Developmental toxicity of cocaine exposure in mid-pregnancy mice.
Abstract
AIM: To investigate the toxic effects of mid-pregnancy cocaine exposure on
embryo-fetus.
METHODS: A transplacental murine model of cocaine exposure on embryo-fetus mice
was established, in which pregnant dams of comparable weight were assigned into
three groups: cocaine with food ad lib (COC), saline and pair-fed with COC (SPF),
and saline with food ad lib (SAL). From embryonic d 8 (E8) to E17, physiological
variables of dams and offspring were recorded and concentrations of dopamine and
serotonin in fetal striatum were examined.
RESULTS: Compared with SAL dams, COC and SPF dams showed lower weight gain. But
only COC fetuses demonstrated low brain weight and low striatum weight on E17, as
well as small biparietal diameter (BPD) on postnatal d1 (P1). Surprisingly, low
brain/body weight ratio was seen in COC offspring, which might reflect
disproportionate growth delay in these fetuses. Neurotransmitter and histological
analysis revealed high level of dopamine and serotonin in COC fetal striatum, as
well as morphological alterations of liver.
CONCLUSION: Mid-pregnancy cocaine exposure induces fetal growth delay in utero,
especially disproportionate brain developmental retardation. Maternal
undernutrition does not play a key role in fetal developmental retardation when
exposed to cocaine in utero.
Keywords:
embryo-fetus.
METHODS: A transplacental murine model of cocaine exposure on embryo-fetus mice
was established, in which pregnant dams of comparable weight were assigned into
three groups: cocaine with food ad lib (COC), saline and pair-fed with COC (SPF),
and saline with food ad lib (SAL). From embryonic d 8 (E8) to E17, physiological
variables of dams and offspring were recorded and concentrations of dopamine and
serotonin in fetal striatum were examined.
RESULTS: Compared with SAL dams, COC and SPF dams showed lower weight gain. But
only COC fetuses demonstrated low brain weight and low striatum weight on E17, as
well as small biparietal diameter (BPD) on postnatal d1 (P1). Surprisingly, low
brain/body weight ratio was seen in COC offspring, which might reflect
disproportionate growth delay in these fetuses. Neurotransmitter and histological
analysis revealed high level of dopamine and serotonin in COC fetal striatum, as
well as morphological alterations of liver.
CONCLUSION: Mid-pregnancy cocaine exposure induces fetal growth delay in utero,
especially disproportionate brain developmental retardation. Maternal
undernutrition does not play a key role in fetal developmental retardation when
exposed to cocaine in utero.