Dopamine and cAMP-regulated phosphoprotein 32 kDa controls both striatal long-term depression and long-term potentiation, opposing forms of synaptic plasticity
P. Calabresi et al., Dopamine and cAMP-regulated phosphoprotein 32 kDa controls both striatal long-term depression and long-term potentiation, opposing forms of synaptic plasticity, J NEUROSC, 20(22), 2000, pp. 8443-8451
A complex chain of intracellular signaling events, critically important in
motor control, is activated by the stimulation of D1-like dopamine (DA) rec
eptors in striatal neurons. At corticostriatal synapses on medium spiny neu
rons, we provide evidence that the D1-like receptor-dependent activation of
DA and cyclic adenosine 3',5' monophosphate-regulated phosphoprotein 32 kD
a is a crucial step for the induction of both long-term depression (LTD) an
d long-term potentiation (LTP), two opposing forms of synaptic plasticity.
In addition, formation of LTD and LTP requires the activation of protein ki
nase G and protein kinase A, respectively, in striatal projection neurons.
These kinases appear to be stimulated by the activation of D1-like receptor
s in distinct neuronal populations.