“Knockout (KO) mice invalidated for the dopamine transporter (DAT) constitute a powerful animal model of neurobiological alterations associated with hyperdopaminergia relevant to schizophrenia and attention-deficit/hyperactivity disorder (ADHD).
CONCLUSIONS:
These data indicate a dysregulated striatal endocannabinoid neurotransmission associated with hyperdopaminergic state.
Restoring endocannabinoid homeostasis in active synapses might constitute an alternative therapeutic strategy for disorders associated with hyperdopaminergia.
In this process, TRPV1 receptors seem to play a key role and represent a novel promising pharmacological target.”