|1.||Snead, O Carter: 10 articles (08/2012 - 01/2002)|
|2.||Cortez, Miguel A: 10 articles (08/2012 - 01/2002)|
|3.||Serbanescu, Irina: 4 articles (12/2006 - 08/2003)|
|4.||Jeon, Daejong: 2 articles (05/2015 - 01/2013)|
|5.||Jung, Seungmoon: 2 articles (05/2015 - 01/2013)|
|6.||Stewart, Lee S: 2 articles (08/2012 - 12/2006)|
|7.||Fliesler, Steven J: 2 articles (10/2011 - 07/2008)|
|8.||Bercovici, Eduard: 2 articles (05/2007 - 12/2006)|
|9.||Persad, Vasan: 2 articles (12/2006 - 01/2002)|
|10.||Burnham, W McIntyre: 2 articles (07/2006 - 08/2003)|
|2.||Absence Epilepsy (Absence Seizure)
05/01/2015 - "Epileptic activity during early postnatal life in the AY-9944 model of atypical absence epilepsy."
01/01/2013 - "Social deficits in the AY-9944 mouse model of atypical absence epilepsy."
08/01/2012 - "Environmental enrichment improves behavioral outcome in the AY-9944 model of childhood atypical absence epilepsy."
05/11/2007 - "5-HT2 modulation of AY-9944 induced atypical absence seizures."
07/10/2006 - "The AY9944 model of chronic atypical absence seizures in rats reliably reproduces the electrographic, behavioral, pharmacological and cognitive features of clinical atypical absence. "
03/01/1998 - "In previous studies, early administration of the 7DHC-reductase inhibitor AY9944 to pregnant rats resulted in a high frequency of holoprosencephaly, relevant to craniofacial anomalies of SLOS. "
03/01/1998 - "The malformations could have been caused by the same mechanism as holoprosencephaly after early treatment with AY9944. "
09/01/1996 - "Our aim is to verify the validity of a rat model proposed for Smith-Lemli-Opitz (SLO) syndrome, a developmental disorder characterized by a defect in 7-dehydrocholesterol-delta 7 (7DHC)-reductase and by facial dysmorphism close to the holoprosencephaly caused by the teratogen AY9944. "
06/01/1988 - "Pituitary agenesis was the most constant element of holoprosencephaly when AY 9944 was administered on d 4 of gestation at two dosages, 50 or 75 mg/kg. The rate of malformed fetuses was dose related. "
05/01/1984 - "A single dose of AY 9944 (50 mg/kg or 75 mg/kg) given to Wistar pregnant rats on the second, fourth, sixth, seventh, or eighth day of gestation induced malformations such as holoprosencephaly. "
10/01/2013 - "AY9944 -treated rats are considered a model for Smith-Lemli-Opitz syndrome (SLOS). "
09/01/1996 - "Inhibition of 7-dehydrocholesterol reductase by the teratogen AY9944: a rat model for Smith-Lemli-Opitz syndrome."
03/01/1998 - "Abnormal cholesterol biosynthesis produced by AY 9944 in the rat leads to skeletal deformities similar to the Smith-Lemli-Opitz syndrome."
10/01/2011 - "Treatment of Sprague-Dawley rats with AY9944, an inhibitor of 3β-hydroxysterol-Δ(7)-reductase (Dhcr7), leads to elevated levels of 7-dehydrocholesterol (7-DHC) and reduced levels of cholesterol in all biological tissues, mimicking the key biochemical hallmark of Smith-Lemli-Opitz syndrome (SLOS). "
04/01/2000 - "Low cholesterol and high 7-dehydrocholesterol (7DHC) levels are associated with a blockade of Delta7-reductase in the Smith-Lemli-Opitz syndrome (SLOS) and in the animals treated with the inhibitor AY9944. "
11/01/2004 - "AY-9944 (AY) exacerbates chronic recurrent seizures in rats that are analogous to atypical absence epilepsy in humans. "
05/01/2015 - "Administration of the cholesterol biosynthesis inhibitor AY-9944 (AY) during the postnatal developmental period induces AAE in animals; however, the neural mechanism of seizure development remains largely unknown. "
12/01/2006 - "We studied daily rhythms of chronic seizure activity and behavior in adult rats and mice treated with the cholesterol biosynthesis inhibitor AY-9944 (AY) during early postnatal development. "
11/01/2004 - "We sought to produce chronic, recurrent, medically refractory seizures by administration of the cholesterol biosynthesis inhibitor AY-9944 (AY) during postnatal development in rats exposed prenatally to MAM. "
07/10/2006 - "These data suggest that GABA(B) receptor-mediated mechanisms are responsible for the cognitive dysfunction in the AY9944 model of chronic atypical absence seizures and further, that their cognitive impairment is independent of the seizure activity. "
|1.||3- beta- (2- (diethylamino)ethoxy)androst- 5- en- 17- one
|2.||Sodium Oxybate (gamma Hydroxybutyrate)
|9.||GABA-B Receptor Antagonists
|10.||GABA-B Receptors (Receptor, GABA-B)