Zn2+ potentiates steady-state ATP activated currents in rat nodose ganglion neurons by increasing the burst duration of a 35 pS channel.
Zn2+ and ATP are normally present in serum at low levels and are released from some neurons during synaptic activity. In whole-cell recordings, 10 microM Zn2+ potentiated steady-state currents in rat nodose ganglion nerve cells by 18% in 0.5 microM ATP and 120% in 2 microM ATP. Fluctuation analysis of whole-cell suggested the mechanism was increased burst duration. In single-channel recordings, 10 microM Zn2+ did not increase the ATP-activated channel conductance but did increase the mean burst duration of the 35 pS primary open conductance state. These observations indicate that Zn2+ potentiates the steady-state response to extracellular ATP by increasing the burst duration of the channels.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D009620:Nodose Ganglion / Q000187:drug effects*; D009622:Noise; D018408:Patch-Clamp Techniques; D017729:Presynaptic Terminals / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015032:Zinc / Q000494:pharmacology*
D007473:Ion Channels; D000255:Adenosine Triphosphate; D015032:Zinc