Mechanisms causing plateau potentials in spinal motoneurones.

Area of Science:

• Neuroscience
• Cellular Physiology
• Ion Channel Function

Background:

• Plateau potentials are crucial for motoneuron excitability.
• These potentials are generated by voltage-sensitive persistent inward currents.
• In spinal motoneurons, calcium influx via L-type calcium channels (Ca(v)1.3) is the primary mechanism.

Purpose of the Study:

• To investigate the role of L-type calcium channels in plateau potential generation.
• To understand the mechanisms of delayed activation (wind-up and warm-up) and hysteresis.
• To explore the modulation of these channels and potentials by neurotransmitter receptors and intracellular factors.

Main Methods:

• Electrophysiological recordings in spinal motoneurons.
• Pharmacological manipulation of L-type calcium channels.
• Investigation of neurotransmitter receptor activation (glutamate, acetylcholine, noradrenaline, serotonin, GABA(B)).
• Assessment of calmodulin's role in channel facilitation.

Main Results:

• Depolarization-induced facilitation of Ca(v)1.3 L-type calcium channels underlies plateau potential wind-up and warm-up.
• This facilitation also explains firing frequency and I-V relation hysteresis during triangular depolarization.
• Metabotropic receptor activation facilitates, while GABA(B) receptor activation down-regulates, L-type calcium channels and plateau potentials.
• Facilitation is dependent on activated calmodulin.

Conclusions:

• Ca(v)1.3 L-type calcium channels are key determinants of plateau potentials in spinal motoneurons.
• Neurotransmitter modulation of these channels significantly impacts motoneuron firing properties.
• Calmodulin plays a critical role in the facilitation of these calcium channels and subsequent plateau potentials.