Synaptic plasticity in the basal ganglia: a similar code for physiological and pathological conditions.

It is widely accepted that the complexity and adaptability of neuronal communication, which is necessary for integrative and higher functions of the brain, is amply represented by plastic changes occurring at synaptic level. Therefore, long-term modifications of synaptic efficacy between neurons have been considered the cellular basis of learning and memory. Accordingly, there is a plethora of experimental evidence supporting this contention. Indeed, synaptic modifications in the hippocampus, the cerebral and cerebellar cortices regulate composite neuronal functions such those related to cognition, awareness, memory storage, and motion. In recent years, the concept that enduring changes of excitatory glutamatergic synaptic potentials [long-term potentiation (LTP) and long-term depression (LTD)] are not limited to the hippocampus and cortices but occur also in other brain areas has emerged. For instance, plasticity at different excitatory pathways has been clearly demonstrated in the basal ganglia. Here we present an overview of the experimental data regarding synaptic plasticity in the basal ganglia and highlight how results reported in the literature are often contradictory, especially when compared to those obtained in the hippocampal area. In trying to propose possible explanations to some of these contradictions, we present a holistic approach that re-interprets the basal ganglia synaptic plasticity in terms of expression of physiological and pathological phenomena and therapeutic effects of drugs.