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cAMP-dependent protein kinase type II-beta regulatory subunit 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 Adenylate cyclase type 10 Sodium- dependent dopamine transporter 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 Dopamine Ca+ Dopamine cAMP Lisdexamfetamine Dopamine Ca+ Lisdexamfetamine Lisdexamfetamine 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 Lisdexamfetamine 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, Lisdexamfetamine selectively activates dopamine neurotransmission Blood-Brain Barrier Diffusion
PRKAR2B DRD4 PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A GNB1 GNG2 ADCY10 SLC6A3 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC Dopamine Calcium Dopamine cAMP Lisdexamfetamine Dopamine Calcium Lisdexamfetamine Lisdexamfetamine L-Tyrosine L-Dopa Carbon dioxide Adenosine triphosphate GNAI1 Neuronal Excitability
PRKAR2B DRD4 PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A GNB1 GNG2 ADCY10 SLC6A3 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC LDP Ca+ LDP cAMP NRP104 LDP Ca+ NRP104 NRP104 Tyr L-Dopa CO2 ATP Mg2+ Fe2+ Pyr-5'P GNAI1 Neu Exc The inhibition of dopamine reuptake receptors by Lisdexamfetamine 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, Lisdexamfetamine selectively activates dopamine neurotransmission Blood-Brain Barrier Diffusion
PRKAR2B DRD4