Ischaemia is known to cause massive neuronal depolarization, termed anoxic depolarization (AD), due to energy failure and loss of membrane ion gradients. The neuromodulator adenosine accumulates extracellularly during ischaemia and… Click to show full abstract
Ischaemia is known to cause massive neuronal depolarization, termed anoxic depolarization (AD), due to energy failure and loss of membrane ion gradients. The neuromodulator adenosine accumulates extracellularly during ischaemia and activates four metabotropic receptors: A1, A2A, A2B and A3. Striatal medium spiny neurons (MSNs) express high levels of A2A receptors and are particularly vulnerable to ischaemic insults. A2A Receptor blockade reduces acute striatal post‐ischaemic damage but the cellular mechanisms involved are still unknown.
               
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