Ok, probably not the answer you're looking for, but here we go.
From: http://www.lclark.edu/~reiness/neurobiology/Lectures/lecture15.htm
"After the pulse of neurotransmitter ends and the transmitter diffuses
away or is taken back up into the nerve terminal, what happens? First
the transmitter dissociates from its receptor. The receptor no longer
activates GTP exchange on the G protein, so the G proteins gets stuck
in the GDP-binding form, preventing it from interacting with adenylyl
cyclase, and so adenylyl cyclase becomes inactive. Thus, cAMP is no
longer being made. In fact cAMP is constantly degraded into the
inactive molecule AMP by an enzyme called phosphodiesterase, so the
cAMP levels begin to fall when cAMP is no longer being made. Once this
happens, cAMP dissociates from the regulatory subunit of PKA, so that
the PKA can reassemble--catalytic and regulatory subunits bind
together. This of course inactivates the catalytic subunit so that it
no longer can phosphorylate proteins. Finally there is a group of
proteins that cut phosphate groups off the serine and threonine
residues that PKA phosphorylated. These phosphatases the ion channels
back to their original unphosphorylated forms which shifts the ion
channel back into the non-conducting state (Fig. 7.12). Thus, using
this elaborate cascade of events, cells can rapidly respond to, and
amplify, signals from the neurotransmitters that impinge upon their
surface, and they can rapidly reverse the response when the signal is
no longer present. Nevertheless, both the activation and inactivation
process are slower than simply opening and closing an ion channel;
thus transmitters that activate G-protein coupled receptors tend to
have slower-to-start and longer-lasting effects on postsynaptic cells
than transmitters that activate ligand-gated ion channels."
As I understand this, the decreased concentrations of cAMP due to the
inhibition of adenylyl cyclase due to the inhibitory G protein linked
to the alpha-2 receptor cause cAMP to dissociate from PKA. This could
be viewed as activation of cAMP in a roundabout way. As I said, I'm
not sure that this is what you want. This looks like a feedback
mechanism more than anything, but I couldn't find anything that stated
that alpha-2 receptor could directly stimulate production of cAMP in
anyway. |
