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J Neurophysiol (October 1, 2003). doi:10.1152/jn.00883.2003
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Submitted on September 9, 2003
Accepted on September 25, 2003

Ionic basis of tonic firing in spinal substantia gelatinosa neurons of rat

Igor V. Melnick1, Sonia Santos1, Karolina Szokol2, Peter Szucs2, and Boris V. Safronov1*

1 Morphophysiology, Instituto de Biologia Molecular e Celular (IBMC), Porto, Portugal
2 Anatomy, Histology and Embryology, Medical and Health Science Centre, University of Debrecen, Debrecen, Hungary

* To whom correspondence should be addressed. E-mail: safronov{at}ibmc.up.pt.

Ionic conductances underlying excitability in tonically firing neurons (TFNs) from substantia gelatinosa (SG) were studied by the patch-clamp method in rat spinal cord slices. Ca2+-dependent K+ (KCA) conductance sensitive to apamin was found to prolong the interspike intervals and stabilize firing evoked by a sustained membrane depolarization. Suppression of Ca2+ and KCA currents, however, did not abolish the basic pattern of tonic firing indicating that it was generated by voltage-gated Na+ and K+ currents. Na+ and K+ channels were further analyzed in somatic nucleated patches. Na+ channels exhibited fast activation and inactivation kinetics, and followed two-exponential time course of recovery from inactivation. The major K+ current was carried through tetraethylammonium (TEA)-sensitive rapidly activating delayed-rectifier (KDR) channels with a slow inactivation. The TEA-insensitive transient A-type K+ (KA) current was very small in patches and was strongly inactivated at resting potential. Block of KDR rather than KA conductance by 1 mM TEA lowered the frequency and stability of firing. Intracellular staining with biocytin revealed at least three morphological groups of TFNs. Finally, on the basis of present data we created a model of TFN and showed that Na+ and KDR currents are sufficient to generate a basic pattern of tonic firing. It is concluded that the balanced contribution of all ionic conductances described here is important for generation and modulation of tonic firing in SG neurons.




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