Work

Low Concentrations of Alcohol Inhibit BDNF-Dependent GABAergic Plasticity via L-type Ca 2+ Channel Inhibition in Developing CA3 Hippocampal Pyramidal Neurons

Year: 2010

Type: article

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 third 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. These findings support the recommendation that even light drinking should be avoided during pregnancy.

Source: Journal of Neuroscience

DOI: 10.1523/jneurosci.5405-09.2010

Authors: Stefano Zucca, C. Fernando Valenzuela

Institutions: University of New Mexico, University of New Mexico Health Sciences Center

Language: English

Topic: Neuroscience and Neuropharmacology Research

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funders: National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism