Drastic facilitation by α-latrotoxin of bovine chromaffin cell exocytosis without measurable enhancement of Ca2+entry or [Ca2+]i
| Autor: | Pedro Michelena, Manuela G. López, Antonio G. García, Baldomero Lara, Luis Gandía, María-Teresa de la Fuente, Teresa Vega |
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| Rok vydání: | 1997 |
| Předmět: |
medicine.medical_specialty
Patch-Clamp Techniques Physiology Chromaffin Cells Latrotoxin Spider Venoms Stimulation Buffers Exocytosis Membrane Potentials Catecholamines Internal medicine medicine Animals Secretion Channel blocker Adenosine Triphosphatases Chemistry Calcium Radioisotopes Sodium Splanchnic Nerves Acetylcholine Electroporation Endocrinology medicine.anatomical_structure Adrenal Medulla Chromaffin cell Potassium Catecholamine Calcium Cattle Calcium Channels Secretory Rate HEPES Ion Channel Gating Signal Transduction Research Article medicine.drug |
| Zdroj: | The Journal of Physiology. 502:481-496 |
| ISSN: | 0022-3751 |
| Popis: | 1. Latrotoxin (LTX, 1-3 nM) caused a gradual increase of the spontaneous catecholamine release rate in bovine adrenal chromaffin cells superfused with normal Krebs-Hepes solution containing 2.5 mM Ca2+. Ca2+ removal abolished this effect. LTX enhanced also the secretory responses to high K+ (35 or 70 mM) and to acetylcholine (ACh, 30 microM). 2. The application of Ca2+ pulses to cells previously superfused with a 0 Ca2+ solution (Krebs-Hepes deprived of CaCl2) induced secretory responses that gradually reached 400-800 nA of catecholamines, provided that LTX was present. The responses to ACh or 35 mM K+ pulses (in the presence of Ca2+) were also enhanced by LTX, from around 100-200 nA to over 1000 nA. Though such enhancement remained in the presence of Ca2+ channel blockers, it disappeared upon the lowering of [Na+]o or in electroporated cells. 3. Using protocols similar to those of secretion, LTX did not enhance basal 45Ca2+ uptake, whole-cell Ca2+ currents or basal [Ca2+]i. In fact, LTX attenuated the K(+)- or ACh-evoked increases in 45Ca2+ uptake and [Ca2+]i. 4. It is proposed that the secretory response to brief periods of Ca2+ reintroductions is triggered by local subplasmalemmal Ca2+i transients, produced by the Na(+)-Ca2+ exchanger of the plasma membrane working in the reverse mode. This situation might be physiologically reproduced during ACh stimulation of chromaffin cells, which is followed by the firing of Na(+)-dependent action potentials. |
| Databáze: | OpenAIRE |
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