NDLI: Low Concentrations of Alcohol Inhibit BDNF-Dependent GABAergic Plasticity via L-type Ca2+ channel Inhibition in Developing CA3 Hippocampal Pyramidal Neurons

Content Provider	PubMed Central
Author	Zucca, Stefano Valenzuela, C. Fernando
Abstract	Fetal Alcohol Spectrum Disorder (FASD) is associated with learning and memory alterations that could be, in part, a consequence of hippocampal damage. The CA3 hippocampal subfield is one of the regions affected by ethanol (EtOH), including exposure during the 3rd trimester-equivalent (i.e. neonatal period in rats). However, the mechanism of action of EtOH is poorly understood. In CA3 pyramidal neurons from neonatal rats, dendritic BDNF release causes long-term potentiation of the frequency of GABAA receptor-mediated spontaneous postsynaptic currents (LTP-GABAA) and this mechanism is thought to play a role in GABAergic synapse maturation. Here, we show that short- and long-term exposure of neonatal male rats to low EtOH concentrations abolishes LTP-GABAA by inhibiting L-type voltage-gated Ca2+ channels (VGCCs). These findings support the recommendation that even light drinking should be avoided during pregnancy.
Related Links	http://dx.doi.org/10.1523/jneurosci.5405-09.2010
Ending Page	6781
Page Count	6
Starting Page	6776
File Format	PDF
ISSN	02706474
e-ISSN	15292401
Journal	The Journal of neuroscience : the official journal of the Society for Neuroscience
Issue Number	19
Volume Number	30
Language	English
Publisher Date	2010-05-12
Access Restriction	Open
Subject Keyword	Neuroscience(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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Low Concentrations of Alcohol Inhibit BDNF-Dependent GABAergic Plasticity via L-type Ca2+ channel Inhibition in Developing CA3 Hippocampal Pyramidal Neurons