Postnatal aniracetam treatment improves prenatal ethanol induced attenuation of AMPA receptor-mediated synaptic transmission

Neurobiology of Disease

Alexander Dityatev¹  Mark Carpenter²  Nayana Wijayawardhane³  Brian C. Shonesy³  Julia Vaglenova³  Vishnu Suppiramaniam³  Thirumalini Vaithianathan³  Charles R. Breese³ 

[1] Department of Mathematics and Statistics, College of Sciences and Mathematics, Auburn University, Auburn, AL 36849, USA;Department of Pharmacology, University of Tennessee Health Science Center, Memphis, TN 38163, USA;Department of Pharmacal Sciences, 401 Walker Building, Harrison School of Pharmacy, Auburn University, Auburn, AL 36849, USA;

关键词: Prenatal ethanol;    Hippocampus;    AMPA receptors;    mEPSCs;    Aniracetam;    Fetal alcohol syndrome;   

DOI  :  

来源: DOAJ

【 摘 要 】

Aniracetam is a nootropic compound and an allosteric modulator of AMPA receptors (AMPARs) which mediate synaptic mechanisms of learning and memory. Here we analyzed impairments in AMPAR-mediated synaptic transmission caused by moderate prenatal ethanol exposure and investigated the effects of postnatal aniracetam treatment on these abnormalities. Pregnant Sprague–Dawley rats were gavaged with ethanol or isocaloric sucrose throughout pregnancy, and subsequently the offspring were treated with aniracetam on postnatal days (PND) 18 to 27. Hippocampal slices prepared from these pups on PND 28 to 34 were used for the whole-cell patch-clamp recordings of AMPAR-mediated spontaneous and miniature excitatory postsynaptic currents in CA1 pyramidal cells. Our results indicate that moderate ethanol exposure during pregnancy results in impaired hippocampal AMPAR-mediated neurotransmission, and critically timed aniracetam treatment can abrogate this deficiency. These results highlight the possibility that aniracetam treatment can restore synaptic transmission and ameliorate cognitive deficits associated with the fetal alcohol syndrome.

【 授权许可】

Unknown