The present study addresses the still unresolved issue of the character of alcohol–thiamine metabolic interferences in the developing central nervous system (CNS).
Investigations compare developmental neurotoxicity evoked by three patterns of maternal thiamine deficiency (pre, peri and postnatal), with two patterns of maternal chronic alcohol intake (alcohol alone and alcohol + thiamine cotreatment), on seven neurodevelopmental abilities in the offspring.
The three patterns of thiamine deficiency, pair-compared with controls, highlight four sequences of development: (1) embryonic–perinatal sequence; (2) perinatal–postnatal sequence; (3) “ontogeny in ontogeny out” sequence; (4) “off and on” developing sequence.
The results suggest a temporally- and regionally emergence of structures and centers underlying functional maturation during CNS ontogenesis.
Furthermore, both developmental thiamine deficiencies and ethanol exposure produce two waves of neurofunctional alterations, peaking at P15 (postnatal day 15) and P25, respectively. The first peak of vulnerability is a prenatal event; it may interfere with the periods of intense cellular proliferation and migration. The second peak represents both perinatal and postnatal events; it may interfere with the periods of cellular differentiation, synaptogenesis, axonogenesis and myelinogenesis. Alcohol + thiamine cotreatment fails to reduce the first peak, but neutralizes essentially the second peak.
The results suggest that alcohol interferes with thiamine during cellular differentiation and membrane developmental processes mainly. Indeed, among the three conditions of thiamine-deficient diet, only perinatal thiamine deficiency exhibits a closer relationship with developmental alcohol exposure.
Together, these observations suggest that the critical period for alcohol–thiamine antagonism occurs perinatally and affects primarily cellular differentiation.
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