Development of anomalous rectification (Ih) and of a tetrodotoxin‐resistant sodium current in embryonic quail neurones.

Abstract

SUMMARY1. The developmental expression of an inwardly rectifying current activated by membrane hyperpolarization (Ih) and of a tetrodotoxin (TTX)-resistant Na+ current (VNa(TR)) was studied using freshly dissociated ganglionic quail neurones of various embryonic ages. This work was carried out on parasympathetic (ciliary) and sensory (trigeminal and dorsal root) ganglion neurones with the whole-cell configuration of the patch-clamp technique.2. In sensory and parasympathetic neurones, Ih was activated at potentials more negative than -60 mV and displayed strong inward rectification. No sign of timeor voltage-dependent inactivation was apparent. Ih was carried by both Na+ and K+ ions and was selectively and reversibly blocked by extracellular Cs+.3. During the development of sensory neurones, Ih was observed for the first time between embryonic day 10 (E1O) and E1i and the percentage of neurones expressing the current increased subsequently, reaching a plateau level of about 80 % at E14. In the parasympathetic neurones of the ciliary ganglion, Ih was already detected at El0 and the percentage of neurones possessing the current increased until E16, a stage at which all neurones were found to express Ih.4. In the presence of TTX (1 /1M), an inward Na+ current, INa(TR), was recorded in sensory neurones after E 12. This current was activated at potentials more depolarized than -30 mV and its amplitude was maximal at + 5 mV. INa(TR) showed time-and voltage-dependent inactivation. Half-maximal steady-state inactivation was observed at -40 mV.5. INa(TR) was observed for the first time after E12 in sensory neurones and the percentage of neurones with INa(TR) increased until E14. Thereafter, 80% of the neurones had the current. In contrast, INa(TR) was never observed in the parasympathetic neurones of the ciliary ganglion during embryonic development.6. Our results with parasympathetic and sensory neurones suggest that the expression of INa(TR) is linked to the phenotype and not to the embryonic origin of a neurone.

Hyperpolarization-Activated Currents in Gonadotropin-Releasing Hormone (GnRH) Neurons Contribute to Intrinsic Excitability and Are Regulated by Gonadal Steroid Feedback

“…Both resulting I-V plots were fit with linear regression and the reversal potential calculated from the point of crossover (n= 11, Figure 3D). The calculated reversal potential was similar to previously reported values in neurons (Spain et al, 1987; Schlichter et al, 1991), and was sensitive to changes in concentration of either Na + or K + ions in the extracellular solution (both manipulations p<0.05, Figure 3E). …”

HCN channels contribute to the intrinsic activity of cochlear pyramidal cells

“…In accordance with the data found in the literature [21,[24][25][26], the channels found here proved to be sensitive to Cs ions, as 1 mM CsCl had a blocking effectivity of ~85% at -140 mV. Moreover, they were also very effectively inhibited by ZD7228, a bradycardic agent known to be specific for the hyperpolarization-activated non-specific cationic current providing the pace-making ability of the sinu-atrial cells [27] and certain neurones [28].…”

Characterization of TTX‐sensitive and TTX‐resistant sodium currents in small cells from adult rat dorsal root ganglia.

“…The results of this study indicate that small diameter DRG cells isolated from adult rats may contain at least two different populations of sodium channel, differing in their sensitivity to the neurotoxin TTX by as much as three orders of magnitude. These findings are in agreement with those of previous studies on both immature (Kostyuk et al 1981a;Meiri et al 1987;Omri & Meiri, 1990;Fedulova et al 1991) and adult rat DRG neurones (McLean et al 1988;Caffrey et al 1991;Fedulova et al 1991), and are similar to those reported for many other vertebrate sensory neurones (Bossu & Feltz, 1984;Ikeda et al 1986;Jones, 1987;Petersen et al 1987;Campbell, 1988;Campbell & Babeu, 1989;Schlichter et al 1991).…”

“…As a result of early action potential studies (Yoshida, Matsuda & Samejima, 1978;Yoshida & Matsuda, 1979;Fukuda & Kameyama, 1980;Baccaglini & Cooper, 1982;Heyer & MacDonald, 1982;Gallego, 1983;Stansfeld & Wallis, 1985) many immature and adult vertebrate sensory neurones have now been shown to express at least two different types of sodium current, distinguishable pharmacologically in terms of their sensitivity to tetrodotoxin (TTX) Bossu & Feltz, 1984;Ikeda, Schofield & Weight, 1986;Jones, 1987;Meiri, Spira, Samma, Namir, Schwartz, Komoriya & Palti, 1987;Petersen, Pierau & Weyrich, 1987;McLean, Bennett & Thomas, 1988;Fedulova, Kostyuk & Veselovsky, 1991;Schlichter, Bader & Bernheim, 1991).…”