afterpotentials in rat trigeminal motoneurons
AU - Kobayashi, Masayuki
AU - Inoue, Tomio
AU - Matsuo, Ryuji
AU - Masuda, Yuji
AU - Hidaka, Osamu
AU - Kang, Youngnam
AU - Morimoto, Toshifumi
PY - 1997
Y1 - 1997
N2 - Intracellular recordings were obtained from rat trigeminal motoneurons in slice preparations to investigate the role of calcium conductances in the depolarizing and hyperpolarizing spike afterpotential (ADP and mAHP, respectively). The mAHP was suppressed by bath application of 1 μM apamin, 2 mM Mn2+, and 2 mM Co2+, and also by intracellular injection of ethylene glycol-bis(b-aminoethylenether)-N,N,N',N'-tetraacetic acid (EGTA), suggesting that the potassium conductance generating the mAHP is activated by Ca2+ influx. Mn2+ (2 mM) or Cd2+ (500 μM) reduced the ADP, whereas the ADP amplitude was increased by raising extracellular Ca2+ concentration from 2 to 8 mM by bath application of Ba2+ (0.5-5 mM) and by intracellular injection of EGTA. This would suggest that Ca2+ itself is likely to be the charge carrier generating the ADP. Focal application of ω-conotoxin GVIA (10-30 μM) suppressed the mAHP and enhanced the ADP, whereas focal application of ω-agatoxin IVA (10-100 μM) reduced the ADP amplitude without apparent effects on the mAHP. We conclude that Ca2+ influx through ω- agatoxin IVA-sensitive calcium channels is at least in part responsible for the generation of the ADP and that Ca2+ influx through ω-conotoxin GVIA- sensitive calcium channels contributes to the generation of the mAHP. Because of the selective suppression of the ADP and mAHP by ω-agatoxin IVA and ω- conotoxin GVIA, respectively, it is suggested that both calcium channels are separated geometrically in rat trigeminal motoneurons.
AB - Intracellular recordings were obtained from rat trigeminal motoneurons in slice preparations to investigate the role of calcium conductances in the depolarizing and hyperpolarizing spike afterpotential (ADP and mAHP, respectively). The mAHP was suppressed by bath application of 1 μM apamin, 2 mM Mn2+, and 2 mM Co2+, and also by intracellular injection of ethylene glycol-bis(b-aminoethylenether)-N,N,N',N'-tetraacetic acid (EGTA), suggesting that the potassium conductance generating the mAHP is activated by Ca2+ influx. Mn2+ (2 mM) or Cd2+ (500 μM) reduced the ADP, whereas the ADP amplitude was increased by raising extracellular Ca2+ concentration from 2 to 8 mM by bath application of Ba2+ (0.5-5 mM) and by intracellular injection of EGTA. This would suggest that Ca2+ itself is likely to be the charge carrier generating the ADP. Focal application of ω-conotoxin GVIA (10-30 μM) suppressed the mAHP and enhanced the ADP, whereas focal application of ω-agatoxin IVA (10-100 μM) reduced the ADP amplitude without apparent effects on the mAHP. We conclude that Ca2+ influx through ω- agatoxin IVA-sensitive calcium channels is at least in part responsible for the generation of the ADP and that Ca2+ influx through ω-conotoxin GVIA- sensitive calcium channels contributes to the generation of the mAHP. Because of the selective suppression of the ADP and mAHP by ω-agatoxin IVA and ω- conotoxin GVIA, respectively, it is suggested that both calcium channels are separated geometrically in rat trigeminal motoneurons.
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M3 - Article
VL - 77
SP - 3273
EP - 3283
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 6
ER -