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Glutathione-induced sodium currents in neocortex

C A Shaw¹, B A Pasqualotto, K Curry

¹Department of Ophthalmology, University of British Columbia, Vancouver, Canada.

|April 26, 1996

Summary

Glutathione (GSH), a known antioxidant, triggers a potent depolarizing potential in brain cortical slices. This effect, mediated by novel GSH receptors, suggests a new pathway in cortical excitatory neurotransmission.

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Area of Science:

Neuroscience
Neurophysiology
Biochemistry

Background:

Glutathione (GSH) is a vital tripeptide known for its role as a potent free radical scavenger.
Excitatory neurotransmission in the cortex is primarily mediated by excitatory amino acid (EAA) receptors like NMDA and AMPA.

Purpose of the Study:

To investigate the electrophysiological effects of glutathione (GSH) on cortical slices.
To determine the mechanism and receptor involvement of GSH-induced neuronal depolarization.

Main Methods:

Application of GSH to cortical slices to measure electrophysiological responses.
Comparison of GSH-induced potentials with those induced by NMDA and AMPA.
Testing the effects of glutamate receptor antagonists (AP5, DNQX), calcium removal, and potassium channel blockers (TEA).

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Main Results:

GSH elicits a large, fast depolarizing potential in cortical slices, exceeding NMDA and AMPA responses.
The GSH-induced current is carried by sodium ions and is not blocked by AP5 or DNQX.
GSH-induced potential is unaffected by calcium removal or TEA blockade of potassium currents.

Conclusions:

GSH acts via its own distinct receptor-mediated channels, independent of known EAA receptors.
These novel GSH receptors represent a previously unrecognized component of cortical excitatory neurotransmission.
GSH's role extends beyond antioxidant functions to actively modulate neuronal excitability.