“Jing-Ning Granules” Can Alleviate Attention Deficit Hyperactivity Disorder in Rats by Modulating Dopaminergic D2/D1-Like Receptor-Mediated Signaling Pathways

Figure 1

A schematic plot of DA transport in the extracellular and intracellular pathways. ① DA is released to the synaptic cleft by vesicular exocytosis, acting on DA receptors on the postsynaptic membrane. DA is then reuptaken by dopamine transporters (DAT) back into neurons, partly reabsorbed, and utilized and partly inactivated by inactivating enzymes (MAO). ② DA in the synaptic cleft acts on D1-like and D2-like receptors, which exert different physiological functions. The Dl-like receptors are coupled to Gs/olf proteins that activate the cAMP/PKA pathway, whereas the D2-like receptors are coupled to Gi/o proteins that inhibit AC activity and eventually lead to reduced PKA levels; similar effects are observed on the Ca²⁺/CAM/CAMKII pathway.