{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,2]],"date-time":"2025-10-02T06:12:58Z","timestamp":1759385578779,"version":"3.41.0"},"reference-count":62,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1997,1,1]]},"abstract":"<jats:p>Hong, Sungwon J. and Gregory A. Lnenicka. Characterization of a P-type calcium current in a crayfish motoneuron and its selective modulation by impulse activity. J. Neurophysiol. 77: 76\u201385, 1997. Previous studies have demonstrated that the voltage-dependent Ca<jats:sup>2+<\/jats:sup>current recorded from the cell body of the crayfish abdominal motoneuron, F3, undergoes a long-term reduction as a result of increased impulse activity. The properties of the Ca<jats:sup>2+<\/jats:sup>channels undergoing this long-term change were examined with the use of two-electrode voltage-clamp techniques. The Ca<jats:sup>2+<\/jats:sup>current was activated at \u221250 to \u221240 mV and its amplitude was maximal at 0 mV (\u2212135.0 \u00b1 25.8 nA, mean \u00b1 SE, n = 14). The current-voltage relationship and the greater sensitivity of the Ca<jats:sup>2+<\/jats:sup>channel to Cd<jats:sup>2+<\/jats:sup>than Ni<jats:sup>2+<\/jats:sup>indicated that Ca<jats:sup>2+<\/jats:sup>influx occurs through high-voltage-activated (HVA) Ca<jats:sup>2+<\/jats:sup>channels. Loose-patch recordings demonstrated that the Ca<jats:sup>2+<\/jats:sup>current was generated by the membrane of the cell body. When Ba<jats:sup>2+<\/jats:sup>was substituted for extracellular Ca<jats:sup>2+<\/jats:sup>, there was a 40% increase in the amplitude of the inward current and a negative shift of \u223c10 mV in the I-V relationship. Application of the P-type Ca<jats:sup>2+<\/jats:sup>channel antagonist \u03c9-agatoxin IVA (\u03c9-AgTX IVA) produced a significant 33% ( n = 6) reduction in the peak amplitude of the Ba<jats:sup>2+<\/jats:sup>current, whereas neither the L-type Ca<jats:sup>2+<\/jats:sup>channel antagonist nifedipine nor the N-type channel antagonist \u03c9-conotoxin GVIA produced a reduction in the Ba<jats:sup>2+<\/jats:sup>current. The voltage-dependent activation of this P-type (\u03c9-AgTX-IVA-sensitive) Ca<jats:sup>2+<\/jats:sup>channel was similar to previously identified P-type channels, but different from that of the non-P-type (\u03c9-AgTX-IVA-resistant) Ca<jats:sup>2+<\/jats:sup>channels. When Ca<jats:sup>2+<\/jats:sup>currents were measured6\u20137 h after an increase in impulse activity (5-Hz stimulation for45\u201360 min), there was a 43% reduction in the amplitude of the P-type current, but no significant changes in the non-P-type current amplitude. These results demonstrate that at least two subtypes of HVA Ca<jats:sup>2+<\/jats:sup>channels contribute to the macroscopic Ca<jats:sup>2+<\/jats:sup>current observed in the cell body of this crayfish phasic motoneuron: one belongs to the previously described P-type Ca<jats:sup>2+<\/jats:sup>channel and the other(s) does not belong to the N-, L-, or P-type Ca<jats:sup>2+<\/jats:sup>channel. The long-term, Ca<jats:sup>2+<\/jats:sup>-dependent reduction in Ca<jats:sup>2+<\/jats:sup>current previously demonstrated in motoneuron F3 is produced by the selective reduction of this P-type Ca<jats:sup>2+<\/jats:sup>current. This activity-dependent reduction in the P-type Ca<jats:sup>2+<\/jats:sup>current is likely involved in the long-term depression of transmitter release observed at the neuromuscular synapses of this motoneuron.<\/jats:p>","DOI":"10.1152\/jn.1997.77.1.76","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T01:09:16Z","timestamp":1514164156000},"page":"76-85","source":"Crossref","is-referenced-by-count":22,"title":["Characterization of a P-Type Calcium Current in a Crayfish Motoneuron and Its Selective Modulation by Impulse Activity"],"prefix":"10.1152","volume":"77","author":[{"given":"Sungwon J.","family":"Hong","sequence":"first","affiliation":[{"name":"Neurobiology Research Center, Department of Biological Sciences, University at Albany, State University of New York, Albany, New York 12222"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory A.","family":"Lnenicka","sequence":"additional","affiliation":[{"name":"Neurobiology Research Center, Department of Biological Sciences, University at Albany, State University of New York, Albany, New York 12222"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(86)90559-8"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.11-03-00746.1991"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.10.4224"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.14-11-06667.1994"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1007\/BF00582548"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1002\/neu.480200402"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1991.66.2.590"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1152\/jn.1995.73.1.178"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.14-08-05011.1994"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(90)90715-L"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1982.sp014052"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1987.sp016551"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0079-6107(89)90008-4"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1986.sp016206"},{"key":"B15","doi-asserted-by":"crossref","first-page":"1483","DOI":"10.1242\/jeb.198.7.1483","volume":"198","author":"Chrachri A.","year":"1995","journal-title":"J. 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