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cAMP-dependent protein kinase type II-beta regulatory subunit 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 Sodium- dependent dopamine transporter D(2) dopamine receptor 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 Guanine nucleotide- binding protein G(I)/G(S)/G(T) subunit beta-1 Guanine nucleotide- binding protein G(i) subunit alpha-1 Ca+ Dopamine cAMP Cocaine Dopamine Dopamine Ca+ L-Tyrosine L-Dopa CO2 ATP Magnesium Fe2+ Pyridoxal 5'-phosphate Neuronal Excitability The inhibition of dopamine reuptake receptors by Cocaine causes more dopamine to accumulate in the synapse, causing the continual activation of the D2 Dopamine receptor Activation of D2 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 Reduced cAMP results in decreased neural excitability. This has been found to be linked to the cause of addiction, especially with cocaine. Synapse Increased dopamine activates D2 dopamine receptorswhich are associated with regulating the reward pathway. Mesolimbic Pathway Mesolimbic pathway
PRKAR2B PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A SLC6A3 DRD2 GNG2 ADCY10 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC GNB1 GNAI1 Calcium Dopamine cAMP Cocaine Dopamine Dopamine Calcium L-Tyrosine L-Dopa Carbon dioxide Adenosine triphosphate Neuronal Excitability
PRKAR2B PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A SLC6A3 DRD2 GNG2 ADCY10 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC GNB1 GNAI1 Ca+ LDP cAMP Cocaine LDP LDP Ca+ Tyr L-Dopa CO2 ATP Mg2+ Fe2+ Pyr-5'P Neu Exc The inhibition of dopamine reuptake receptors by Cocaine causes more dopamine to accumulate in the synapse, causing the continual activation of the D2 Dopamine receptor Activation of D2 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 Reduced cAMP results in decreased neural excitability. This has been found to be linked to the cause of addiction, especially with cocaine. Synapse Increased dopamine activates D2 dopamine receptorswhich are associated with regulating the reward pathway. Mesolimbic Pathway Mesolimbic pathway
PRKAR2B PRKACA PRKACB PRKAR1A PRKACG PRKAR1B PRKAR2A SLC6A3 DRD2 GNG2 ADCY10 SLC18A2 CACNA2D1 CACNA2D2 CACNA1B TH DDC GNB1 GNAI1 Ca2+ LDP cAMP Cocaine LDP LDP Ca2+ Tyr L-Dopa CO2 ATP Neu Exc