Activity-dependent initiation of a prolonged depolarization in aplysia bag cell neurons: role for a cation channel.
The translation of prior activity into changes in excitability is essential for memory and the initiation of behavior. After brief synaptic input, the bag cell neurons of Aplysia californica undergo a nearly 30-min afterdischarge to release egg-laying hormone. The present study examines a prolonged depolarization in cultured bag cell neurons. A 5-Hz, 10-s action potential train elicited a depolarization of about 10 mV, which lasted </=30 min and was reduced by calmodulin kinase inhibition. Very broad action potentials (resulting from TEA application) decreased prolonged depolarization amplitude, indicating that strong Ca(2+) influx did not necessarily promote the response. The prolonged depolarization current (I(PD)) was recorded after 5-Hz, 10-s trains of square voltage pulses of varying duration (10-150 ms). Despite Ca(2+) influx increasing steadily with pulse duration, I(PD) was most reliably initiated at 100 ms, suggesting a Ca(2+) window or limit exists for triggering I(PD). Consistent with this, modestly broader action potentials, evoked by lengthening the train current-pulse duration, resulted in smaller prolonged depolarizations. With respect to the properties of I(PD), it displayed a linear current-voltage relationship with a reversal potential of about -45 mV that was shifted to approximately -25 mV by lowering internal K(+) or about -56 mV by lowering external Na(+) and Ca(2+). I(PD) was blocked by Gd(3+), but was not antagonized by MDL-123302A, SKF-96365, 2-APB, tetrodotoxin, or flufenamic acid. Optimal Ca(2+) influx may activate calmodulin kinase and a voltage-independent, nonselective cation channel to initiate the prolonged depolarization, thereby contributing to the afterdischarge and reproduction.
Hung
Anne Y
AY
Department of Physiology, Queen's University, 4th Floor, Botterell Hall, 18 Stuart Street, Kingston, ON, K7L 3N6, Canada.
Magoski
Neil S
NS
D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001048:Aplysia / Q000166:cytology*; D002148:Calmodulin-Binding Proteins / Q000494:pharmacology; D002412:Cations / Q000378:metabolism; D002478:Cells, Cultured; D002614:Chelating Agents / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004307:Dose-Response Relationship, Radiation; D004533:Egtazic Acid / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D049990:Membrane Transport Modulators / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology; D013997:Time Factors
D002148:Calmodulin-Binding Proteins; D002412:Cations; D002614:Chelating Agents; D004791:Enzyme Inhibitors; D007473:Ion Channels; D049990:Membrane Transport Modulators; D026902:Potassium Channel Blockers; D004533:Egtazic Acid; C063302:KN 62; D019789:Tetraethylammonium; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine