Do neurons from rat neostriatum express both A TTX-sensitive and a TTX- insensitive slow Na + current ? Chao, T. Ivo, and Christian Alzheimer. Department of Physiology, University of Munich, Pettenkoferstr. 12, D-80336 Munich, Germany.
APStracts 2:0087N, 1995.
SUMMARY AND CONCLUSIONS
1. The properties of a TTX-sensitive, persistent Na + current and a purported TTX-insensitive slow Na + current were studied in acutely isolated neurons from rat neostriatum using the whole-cell configuration of the patch-clamp technique. 2. A TTX-sensitive, persistent Na + current (I NaP ) was activated positive to -60 mV and reached a peak amplitude of -40 to -120 pA at about -40 mV. As indicated by slow depolarizing voltage ramps, activation of I NaP did not require preceding activation of the fast, rapidly inactivating Na + current. 3. The current-voltage (I-V) relationship of I NaP displayed an unexpected inflection after passing through its peak value near -40 mV. Between -40 mV and -10 mV, I NaP declined more rapidly with depolarization than it did at more depolarized potentials. The corresponding conductance ( G NaP ) peaked at -40 mV and declined to a smaller limiting value at potentials positive to about -10 mV. 4. This behavior is not consistent with the notion that I NaP arises solely from a bell-shaped window conductance which results from the overlapping steady-state activation and inactivation curves of the fast Na + current in a narrow voltage range, nor with the notion that I NaP is generated by a single uniform conductance independent of the fast Na + current. 5. In addition to I NaP , a second slow inward current ( I S ) was evoked when small monovalent cations were omitted from the internal solution. I NaP and I S were present both in cells resembling medium spiny neurons and in cells resembling aspiny interneurons. 6. I S was insensitive to TTX (1.2 [mu]M) and the Ca 2+ channel blocker, cadmium. I S was activated positive to about -45 mV, and attained a maximum amplitude of -200 to -500 pA close to 0 mV. The kinetic and pharmacologic profile of this current was almost identical to that of a slow Na + current ( I NaS ) recently described in the same preparation (Hoehn et al. 1993). 7. To our surprise, I S , but not I NaP , disappeared when whole-cell recordings were performed in solutions with physiological cation concentrations, or when high Cs + was present in the internal solution. 8. Our data provide evidence for a persistent, TTX- sensitive Na + current the features of which suggest that it should influence the intrinsic excitability of neostriatal neurons in the subthreshold voltage region. We failed, however, to identify a TTX-insensitive slow Na + current when physiological cation gradients were established. 

Received 21 December 1994; accepted in final form 13 April 1995.
APS Manuscript Number J798-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.