Potentiation of Ca2+ transients in the presynaptic terminals of goldfish retinal bipolar cells.
AUTOR(ES)
Kobayashi, K
RESUMO
1. To study a possible contribution of intracellular Ca2+ stores to the presynaptic Ca2+ regulation, the Ca2+ current (ICa) and the intracellular free Ca2+ concentration ([Ca2+]i) were simultaneously monitored in isolated goldfish retinal bipolar cells using the whole-cell voltage clamp procedure and fura-2 fluorimetry. 2. The Ca2+ transient triggered by the activation of ICa was potentiated when [Ca2+]i was increased by applying either a prepulse or a small steady depolarization. The potentiation seemed to be partly due to the release of Ca2+ from intracellular Ca2+ stores. 3. The intracellular Ca2+ release was reversibly inhibited by caffeine but was not affected by ryanodine, suggesting that Ca2+ is released through intracellular Ca2+ channels which differ from ryanodine receptor channels. 4. These results suggest that the intracellular Ca2+ release may contribute to the facilitation of transmitter release.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1157749Documentos Relacionados
- Ca2+ regulation in the presynaptic terminals of goldfish retinal bipolar cells.
- Local Ca2+ transients (Ca2+ sparks) originate at transverse tubules in rat heart cells.
- Electrical resonance and Ca2+ influx in the synaptic terminal of depolarizing bipolar cells from the goldfish retina.
- Calcium influx and calcium current in single synaptic terminals of goldfish retinal bipolar neurons.
- Clustering of Ca2+ channels and Ca(2+)-activated K+ channels at fluorescently labeled presynaptic active zones of hair cells.