Amantadine indirectly increases dopamine levels in the synapse. It doesn’t directly stimulate dopamine release; instead, it blocks NMDA receptors. This NMDA receptor blockade reduces the reuptake of dopamine, leading to higher concentrations of dopamine available to postsynaptic receptors.
Specifically, amantadine’s action on NMDA receptors influences dopamine reuptake by modulating the activity of dopamine transporters (DAT). Reduced NMDA receptor activity indirectly inhibits the function of DATs, thereby decreasing dopamine removal from the synaptic cleft.
Further research suggests amantadine may also influence dopamine release by affecting other receptors, such as those for glutamate and adenosine. This interaction creates a complex interplay influencing dopamine availability. However, the primary mechanism remains its NMDA receptor antagonism and subsequent impact on dopamine reuptake.
This mechanism makes amantadine a useful medication for conditions where dopamine deficiency plays a role, such as Parkinson’s disease. However, remember its indirect action on dopamine and its potential side effects.
