Neuronal membrane potential is mildly depolarized in the anoxic turtle cortex.

Area of Science:

• Neuroscience
• Cellular Physiology

Background:

• Neuronal membrane potential (E(m)) is critical for regulating neuronal excitability and preventing excitotoxic cell death (ECD).
• Mammalian neurons experience severe E(m) loss and ECD during anoxia, while anoxia-tolerant turtle neurons reduce excitability to avoid damage.

Purpose of the Study:

• To investigate the mechanisms underlying the mild anoxic depolarization (MAD) in anoxia-tolerant turtle cortical neurons.
• To determine if single ion channel or pump modulations prevent MAD or if it results from a summation of altered conductances.

Main Methods:

• Whole-cell patch clamp technique to record E(m) in turtle cortical neurons.
• Transition from normoxic to anoxic conditions with various ion channel/pump modulators and reactive oxygen species scavengers.

Main Results:

• Anoxic perfusion caused a reversible, mild depolarization (8.1 mV) in turtle cortical neurons.
• MAD was not prevented by manipulating single ionic conductances.
• MAD was partially reduced by GABA(A) receptor antagonists, bicarbonate production inhibitors, K(+) channel blockers, or reactive oxygen species scavengers.
• These treatments induced depolarization in normoxic neurons.

Conclusions:

• The mild anoxic depolarization in turtle neurons is likely caused by the summation of multiple altered ion conductance states during anoxia.
• This adaptive response contributes to anoxia tolerance by modulating neuronal excitability.