These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Calcium-induced inactivation of calcium current causes the inter-burst hyperpolarization of Aplysia bursting neurones.
    Author: Kramer RH, Zucker RS.
    Journal: J Physiol; 1985 May; 362():131-60. PubMed ID: 2410598.
    Abstract:
    A triphasic series of tail currents which follow depolarizing voltage-clamp pulses in Aplysia neurones L2-L6 was described in the preceding paper (Kramer & Zucker, 1985). In this paper, we examine the nature of the late outward component of the tail current (phase III) which generates the inter-burst hyperpolarization in unclamped cells. The phase III tail current does not reverse between -30 and -90 mV, and is relatively insensitive to the external K+ concentration. In contrast, Ca2+-dependent K+ current (IK(Ca)), elicited by intracellular Ca2+ injection, reverses near -65 mV, and the reversal potential is sensitive to the external K+ concentration. Addition of 50 mM-tetraethylammonium (TEA) to the bathing medium causes a small increase in the phase III tail current. In contrast, IK(Ca) is completely blocked by addition of 50 mM-TEA. The phase III tail current is suppressed by depolarizing pulses which approach ECa, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA. The phase III tail current is reduced by less than 10% after complete removal of extracellular Na+. These bursting neurones have a voltage-dependent Ca2+ conductance which exhibits steady-state activation at a membrane potential similar to the average resting potential of the unclamped cell (i.e. -40 mV). The steady-state Ca2+ conductance can be inactivated by Ca2+ injection, or by depolarizing pre-pulses which generate a large influx of Ca2+. The steady-state Ca2+ conductance has a voltage dependence similar to that of the phase III tail current. The Ca2+-dependent inactivation of the steady-state Ca2+ conductance occurs in parallel with the phase III tail current; both have a similar sensitivity to Ca2+ influx, and both processes decay with similar rates after a depolarizing pulse. Hence, we propose that the phase III tail current is due to the Ca2+- dependent inactivation of a steady-state Ca2+ conductance. The decay of IK(Ca) following simulated spikes or bursts of spikes is rapid (less than 1 s) compared to the time course of the phase III tail current and the inter-burst hyperpolarization (tens of seconds). Thus, we conclude that IK(Ca) does not have a major role in terminating bursts or generating the inter-burst hyperpolarization in these cells. We present a qualitative model of the ionic basis of the bursting pace-maker cycle. The central features of the model are the voltage-dependent activation and the Ca2+-dependent inactivation of a Ca2+ current.
    [Abstract] [Full Text] [Related] [New Search]