ArticlePflugers Archiv : European journal of physiology1992
Parathyroid hormone enhances calcium current in snail neurones--simulation of the effect by phorbol esters.
Article in Pflugers Archiv : European journal of physiology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 34 citations in OpenAlex.
- Oxygen deprivation inhibits Na+ current in rat hippocampal neurones via protein kinase C.The Journal of physiology · 1997Article
- The effect of the PKC inhibitor GF109203X on the release of Ca2+ from internal stores and Ca2+ entry in DDT1 MF-2 cells.British journal of pharmacology · 1996Article
- Voltage gated calcium channels in molluscs: classification, Ca2+ dependent inactivation, modulation and functional roles.Invertebrate neuroscience : IN · 1996Review
- Mechanisms of antagonistic action of internal Ca2+ on serotonin-induced potentiation of Ca2+ currents in Helix neurones.Pflugers Archiv : European journal of physiology · 1993Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Effects of parathyroid hormone substance (PTH) on the voltage-activated calcium current (ICa) were studied on intracellularly perfused neurones of the snail, Helix pomatia, under voltage-clamp conditions. Application of 0.1 nM PTH produced a marked potentiation of the current. The effect developed slowly (60-70 min) and remained after removal of PTH. Potentiation could be observed in most neurones, but varied considerably from cell to cell; in some neurones ICa was increased 2- to 3-fold. Addition of ethylenebis(oxonitrilo)tetraacetate (EGTA, 10 mM) to, or removal of adenosine 5'-triphosphate (ATP, 2 mM) from the intracellular perfusing solution resulted in a suppression or attenuation of the potentiating effect. The effect could be reproduced by the synthetic 1-34 amino acid fragment of PTH. Extracellularly applied protein kinase-C (PK-C) activator phorbol ester phorbol 12-myristate 13-acetate (PMA, 0.1-10 microM) produced a similar slow increase in ICa (up to 1.5- to 2-fold), while its inactive analogue (4 alpha-phorbol ester) had no effect on ICa. The effects of PTH and PMA were not additive. PK-C inhibitors [1-(5-isoquinoline-sulphonyl)-2-methylpiperazine hydrochloride] (H-7, 100 microM) and staurosporine (100 microM) as well as calcium channel antagonists Cd2+, verapamil, nifedipine and nimodipine depressed the effect of PTH. The chloride channel blocker 4,4'-diisothiocyanato-stilbene-2,2'-disulphonic acid (DIDS, 1 mM) did not affect the potentiating action of PTH. Activation of the adenylate cyclase system also potentiated ICa in some neurones, but this effect had a different time course and was additive to the effect of PTH.2=
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