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6387043 
Journal Article 
Reflex responsiveness of CF-1 mouse neonates following maternal aspartame exposure 
Mahalik, MP; Gautieri, RF 
1984 
0 
Research Communications in Psychology, Psychiatry and Behavior
ISSN: 0362-2428 
9 
385-403 
Brain dysfunction may be a sign of neurotoxic effects observed following late-gestational administration of a suspected teratogenic agent. Mice exposed to teratogenic insults during early gestation exhibit anomalies of structures that develop during this part of gestation, including ocular and craniofacial malformations. Likewise, exposure to a teratogen late in gestation would affect other specific areas, most notably brain myelination and development. Because the end-products of aspartame (APM) metabolism (methanol, aspartic acid and phenylalanine) can affect neuronal myelination and produce hypothalamic lesions in laboratory animals, the possibility exists that neonates born to mothers exposed to APM during the period of ontogenesis critical for brain development could display poor performance in behavioral and reflex testing routines. APM was given by intubation to gravid mice on days 15-18 of gestation in doses of 1 4 g APM/kg body weight. There were no significant differences among the untreated, saline, 1 or 4 g/kg APM test groups in three of the four procedures used to evaluate responsiveness, including negative geotaxis, or surface and air righting. The achievement age for visual placing, however, a barometer of neurosensory development, was significantly later in both the 1 and 4 g/kg APM groups with respect to either the untreated or saline control groups. In addition, the achievement age for this parameter with the higher APM dose was significantly later than that for the 1 g/kg APM dose. Failure of the neonates to perform this basic physiologic task within normal limits may indicate diminished functional ability. Therefore, although pathoanatomic alterations in brains of APM-treated animals and their offspring may not be histologically apparent, the possibility of brain dysfunction appears to be a viable sequela to excessive APM exposure.