ArticleAlcoholism, clinical and experimental research2010
Phosphodiesterase type 4 inhibition does not restore ocular dominance plasticity in a ferret model of fetal alcohol spectrum disorders.
Article in Alcoholism, clinical and experimental research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Phosphodiesterase regulation of alcohol drinking in rodents.Alcohol (Fayetteville, N.Y.) · 2015Review
- Fetal alcohol spectrum disorders and abnormal neuronal plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2011Review
- Overexpression of serum response factor restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThere is growing evidence that deficits in neuronal plasticity account for some of the neurological problems observed in fetal alcohol spectrum disorders (FASD). Recently, we showed that early alcohol exposure results in a permanent impairment in visual cortex ocular dominance (OD) plasticity in a ferret model of FASD. This disruption can be reversed, however, by treating animals with a Phosphodiesterase (PDE) type 1 inhibitor long after the period of alcohol exposure.
aimBecause the mammalian brain presents different types of PDE isoforms we tested here whether inhibition of PDE type 4 also ameliorates the effects of alcohol on OD plasticity. MATERIAL AND
methodsFerrets received 3.5 g/Kg alcohol i.p. (25% in saline) or saline as control every other day between postnatal day (P) 10 to P30, which is roughly equivalent to the third trimester equivalent of human gestation. Following a prolonged alcohol-free period (10 to 15 days), ferrets had the lid of the right eye sutured closed for 4 days and were examined for ocular dominance changes at the end of the period of deprivation.
resultsUsing in vivo electrophysiology we show that inhibition of PDE4 by rolipram does not restore OD plasticity in alcohol-treated ferrets.
conclusionThis result suggests that contrary to PDE1, PDE4 inhibition does not play a role in the restoration of OD plasticity in the ferret model of FASD.
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