Xx. Tan et al., INTERACTION OF ETHANOL WITH MUSCARINIC RECEPTOR-STIMULATED PHOSPHOINOSITIDE METABOLISM DURING THE BRAIN GROWTH SPURT IN THE RAT - ROLE OF ACETALDEHYDE, Neuroscience letters, 156(1-2), 1993, pp. 13-16
The developing brain is extremely sensitive to the neurotoxicity of et
hanol; however, the mechanism(s) of its developmental neurotoxicity ar
e still elusive. In the developing rat brain, ethanol exerts an age-,
brain region-, and receptor-specific inhibitory effect on muscarinic r
eceptor-stimulated phosphoinositide metabolism, which may be linked to
some of the neurotoxic effects of ethanol found in children with feta
l alcohol syndrome. Since some studies have suggested that the ethanol
metabolite acetaldehyde may mediate, at least in part, the developmen
tal effects of ethanol, in the present study we have examined whether
acetaldehyde would inhibit carbachol-stimulated phosphoinositide metab
olism in brain slices from immature rats. We also tested propionaldehy
de, the corresponding aldehyde of n-propanol, another alcohol shown to
cause microencephaly and to affect phosphoinositide metabolism in the
developing rat. Neither acetaldehyde nor propionaldehyde, at concentr
ations up to 1 mM, had any inhibitory effect on this system, while the
two alcohols did, as previously reported. These results suggest that
ethanol itself may be the primary agent responsible for its developmen
tal neurotoxicity.