The Journal of Neurophysiology Vol. 77 No. 1 January 1997, pp. 465-475
Copyright ©1997 The American Physiological Society

High-Voltage-Activated Calcium Currents in Neurons Acutely Isolated From the Ventrobasal Nucleus of the Rat Thalamus

Paul J. Kammermeier¹ and Stephen W. Jones²

Departments of ¹ Neurosciences and ² Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106

Kammermeier, Paul J. and Stephen W. Jones. High-voltage-activated calcium currents in neurons acutely isolated from the ventrobasal nucleus of the rat thalamus. J. Neurophysiol. 77: 465-475, 1997. We studied the high-voltage-activated (HVA) calcium currents in cells isolated from the ventrobasal nucleus of the rat thalamus with the use of the whole cell patch-clamp technique. Low-voltage-activated current was inactivated by the use of long voltage steps or 100-ms prepulses to 20 mV. We used channel blocking agents to characterize the currents that make up the HVA current. The dihydropyridine (DHP) antagonist nimodipine (5 µM) reversibly blocked 33 ± 1% (mean ± SE), and -conotoxin GVIA (1 µM) irreversibly blocked 25 ± 5%. 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 -agatoxin IVA (54 ± 4% block at 1 µM). We conclude that there are at least four main HVA currents in thalamic neurons: N current, L current, and two -conotoxin MVIIC-sensitive currents that differ in their sensitivity to -agatoxin 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 guanosine 5-O-(3-thiotriphosphate) (GTP--S) in the intracellular solution, brief (~20 ms), strong depolarization produced a voltage-dependent facilitation of the current (44 ± 5%), compared with cells with GTP (22 ± 7%) or guanosine 5-O-(2-thiodiphosphate) (7 ± 4%). However, the HVA current was inhibited only weakly by 100 µM acetylcholine (8 ± 4%). Effects of the -aminobutyric acid-B agonist baclofen were variable (3-39% inhibition, n = 12, at 10-50 µM).

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