XXXX alters bursting pacemaker activity in Aplysia neurons: voltage-clamp analysis of effects on calcium currents.

@entity9421 @entity671 @entity1041 @entity10977 @entity5128 @entity1022 @entity4524 @entity4527 @entity515 @entity141
1. The left upper-quadrant bursting neurons (cells L2, L3, L4, and L6) of the abdominal ganglion of Aplysia display a regular burst-firing pattern that is controlled by cyclic changes of intracellular @entity141 that occur during the bursting rhythm. The characteristic bursting pattern of these neurons occurs within a range of membrane potentials (-35 to -50 mV) called the pacemaker range. 2. Intracellular pressure injection of @entity671 ( @entity9421 ) altered the bursting rhythm of the left upper-quadrant bursting (LUQB) cells for up to 15 min. Injection of IP3 induced a brief depolarization that was followed by a long-lasting (2-15 min) hyperpolarization. The hyperpolarizing phase of the response was accompanied by prolonged interburst intervals. 3. When cells were voltage-clamped at potentials within the pacemaker range, injection of IP3 generally induced a biphasic response that had a total duration of 2-15 min. An initial inward shift in holding current (Iin), which lasted 5-120 s, was followed by a slow outward shift in holding current (Iout). 4. At membrane potentials more negative than -40 mV, Iin was associated with a small and relatively voltage-independent increase in membrane conductance. Iin was not blocked by bath application of @entity1022 ( @entity4524 ) or @entity515 . Although Iin was activated by injection of IP3, we were unable to block it by iontophoretic injection of @entity10977 -bis (beta-aminoethyl ether)-N,N,N',N'-tetra-acetic acid ( @entity4527 ) sufficient to block the @entity141 -activated inward tail current (IB). The ionic mechanism that produces Iin has not been analyzed. 5. In normal bathing solution, Iout was present at membrane potentials more positive than approximately -50 mV. Iout was not blocked by 50 mM @entity5128 ( @entity1041 ), which is known to block @entity141 -activated K+ currents (IK,Ca) in these cells. However, it was blocked by 30 mM @entity515 , which blocks ICa. These results indicate that a steady-state ICa is necessary for the generation of Iout following injection of IP3, suggesting that Iout is due to inactivation of ICa and not to activation of a K+ conductance. 6. Intracellular iontophoresis of @entity4527 abolished Iout indicating that elevation of intracellular @entity141 is necessary.(ABSTRACT TRUNCATED AT 400 WORDS)
