{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T03:51:15Z","timestamp":1776743475197,"version":"3.51.2"},"reference-count":0,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1971,11,1]],"date-time":"1971-11-01T00:00:00Z","timestamp":57801600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1971,11]]},"abstract":"1. Changes in ionized calcium in giant axons were followed by recording the light produced by injected aequorin.<\/jats:p>2. From the effect of injecting calcium buffers the internal concentration of ionized calcium was found to be about the same as in a mixture of 45 Ca EGTA:55 free EGTA, i.e. about 0\u00b73 \u03bc\nM<\/jats:sc>.<\/jats:p>3. After an axon had been exposed to cyanide for 50\u2013100 min the velocity of the aequorin reaction increased about 500 times. This effect, which could be reversed rapidly by removing cyanide, was probably brought about by release of calcium from an internal store.<\/jats:p>4. Injecting 30 \u03bcmole ATP per litre of axoplasm into a cyanide\u2010poisoned axon caused a transient lowering of light intensity; oligomycin blocked the effect.<\/jats:p>5. Raising external calcium or replacing external sodium by choline or lithium reversibly increased the light produced by axons injected with aequorin.<\/jats:p>6. Stimulation at 50\u2013200 impulses\/sec in a solution containing 112 m\nM<\/jats:sc>\u2010Ca caused the light intensity to increase to a new steady level; after stimulation the light intensity returned to its original level with a time constant of 10\u201330 sec. Similar but smaller effects were seen in solutions containing less external calcium. The recovery after stimulation is probably due to uptake of calcium by the internal store.<\/jats:p>7. Injecting 3 m\u2010mole EGTA per litre axoplasm lowered the resting glow and abolished the aequorin response to stimulation.<\/jats:p>8. There was no light response to stimulation immediately after an axial injection of aequorin and the effect increased to a \u2018steady\u2019 level with a half\u2010time of about 5 min. The conclusion is that the rise in calcium concentration resulting from stimulation is confined to the peripheral part of the axon and that the diffusion coefficient of aequorin in axoplasm is about 4 \u00d7 10\u22127<\/jats:sup> cm2<\/jats:sup>\/sec.<\/jats:p>9. The increment in light per impulse often increased markedly during the course of a long experiment and there was also considerable variation between axons.<\/jats:p>10. If the light response to stimulation was small it was proportional to the frequency of stimulation; if large to the square of the frequency.<\/jats:p>11. Voltage\u2010clamp experiments showed that the calcium entry associated with a depolarizing pulse could be divided into an early component which was abolished by tetrodotoxin (TTX), and a late component which was unaffected by this inhibitor.<\/jats:p>12. The time relations of the early calcium entry were consistent with its being a leak of calcium ions through the sodium channel; the permeability of the sodium channel to calcium was about 1% of the permeability to sodium.<\/jats:p>13. The late entry of calcium was little changed by injecting enough tetraethylammonium (TEA) to block the outward potassium current; it was greatly reduced by external concentrations of manganese which had little effect on the maximum potassium conductance.<\/jats:p>14. The voltage\u2014response curve for the late entry of calcium had a well defined maximum and was similar in shape to the curve relating calcium entry to depolarization at the presynaptic ending (Katz & Miledi, 1969, 1970).<\/jats:p>","DOI":"10.1113\/jphysiol.1971.sp009641","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T11:13:51Z","timestamp":1418987631000},"page":"709-755","source":"Crossref","is-referenced-by-count":466,"title":["Depolarization and calcium entry in squid giant axons"],"prefix":"10.1113","volume":"218","author":[{"given":"P. F.","family":"Baker","sequence":"first","affiliation":[]},{"given":"A. L.","family":"Hodgkin","sequence":"additional","affiliation":[]},{"given":"E. B.","family":"Ridgway","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[1971,11]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1971.sp009641","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1971.sp009641","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,8]],"date-time":"2023-11-08T15:02:56Z","timestamp":1699455776000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1971.sp009641"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1971,11]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1971,11]]}},"alternative-id":["10.1113\/jphysiol.1971.sp009641"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1971.sp009641","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1971,11]]}}}