Effects of depolarization evoked Na+ influx on intracellular Na+ concentration at neurosecretory nerve endings.
Effects of depolarization evoked Na+ influx on intracellular Na+ concentration at neurosecretory nerve endings.
复制标题
去极化引起的 Na 内流对神经分泌神经末梢细胞内 Na 浓度的影响。
DOI:
10.1016/s0306-4522(98)00065-7
复制
发表时间:
1998
期刊:
影响因子:
3.3
通讯作者:
Stuenkel,EL
中科院分区:
文献类型:
--
作者:
Turner,D;Stuenkel,EL
Electrophysiological measurements of voltage-dependent Na+influx using patch-clamp methodology were combined with optical monitoring of the free intracellular Na+concentration in isolated rat neurohypophysial nerve endings to determine the relationship between Na+influx generated by repetitive stimulation and change in [Na+]i. Application of step depolarizations under voltage-clamp-evoked tetrodotoxin-sensitive inward currents that were dependent upon extracellular Na+and that exhibited rapid activation and inactivation properties. These characteristics substantiated the evoked current as a voltage-dependent Na+current. Application of stimulus trains consisting of step depolarizations that mimick in frequency and duration those of action potentials were found to result in increases in [Na+]i. The induced change in [Na+]iwas found to be related to the frequency and period of stimulation. Changes in [Na+]iwere greatest at frequencies of 40Hz and gave maximal changes with 30s of continuous stimulation of approximately 2.4mM. Sodium influx expressed as a molar quantity resulted in a nearly directly proportional increase in [Na+]iduring the initial period of stimulation at low Na+loads. When expressed as a charge density (pC/mm2) Na+influx was found to increase with smaller diameter nerve endings as did the rate of change in [Na+]iin response to applied repetitive step depolarizations. Repetitive step depolarizations which simulate impulse activity that invade neuroendocrine nerve endings in vivo in response to physiological demand for hormone secretion resulted in an increased [Na+]i. It is postulated that this increased [Na+]imay provide a modulatory influence on the secretory response indirectly via alteration of intracellular calcium regulation or, perhaps, via a direct action on the secretory mechanism.