ArticleThe Journal of membrane biology1994
Guanine nucleotides modulate steady-state inactivation of voltage-gated sodium channels in frog olfactory receptor neurons.
Article in The Journal of membrane biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 15 citations in OpenAlex.
- The effect of recombinant neurotoxins from the sea anemone Anthopleura sp. on sodium currents of rat cerebral cortical neurons.Cellular and molecular neurobiology · 2008Article
- An estimate of the resting membrane resistance of frog olfactory receptor neurones.The Journal of physiology · 2004Article
- Contribution of cyclic-nucleotide-gated channels to the resting conductance of olfactory receptor neurons.Biophysical journal · 2003Article
- Odorant-induced currents in intact patches from rat olfactory receptor neurons: theory and experiment.Biophysical journal · 1997Article
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3 authors at 1 institution in 1 country.
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Abstract
The voltage for half-inactivation (V1/2) of Na+ currents in frog olfactory receptor neurons (ORNs) under whole-cell voltage clamp showed a shift to more negative potentials with time. Inclusion of guanosine triphosphate (GTP) or its nonhydrolyzable analogue, guanosine-5'-O-3-thiotriphosphate (GTP-gamma-S), which activates G proteins, in the recording pipette, not only gave a more positive V1/2, but also reduced and delayed the negative shift observed in the absence of nucleotides. Guanosine-5'-O-2-thiodiphosphate (GDP-beta-S), a nonhydrolyzable analogue that prevents the binding of GTP to G proteins, did not affect the V1/2 significantly by itself but blocked the positive shift induced by GTP. Since the steady-state activation was not affected, our results indicate that a G protein or a G-protein-dependent process may be important in regulating the steady-state inactivation of Na+ channels in ORNs of the frog.
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