the activated adenylate cyclase manufactures cyclic adenosine mono-phosphate (cAMP),
which in turn catalyzes the activity of another protein, kinase A (or PKA).
In other words, there is a typical cascade of biochemical reactions which can
have many different effects.
For example, PKA phosphorylates
the AMPA receptors, allowing them to remain open longer after glutamate binds
to them. As a result, the postsynaptic neuron becomes further depolarized, thus
contributing to LTP.
Other experiments have shown that
CREB protein is another target of PKA. CREB plays a major role in gene
transcription, and its activation leads to the creation of new AMPA receptors
that can increase synaptic efficiency still further.
other enzyme activated by Ca2+/calmodulin, CaM kinase II, has a property that
is decisive for the persistence of LTP: it can phosphorylate itself! Its enzymatic
activity continues long after the calcium has been evacuated from the cell and
the Ca2+/calmodulin has been deactivated.
II can then in turn phosphorylate the AMPA receptors and probably other proteins
such as MAP kinases, which are involved in the building of dendrites, or the NMDA
receptors themselves, whose calcium conductance would be increased by this phosphorylation.