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cAMP-dependent protein kinase type II-beta regulatory subunit Sodium- dependent dopamine transporter D(4) dopamine receptor cAMP-dependent protein kinase catalytic subunit alpha cAMP-dependent protein kinase catalytic subunit beta cAMP-dependent protein kinase type I-alpha regulatory subunit cAMP-dependent protein kinase catalytic subunit gamma cAMP-dependent protein kinase type I-beta regulatory subunit cAMP-dependent protein kinase type II-alpha regulatory subunit Guanine nucleotide- binding protein G(I)/G(S)/G(T) subunit beta-1 Gγ Adenylate cyclase type 10 Synaptic vesicular amine transporter Voltage- dependent calcium channel subunit alpha-2/delta-1 Voltage- dependent calcium channel subunit alpha-2/delta-2 Voltage- dependent N-type calcium channel subunit alpha-1B Tyrosine 3-monooxygenase Aromatic-L- amino-acid decarboxylase Methylphenidate Dopamine Ca+ Dopamine cAMP Dopamine Ca+ Methylphenidate Methylphenidate L-Tyrosine L-Dopa CO2 ATP Magnesium Fe2+ Pyridoxal 5'-phosphate Guanine nucleotide- binding protein G(i) subunit alpha-1 Neuronal Excitability The inhibition of dopamine reuptake receptors by Methylphenidate causes more dopamine to accumulate in the synapse, causing the continual activation of the D4 Dopamine receptor Activation of D4 dopamine receptors activates the Gi signalling cascade which leads to reduced cAMP. Presynaptic Neuron Cytosol Synaptic Vesicle Postsynaptic Neuron Cytosol Dopamine is produced in the Ventral Tegmental Area of the brain Prefrontal Cortex Reduced cAMP results in decreased neural excitability. This results in reduced movement and impulsivity. Although the exact mechanisms are unknown. Synapse Prefrontal Cortex Increased dopamine activates D4 dopamine receptors in the prefrontal cortex which are the main receptor involved in ADHD In low doses, Methylphenidate selectively activates dopamine neurotransmission, Blood-Brain Barrier Diffusion
PRKAR2B SLC6A3 DRD4 PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A GNB1 GNG2 ADCY10 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC Methylphenidate Dopamine Calcium Dopamine cAMP Dopamine Calcium Methylphenidate Methylphenidate L-Tyrosine L-Dopa Carbon dioxide Adenosine triphosphate GNAI1 Neuronal Excitability
PRKAR2B SLC6A3 DRD4 PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A GNB1 GNG2 ADCY10 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC Phenidy LDP Ca+ LDP cAMP LDP Ca+ Phenidy Phenidy Tyr L-Dopa CO2 ATP Mg2+ Fe2+ Pyr-5'P GNAI1 Neu Exc The inhibition of dopamine reuptake receptors by Methylphenidate causes more dopamine to accumulate in the synapse, causing the continual activation of the D4 Dopamine receptor Activation of D4 dopamine receptors activates the Gi signalling cascade which leads to reduced cAMP. Presynaptic Neuron Cytosol Synaptic Vesicle Postsynaptic Neuron Cytosol Dopamine is produced in the Ventral Tegmental Area of the brain Prefrontal Cortex Reduced cAMP results in decreased neural excitability. This results in reduced movement and impulsivity. Although the exact mechanisms are unknown. Synapse Prefrontal Cortex Increased dopamine activates D4 dopamine receptors in the prefrontal cortex which are the main receptor involved in ADHD In low doses, Methylphenidate selectively activates dopamine neurotransmission, Blood-Brain Barrier Diffusion