Final answer:
Glutamate is the excitatory biogenic amine in the CNS that causes EPSP. When dopamine binds to its receptor, cAMP concentration increases. Before tyrosine phosphorylation, insulin receptor dimerization and autophosphorylation occur.
Step-by-step explanation:
The excitatory biogenic amine in the CNS that causes EPSP is glutamate. Glutamate is known to be excitatory because when it binds to its receptors, it causes depolarization of the postsynaptic cell. On the other hand, GABA (gamma-aminobutyric acid) is the main inhibitory neurotransmitter in the CNS, which works opposite to glutamate, causing hyperpolarization when it binds to its receptors. Dopamine, which can have either excitatory or inhibitory effects depending on the type of receptor it binds to, is not the neurotransmitter that is associated with causing EPSPs.
In the context of dopamine binding its receptor, you would expect an increase in the concentration of cAMP (cyclic Adenosine Monophosphate) following this event. Dopamine receptors that are G-protein-linked can activate adenylate cyclase enzymes, which convert ATP to cAMP, serving as a secondary messenger in various signalling pathways in the cell.
Before phosphorylation of tyrosine residues when insulin binds to its receptor, which is a receptor tyrosine kinase, dimerization and autophosphorylation of the receptor occur. Following this event, the tyrosine residues of the insulin receptor are phosphorylated, initiating a sigsignallingscade that has multiple effects within the cell.