The mechanism that caffeine increases activity by is via antagonizing adenosine A2 A receptors (the standard mechanism of caffeine). Adenosine normally suppresses the effects of dopamine on locomotion (via working in opposition on neuronal excitation  ) in the striatum where A2 A and dopaminergic neurons co-exist, and preventing this suppression with an antagonist increases the effects of dopamine on D2, of which include spontaneous activity and (in rats) rotational behaviour when unilateral lesions are induced in the striatum.   Non-caffeine adenosine antagonists also share this effect on locomotion, further implicating A2A antagonism and dopamine as the cause rather than a separate, unseen effect of caffeine.  As for why A2 A is mentioned more frequently than A1 in this section, it is since A2 A receptors appear to co-exist with dopamine receptors in many parts of the brain (nuclear accumbens, striatum, tuberculum olfactorium) whereas although A1 are heterogeneously expressed in the brain, there is no pattern with dopamine receptors.  Interactions with motor control appear to be highly relevant to the striatum, where A2 A predominates.
Hello. I’m curious what you mean that you still suffer from the clot you had years ago. It didn’t dissolve with the Nattokinase and Serrapeptace? Do you suffer from the medicine they had you on? This concerns me because I’m trying to decide if I should take the xarelto my doctor prescribed for the small clot I got from a vein surgery I recently had or if I should stay on the Nattokinase and Serrapeptace I started two days ago. I felt nauseous and scared this morning because my dr told me I’ll be fine as long as I take xarelto. I also might have taken too much. 3times yesterday and also Vit. E, fish oil and aspirin. I might have overdone it. Your opinion would be appreciated.