Electrophysiology of dopamine in normal and denervated striatal neurons.
Parkinson's disease (PD) symptoms originate from the loss of the dopaminergic control of neuronal activity in the striatum. Permanent loss of dopaminergic terminals in the striatum results in an abnormal activity of striatal neurons. The therapeutic treatment with exogenous dopamine, therefore, temporarily restores a balanced synaptic excitation of striatal neurons, counteracting pre- and postsynaptically the excessive glutamate release caused by the degeneration of nigrostriatal dopaminergic fibers. However, chronic treatment is associated with adverse effects that might reflect nonphysiological dopamine replacement. Basic studies on experimental animal models of PD are of crucial importance for the development of therapeutic agents able to provide relief to individuals with PD, without the adverse effects associated with currently available drugs.
Calabresi
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P
Cliníca Neurologica, Dipartimento di Neuroscienze, Università di Roma Tor Vergata, Rome, Italy.
Centonze
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D
Bernardi
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G
D000818:Animals; D000978:Antiparkinson Agents / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D004298:Dopamine / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004409:Dyskinesia, Drug-Induced / Q000378:metabolism* / Q000503:physiopathology; D004594:Electrophysiology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage / Q000009:adverse effects* / Q000494:pharmacology; D008959:Models, Neurological; D009474:Neurons / Q000378:metabolism*; D010300:Parkinson Disease / Q000378:metabolism* / Q000503:physiopathology
D000978:Antiparkinson Agents; D018698:Glutamic Acid; D007980:Levodopa; D004298:Dopamine