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Tetrodotoxin resistant propagation and extracellular sodium changes during spreading depression in rat cerebellum
Abstract:
Spreading depression (SD) was elicited in the benzoate-conditioned rat cerebellum by microinjection of KC1. Median SD propagation velocity was 9.2 mm . min-1. [Na+]0 decreases, median value 77.5 mM, were measured with ion-selective micropipettes. Superfusion of the cerebellum with 10-5 M tetrodotoxin did not modify the propagation velocity or decrease the [Na+]0 change. This confirms that classical voltage-mediated Na+ conductances are not involved in SD.
Insights
Spreading depression (SD) in rat cerebellum propagates rapidly. Tetrodotoxin, a sodium channel blocker, did not affect SD velocity or sodium changes, suggesting non-classical mechanisms are involved.
Area of Science:
- Neuroscience
- Physiology
Background:
- Spreading depression (SD) is a wave of neuronal and glial depolarization.
- The precise ionic mechanisms underlying SD propagation in the cerebellum remain incompletely understood.
Purpose of the Study:
- To investigate the role of classical voltage-gated sodium channels in cerebellar SD.
- To measure SD propagation velocity and associated extracellular sodium changes in vivo.
Main Methods:
- Spreading depression was induced in benzoate-conditioned rat cerebellum via KCl microinjection.
- Extracellular sodium concentration ([Na+]0) changes were measured using ion-selective microelectrodes.
- The effect of tetrodotoxin (TTX) on SD propagation was assessed.
Main Results:
- The median SD propagation velocity was 9.2 mm/min.
- A median decrease in [Na+]0 of 77.5 mM was observed.
- Superfusion with 10-5 M tetrodotoxin did not alter SD propagation velocity or the magnitude of [Na+]0 decrease.
Conclusions:
- Classical voltage-gated sodium conductances are not essential for cerebellar SD propagation.
- These findings suggest alternative ion transport mechanisms contribute to SD in this brain region.