Restoration of neuronal plasticity by a phosphodiesterase type 1 inhibitor in a model of fetal alcohol exposure.
Although some studies showed the efficacy of phosphodiesterase (PDE) inhibitors as neuronal plasticity enhancers, little is known about the effectiveness of these drugs to improve plasticity in cases of mental retardation. Fetal alcohol syndrome (FAS) is the leading cause of mental retardation in the western world. Using a combination of electrophysiological and optical imaging techniques, we show here that vinpocetine, a PDE type I inhibitor, restores ocular dominance plasticity in the ferret model of fetal alcohol exposure. Our finding should contribute to a better understanding and treatment of cognitive deficits associated with mental disorders, such as FAS.
Medina
Alexandre E
AE
Department of Anatomy and Neurobiology, School of Medicine, Virginia Commonwealth University, Richmond, Virginia 23298, USA. amedina@vcu.edu
Krahe
Thomas E
TE
Ramoa
Ary S
AS
D000818:Animals; D004195:Disease Models, Animal; D000431:Ethanol / Q000633:toxicity; D005260:Female; D005289:Ferrets; D063647:Fetal Alcohol Spectrum Disorders / Q000188:drug therapy / Q000201:enzymology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D043264:Phosphodiesterase I / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D011247:Pregnancy; D014748:Vinca Alkaloids / Q000494:pharmacology*
D010726:Phosphodiesterase Inhibitors; D014748:Vinca Alkaloids; D000431:Ethanol; C013983:vinpocetine; D043264:Phosphodiesterase I