Riluzole-induced oscillations in spinal networks.

Area of Science:

• Neuroscience
• Computational Neuroscience

Background:

• Disinhibition-induced bursting in spinal cord networks relies on intrinsic spiking, network recruitment, and refractory periods.
• A persistent sodium current (I(NaP)) is crucial for intrinsic spiking and subsequent bursting activity.

Purpose of the Study:

• Investigate the mechanisms by which partial blockade of I(NaP) with low-dose riluzole alters bursting activity.
• Determine the role of spike-frequency adaptation and depolarization block in riluzole-induced intraburst oscillations.

Main Methods:

• Utilized dissociated fetal rat spinal cord cultures.
• Applied low doses of riluzole and phenytoin to block I(NaP).
• Simulated bursting via current injection in single neurons and employed a theoretical network model.

Main Results:

• Low-dose riluzole maintained bursting but shifted it from persistent to oscillatory activity (~5 Hz).
• Riluzole increased spike-frequency adaptation and induced depolarization block, unlike phenytoin.
• Phenytoin did not induce intraburst oscillations or affect adaptation/depolarization block.

Conclusions:

• Riluzole-induced intraburst oscillations are a network phenomenon.
• Depolarization block, driven by sodium channel inactivation, is the primary accommodation mechanism responsible for these oscillations.