Synaptic transmission in the striatum: from plasticity to neurodegeneration

Striatal neurones receive myriad of synaptic inputs originating from differ ent sources. Massive afferents from all areas of the cortex and the thalamu s represent the most important source of excitatory amino acids, whereas th e nigrostriatal pathway and intrinsic circuits provide the striatum with do pamine, acetylcholine, GABA, nitric oxide and adenosine. All these neurotra nsmitter systems interact each other and with voltage-dependent conductance s to regulate the efficacy of the synaptic transmission within this nucleus . The integrative action exerted by striatal projection neurones on this co nverging information dictates the final output of the striatum to the other basal ganglia structures. Recent morphological, immunohistochemical and el ectrophysiological findings demonstrated that the striatum also contains di fferent interneurones, whose role in physiological and pathological conditi ons represents an intriguing challenge in these years. The use of the in vi tro brain slice preparation has allowed not only the detailed investigation of the direct pre- and postsynaptic electrophysiological actions of severa l neurotransmitters in striatal neurones, but also the understanding of the ir role in two different forms of corticostriatal synaptic plasticity, long -term depression and long-term potentiation. These long-lasting changes in the efficacy of excitatory transmission have been proposed to represent the cellular basis of some fc,rms of motor learning and are altered in animal models of human basal ganglia disorders, such as Parkinson's disease. The s triatum also expresses high sensitivity to hypoxic-aglycemic insults. Durin g these pathological conditions, striatal synaptic transmission is altered depending on presynaptic inhibition of transmitter release and opposite mem brane potential changes occur in projection neurones and in cholinergic int erneurones. These ionic mechanisms might partially explain the selective ne uronal vulnerability observed in the striatum during global ischemia and Hu ntington's disease. (C) 2000 Elsevier Science Ltd. All rights reserved.