ArticlePflugers Archiv : European journal of physiology2005
Frequency-dependent potentiation of voltage-activated responses only in the intact neurohypophysis of the rat.
Article in Pflugers Archiv : European journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Advances in the neurophysiology of magnocellular neuroendocrine cells.Journal of neuroendocrinology · 2020Review
- Kisspeptin inhibits a slow afterhyperpolarization current via protein kinase C and reduces spike frequency adaptation in GnRH neurons.American journal of physiology. Endocrinology and metabolism · 2013Article
- Voltage-dependent kappa-opioid modulation of action potential waveform-elicited calcium currents in neurohypophysial terminals.Journal of cellular physiology · 2010Article
- Ionic conditions modulate stimulus-induced capacitance changes in isolated neurohypophysial terminals of the rat.The Journal of physiology · 2010Article
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The loose-patch-clamp technique was used with multiple-pulse protocols to study the frequency dependence of currents from the surface of the intact rat neurohypophysis (NH) and hypothalamus. In the NH, but not in the corresponding supraoptic nucleus of the hypothalamus, an initial, single pulse of 3-8 ms duration (long pulse) potentiated a secondary pulse response starting 20-50 ms after the initial pulse. Potentiation was abolished by 4-aminopyridine (4-AP), but not by tetraethylammonium (TEA) chloride or tetrandrine, indicating the participation of A-type potassium currents. Potentiation was also abolished by CdCl2, CoCl2 or 1 microM nicardipine, indicating the participation of calcium currents. The potentiation was reduced significantly in the presence of 4-6 mM extracellular CaCl2, indicating that the potentiation is not due to calcium influx. An initial train with as few as two pulses, each of 0.3-0.7 ms duration (short pulses) at 64-1,100 Hz also potentiated the secondary short pulse response significantly. We conclude that voltage-gated channels underlie this potentiation, which is due to interstitial calcium and potassium homeostasis changes induced by action potential activity and occurs only in the intact NH. A model is proposed for the participation of calcium and potassium channels in the burst patterning that is optimal for secretion from the NH.
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