{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T05:47:32Z","timestamp":1789451252616,"version":"build-2803163510"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,12,6]],"date-time":"2007-12-06T00:00:00Z","timestamp":1196899200000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,12]]},"abstract":"<jats:p>Luteinizing hormone (LH) regulates testosterone synthesis in Leydig cells by inducing an intracellular increase in cAMP concentration. LH also increases the intracellular calcium concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), dependent on the presence of Ca<jats:sup>2+<\/jats:sup> in the extracellular medium ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>e<\/jats:sub>) for its effect. Despite these evidences, the identity of a pathway for calcium entry has remained elusive and the relationship between cAMP and [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> has been questioned. Here we show that mice Leydig cells do have an inward Ca<jats:sup>2+<\/jats:sup> current carried by T\u2010type Ca<jats:sup>2+<\/jats:sup> channels. In 10 m<jats:sc>m<\/jats:sc>[Ca<jats:sup>2+<\/jats:sup>]<jats:sub>e<\/jats:sub>, the currents start to be activated at \u221260 mV, reaching maximal amplitude of 1.8 \u00b1 0.3 pA pF<jats:sup>\u22121<\/jats:sup> at \u221220 mV. Currents were not modified by Ba<jats:sup>2+<\/jats:sup> or Sr<jats:sup>2+<\/jats:sup>, were suppressed in Ca<jats:sup>2+<\/jats:sup>\u2010free external solution, and were blocked by 100 \u03bc<jats:sc>m<\/jats:sc> nickel or 100 \u03bc<jats:sc>m<\/jats:sc> cadmium. The <jats:italic>K<\/jats:italic><jats:sub>i<\/jats:sub> for Ni<jats:sup>2+<\/jats:sup> is 2.6 \u03bc<jats:sc>m<\/jats:sc> and concentrations of Cd<jats:sup>2+<\/jats:sup> smaller than 50 \u03bc<jats:sc>m<\/jats:sc> have a very small effect on the currents. The calcium currents displayed a window centred at \u221240 mV. The half\u2010voltage (<jats:italic>V<\/jats:italic><jats:sub>0.5<\/jats:sub>) of activation is \u221230.3 mV, whereas the half\u2010voltage steady\u2010state inactivation is \u221251.1 mV. The deactivation time constant (\u03c4<jats:sub>deactivation<\/jats:sub>) is around 3 ms at \u221235 mV. Confocal microscopy experiments with Fluo\u20103 loaded cells reveal that both LH and dibutyryl\u2010cAMP (db\u2010cAMP) increase [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. The db\u2010cAMP induced calcium increase was dependent on Ca<jats:sup>2+<\/jats:sup> influx since it was abolished by removal of extracellular Ca<jats:sup>2+<\/jats:sup> and by 400 \u03bc<jats:sc>m<\/jats:sc> Ni<jats:sup>2+<\/jats:sup>. [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> increases in regions close to the plasma membrane and in the cell nucleus. Similar effects are seen when Leydig cells are depolarized by withdrawing K<jats:sup>+<\/jats:sup> from the extracellular solution. Altogether, our studies show that Ca<jats:sup>2+<\/jats:sup> influx through T\u2010type Ca<jats:sup>2+<\/jats:sup> channels in the plasma membrane of Leydig cells plays a crucial role in the intracellular calcium concentration changes that follow binding of LH to its receptor.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.137950","type":"journal-article","created":{"date-parts":[[2007,10,12]],"date-time":"2007-10-12T00:58:37Z","timestamp":1192150717000},"page":"339-349","source":"Crossref","is-referenced-by-count":30,"title":["Intracellular calcium changes in mice Leydig cells are dependent on calcium entry through T\u2010type calcium channels"],"prefix":"10.1113","volume":"585","author":[{"given":"Roberta Ribeiro","family":"Costa","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wamberto 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