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Prenatal ethanol exposure persistently impairs NMDA receptor‐dependent activation of extracellular signal‐regulated kinase in the mouse dentate gyrus
Author(s) -
SamudioRuiz Sabrina L.,
Allan Andrea M.,
Valenzuela Carlos Fernando,
PerroneBizzozero Nora I.,
Caldwell Kevin K.
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2009.06049.x
Subject(s) - dentate gyrus , nmda receptor , long term potentiation , hippocampal formation , hippocampus , neuroscience , receptor , endocrinology , medicine , biology
The dentate gyrus (DG) is the central input region to the hippocampus and is known to play an important role in learning and memory. Previous studies have shown that prenatal alcohol is associated with hippocampal‐dependent learning deficits and a decreased ability to elicit long‐term potentiation (LTP) in the DG in adult animals. Given that activation of the extracellular signal‐regulated kinase 1/2 (ERK1/2) signaling cascade by NMDA receptors is required for various forms of learning and memory, as well as LTP, in hippocampal regions, including the DG, we hypothesized that fetal alcohol‐exposed adult animals would have deficits in hippocampal NMDA receptor‐dependent ERK1/2 activation. We used immunoblotting and immunohistochemistry techniques to detect NMDA‐stimulated ERK1/2 activation in acute hippocampal slices prepared from adult fetal alcohol‐exposed mice. We present the first evidence linking prenatal alcohol exposure to deficits in NMDA receptor‐dependent ERK1/2 activation specifically in the DG of adult offspring. This deficit may account for the LTP deficits previously observed in the DG, as well as the life‐long cognitive deficits, associated with prenatal alcohol exposure.