TY - JOUR
TI - Postnatal increases in axonal conduction velocity of an identified drosophila interneuron require fast sodium, L-type calcium and shaker potassium channels
AU - Kadas, D.
AU - Duch, C.
AU - Consoulas, C.
JO - eNeuro
PY - 2019
VL - 6
TODO - 4
SP - null
PB - Society for Neuroscience
SN - null
TODO - 10.1523/ENEURO.0181-19.2019
TODO - calcium channel L type;  Shaker potassium channel;  sodium channel;  voltage gated sodium channel;  calcium channel L type;  Shaker potassium channel;  voltage gated sodium channel, adult;  alpha nerve fiber;  animal cell;  Article;  beta nerve fiber;  controlled study;  Drosophila;  gene knockdown;  genetic manipulation;  interneuron;  ion conductance;  motoneuron;  nerve conduction velocity;  nerve fiber membrane potential;  nonhuman;  perinatal period;  protein expression;  regulatory mechanism;  RNA interference;  sensory nerve cell;  action potential;  animal;  axon;  female;  growth, development and aging;  interneuron;  larva;  male;  nerve conduction;  physiology, Action Potentials;  Animals;  Axons;  Calcium Channels, L-Type;  Drosophila;  Female;  Interneurons;  Larva;  Male;  Neural Conduction;  Shaker Superfamily of Potassium Channels;  Voltage-Gated Sodium Channels
TODO - During early postnatal life, speed up of signal propagation through many central and peripheral neurons has been associated with an increase in axon diameter or/and myelination. Especially in unmyelinated axons postnatal adjustments of axonal membrane conductances is potentially a third mechanism but solid evidence is lacking. Here, we show that axonal action potential (AP) conduction velocity in the Drosophila giant fiber (GF) interneuron, which is required for fast long-distance signal conduction through the escape circuit, is increased by 80% during the first day of adult life. Genetic manipulations indicate that this postnatal increase in AP conduction velocity in the unmyelinated GF axon is likely owed to adjustments of ion channel expression or properties rather than axon diameter increases. Specifically, targeted RNAi knock-down of either Para fast voltage-gated sodium, Shaker potassium (Kv1 homologue), or surprisingly, L-type like calcium channels counteracts postnatal increases in GF axonal conduction velocity. By contrast, the calcium-dependent potassium channel Slowpoke (BK) is not essential for postnatal speeding, although it also significantly increases conduction velocity. Therefore, we identified multiple ion channels that function to support fast axonal AP conduction velocity, but only a subset of these are regulated during early postnatal life to maximize conduction velocity. Despite its large diameter (~7 μm) and postnatal regulation of multiple ionic conductances, mature GF axonal conduction velocity is still 20–60 times slower than that of vertebrate Aβ sensory axons and α motoneurons, thus unraveling the limits of long-range information transfer speed through invertebrate circuits. © 2019 Kadas et al.
ER -