Dopamine-mediated regulation of corticostriatal synaptic plasticity

Abstract

The striatum represents the main input into the basal ganglia. Neurons projecting from the striatum receive a large convergence of afferents from all areas of the cortex and transmit neural information to the basal ganglia output structures. Corticostriatal transmission is essential in the regulation of voluntary movement, in addition to behavioural control, cognitive function and reward mechanisms. Long-term potentiation (LTP) and long-term depression (LTD), the two main forms of synaptic plasticity, are both represented at corticostriatal synapses and strongly depend on the activation of dopamine receptors. Here, we discuss possible feedforward and feedback mechanisms by which striatal interneurons, in association with striatal spiny neurons and endogenous dopamine, influence the formation and maintenance of both LTP and LTD. We also propose a model in which the spontaneous membrane oscillations of neurons projecting from the striatum (named 'up' and 'down' states), in addition to the pattern of release of endogenous dopamine, bias the synapse towards preferential induction of LTP or LTD. Finally, we discuss how endogenous dopamine crucially influences changes in synaptic plasticity induced by pathological stimuli, such as energy deprivation.