Abstract
The anatomo-physiological disruptions inherent to different categories of the Fetal Alcohol Spectrum Disorder do not encompass all the negative consequences derived from intrauterine ethanol (EtOH) exposure. Preclinical, clinical and epidemiological studies show that prenatal EtOH exposure also results in early programming of alcohol affinity. This affinity has been addressed through the examination of how EtOH prenatally exposed organisms recognize and prefer the drug’s chemosensory cues and their predisposition to exhibit heightened voluntary EtOH intake during infancy and adolescence. In altricial species these processes are determined by the interaction of at least three factors during stages equivalent to the 2nd and 3rd human gestational trimester: (i) fetal processing of the drug’s olfactory and gustatory attributes present in the prenatal milieu; (ii) EtOH’s recruitment of central reinforcing effects that also imply progressive sensitization to the drug’s motivational properties; and (iii) an associative learning process involving the prior two factors. This Pavlovian learning phenomenon is dependent upon the recruitment of the opioid system and studies also indicate a significant role of EtOH’s principal metabolite (acetaldehyde, ACD) which is rapidly generated in the brain via the catalase system. The central and rapid accumulation of this metabolite represents a major factor involved in the process of fetal alcohol programming. According to recent investigations, it appears that ACD exerts early positive reinforcing consequences and antianxiety effects (negative reinforcement). Finally, this review also acknowledges human clinical and epidemiological studies indicating that moderate and binge-like drinking episodes during gestation result in neonatal recognition of EtOH’s chemosensory properties coupled with a preference towards these cues. As a whole, the studies under discussion emphasize the notion that even subteratogenic EtOH exposure during fetal life seizes early functional sensory and learning capabilities that pathologically shape subsequent physiological and behavioral reactivity towards the drug.
Highlights
Two drug-related phenomena act as the foundation for the present review: (i) among other drugs of abuse, ethanol (EtOH) recruits non-associative and associative learning capabilities of the organism; and (ii) age of onset of EtOH-related experiences represents a critical factor determining later use and abuse of this psychotropic agent
It is our expectation that the present review will provide at least partially, notions related with the fact that early experiences with the drug recruit functional capabilities of the organism that result in subsequent alcohol affinity
When configuring the neurophysiological and behavioral studies conducted by Youngentob and Glendinning (2009) the title of one of their articles clearly summarizes the impact of chronic fetal alcohol exposure upon EtOH affinity: ‘‘Fetal EtOH exposure increases EtOH intake by making it smell and taste better.’’
Summary
Two drug-related phenomena act as the foundation for the present review: (i) among other drugs of abuse, ethanol (EtOH) recruits non-associative and associative learning capabilities of the organism; and (ii) age of onset of EtOH-related experiences represents a critical factor determining later use and abuse of this psychotropic agent. According to the US National Institutes of Health (ncbi.nlm.nih.gov; October 2019), approximately 17,000 articles arise when linking the terms ‘‘fetal’’ and ‘‘alcohol.’’ Within this considerable number of peer-reviewed studies, it is possible to detect an early publication that explicitly examined the consequences of fetal chronic exposure to EtOH upon subsequent intake patterns of the drug (Bond and Di Giusto, 1976) According to these authors, and based on an animal model frequently employed to assess EtOH’s teratogenic properties, voluntary intake of the drug in an altricial species such as the rat, increases as a function of prenatal exposure to this psychotropic agent. When configuring the neurophysiological and behavioral studies conducted by Youngentob and Glendinning (2009) the title of one of their articles clearly summarizes the impact of chronic fetal alcohol exposure upon EtOH affinity: ‘‘Fetal EtOH exposure increases EtOH intake by making it smell and taste better.’’
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