Abstract
Pregnant CD-1 mice were given 32 mg/kg of 3,4,3',4'-tetrachlorobiphenyl (TCB) or corn oil vehicle, by gavage, on days 10–16 of gestation. At 1 year of age, the offspring were tested for spontaneous motor activity; the mice were then killed and dopamine (DA) levels and specific DA receptor binding were measured in the corpus striatum. Mice exposed to TCB in utero had elevated levels of motor activity, which were associated with decreased DA levels and DA receptor binding sites. The results indicate that in utero exposure to TCB might permanently alter the development of striatal synapses.
Highlights
Mice exposed to TCB during gestation have been reported to exhibit a longlasting neurobehavioral syndrome consisting of stereotypic head movements, rotational behavior, increased motor activity, impaired neuromuscular strength and coordination, and learning deficits [1]
Possible alterations in dopaminergic function were suggested by the observation that haloperidol, a DA receptor antagonist, decreased the overall motor activity of mice exposed to TCB more than controls
That TCB might produce persistent alterations in DA receptor function correlated with a neurological syndrome consisting of hyperactivity prompted us to explore the long-term effect of TCB on the levels of DA and specific dopamine receptor binding in the corpus striatum, an area believed to be involved in the control of stereotypic motor movements
Summary
Mice exposed to TCB during gestation have been reported to exhibit a longlasting neurobehavioral syndrome consisting of stereotypic head movements, rotational behavior, increased motor activity, impaired neuromuscular strength and coordination, and learning deficits [1]. Exposed in utero to TCB; these observations suggest that TCB might have interfered with the synaptogenesis of dopaminergic systems. Possible alterations in dopaminergic function were suggested by the observation that haloperidol, a DA receptor antagonist, decreased the overall motor activity of mice exposed to TCB more than controls. That TCB might produce persistent alterations in DA receptor function correlated with a neurological syndrome consisting of hyperactivity prompted us to explore the long-term effect of TCB on the levels of DA and specific dopamine receptor binding in the corpus striatum, an area believed to be involved in the control of stereotypic motor movements. The present experiment extended this period of observation to 1 year postnatally in order to assess the irreversible nature of the neurological syndrome
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