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Modulation of a Ca2+-dependent K+-current by intracellular cAMP in rat thalamocortical relay neurons

Published online by Cambridge University Press:  12 April 2006

Gerardo Biella ,
Susanne Meis  and
Hans-Christian Pape
Gerardo Biella
Affiliation:
Institut für Physiologie, Otto-von-Guericke Universität Magdeburg, Leipzier Strasse 44, 39120 Magdeburg, Germany Present address: Department of Experimental Neurophysiology, Istituto Nazionale Neurologico, “C. Besta”, Via Celoria 11,1-20133 Milano, Italy.
Susanne Meis
Affiliation:
Institut für Physiologie, Otto-von-Guericke Universität Magdeburg, Leipzier Strasse 44, 39120 Magdeburg, Germany
Hans-Christian Pape
Affiliation:
Institut für Physiologie, Otto-von-Guericke Universität Magdeburg, Leipzier Strasse 44, 39120 Magdeburg, Germany
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Abstract

Voltage-activated calcium channels in thalamic neurons are considered important elements in the generation of thalamocortical burst firing during periods of electroencephalographic synchronization. A potent counterpart of calcium-mediated depolarization may reside in the activation of calcium-dependent potassium conductances. In the present study, thalamocortical relay cells that were acutely disso-ciated from the rat ventrobasal thalamic complex (VB) were studied using whole-cell patch-clamp techniques. The calcium-dependent potassium-current (IK(Ca)) was evident as a slowly activating component of outward current sensitive to the calcium ions (Ca2+)-channel blocker methoxyverapamil (10 μM) and to substitution of external calcium by manganese. The IK(Ca) was blocked by tetraethylam-monium chloride (1 mM) and iberiotoxin (100 nM), but not apamin (1 μM). In addition, isolated VB neurons were immunopositive to anti-α(913–926) antibody, a sequence-directed antibody to the a-subunit of “big” Ca2+-dependent K+-channel (BKCa) channels. Activators of the adenylyl cyclase cyclic adenosine monophosphate (cAMP) system, such as forskolin (20 μM), dibutyryl-cAMP (10 mM) and 3-isobutyl-1 -methylxanthine (500 μM), selectively and reversibly suppressed IK(Ca). These results suggest that a rise in intracellular cAMP level leads to a decrease in a calcium-dependent potassium conductance presumably mediated via BKCa type channels, thereby providing an additional mechanism by which neurotransmitter systems are able to control electrogenic activity in thalamocortical neurons and circuits during various states of electroencephalographic synchronization and de-synchronization.

Keywords

ThalamusElectrophysiologyPatch-clampPharmacologyCalcium-activated potassium-current
Type
Research Article
Information
Thalamus & Related Systems , Volume 1 , Issue 2 , June 2001 , pp. 157 - 167
Copyright
2001 Elsevier Science Ltd

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