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J Neurophysiol 60: 86-104, 1988;
0022-3077/88 $5.00
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Journal of Neurophysiology, Vol 60, Issue 1 86-104, Copyright © 1988 by APS

ARTICLES

Inositol 1,4,5-trisphosphate alters bursting pacemaker activity in Aplysia neurons: voltage-clamp analysis of effects on calcium currents

K. P. Scholz, L. J. Cleary and J. H. Byrne
Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225.

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 Ca2+ 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 inositol-1,4,5-trisphosphate (IP3) 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 tetrodotoxin (TTX) or Co2+. Although Iin was activated by injection of IP3, we were unable to block it by iontophoretic injection of ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetra-acetic acid (EGTA) sufficient to block the Ca2+-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 tetraethylammonium (TEA), which is known to block Ca2+-activated K+ currents (IK,Ca) in these cells. However, it was blocked by 30 mM Co2+, 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 EGTA abolished Iout indicating that elevation of intracellular Ca2+ is necessary.(ABSTRACT TRUNCATED AT 400 WORDS)


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K. Nakanishi, F. Zhang, D. A. Baxter, A. Eskin, and J. H. Byrne
Role of Calcium-Calmodulin-Dependent Protein Kinase II in Modulation of Sensorimotor Synapses in Aplysia
J Neurophysiol, July 1, 1997; 78(1): 409 - 416.
[Abstract] [Full Text] [PDF]


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