B6 mice have been also shown to be less susceptible than D2 mice to the proconvulsant effects of the glutamate agonist N-methyl-D-aspartate (NMDA) and the potassium channel antagonist 4-aminopyridine (Kosobud and Crabbe, 1990; Metten and Crabbe, 2005). These data suggest that, compared to D2 mice, B6 mice have deficits in neural mechanisms mediating inhibitory (e.g., GABAergic system) and excitatory (e.g., NMDA and potassium channel functions) neurotransmission in the CNS. Moreover, microdialysis studies have also shown that B6 mice exhibit lower basal levels of acetylcholine (ACh) in the hippocampus than D2 mice (Imperato et al., 1996). Evidence from human studies has implicated genes regulating glutamatergic and cholinergic function with delta and theta oscillatory activity in individuals at risk of alcohol dependence (for review, see Rangaswamy and Porjesz, 2008). However, further research is needed to determine the relationship between these neurotransmitter systems, cortical oscillatory activity and alcohol preference in B6 and D2 mice.
