Moreover, studies on the effects of pharmacological interventions in animals with supra-pontine lesions caused by decerebration or cerebral infarction have shown that such lesions can result in increased activity of excitatory mechanisms involving the NMDA-glutamate and D2-dopamine receptors, while the activity of inhibitory mechanisms involving the NMDA-glutamate and M1-muscarinic receptors in the brain is reduced [26]. This evidence concerns the gene DRD2 and cerebral infarction.