Under normal conditions, hippocampal CA1 activation leads to monosynaptic activation of mPFC pyramidal neurons (Jay et al., 1996, Laroche, 1990, Parent et al., 2010). Retrieval and consolidation of hippocampal-dependent memory has been shown to be dependent on mPFC activation (Mameli and Valenzuela, 2006) with coordinated firing increasing with task difficulty (Jones and Wilson 2005). Alcohol exposure during development compromises the hippocampus (Miller 1989; for reviews see Gil-Mohapal et al., 2011, Berman and Hannigan 2000) resulting in inhibited glutamatergic signaling, LTP induction (Puglia et al., 2010) and permanent immature spines (Mameli and Valenzuela, 2006). Together, these findings would predict altered CA1 output in animal models of FASD which could result in adaptive changes in the mPFC including reductions in dendritic spines near the soma of neurons as described in the current study.
