HIGH VOLTAGE-ACTIVATED CALCIUM CURRENTS IN NEURONS ACUTELY ISOLATED FROM
THE VENTROBASAL NUCLEUS OF THE RAT THALAMUS.
Kammermeier, Paul J. and Stephen W. Jones[angstrom]a.
Departments of Neurosciences and [angstrom]aPhysiology and Biophysics, Case
Western Reserve University, Cleveland, OH 44106.
APStracts 3:0203N, 1996.
ABSTRACT
We studied the high voltage-activated (HVA) calcium currents in cells isolated
from the ventrobasal nucleus of the rat thalamus, using the whole-cell patch-
clamp technique. Low voltage-activated current was inactivated by using long
voltage steps, or 100 ms prepulses to -20 mV. We used channel blocking agents
to characterize the currents that make up the HVA. 33 1% was blocked
reversibly by the dihydropyridine (DHP) antagonist nimodipine (5 M), and 25
5% was blocked irreversibly by (-conotoxin GVIA (1 M). The current resistant
to DHPs and (-conotoxin GVIA was inhibited almost completely by (-conotoxin
MVIIC (90 5% at 3-5 µM), and was partially inhibited by (-Aga IVA (54 4%
block at 1 M). We conclude that there are at least 4 main HVA currents in
thalamic neurons: N-current, L-current, and two (-conotoxin MVIIC-sensitive
currents that differ in their sensitivity to (-Aga IVA. We also examined
modulation of HVA currents by strong depolarization and by G protein
activation. Long (1 s), strong depolarizations elicited large, slowly
deactivating tail currents, which were sensitive to DHP antagonists. With GTP-
(-S in the intracellular solution, brief (20 ms) strong depolarization
produced a voltage-dependent facilitation of the current (44 5%), compared to
cells with GTP (22 7%) or GDP-(-S (7 4%). However, the HVA current was
inhibited only weakly by 100 µM acetylcholine (8 4%). Effects of the GABAB
agonist baclofen were variable (3% to 39% inhibition, n=12, at 10-50 M).
Received 13 June 1996; accepted in final form 13 September 1996.
APS Manuscript Number J469-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996