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As of 2006 (the latest
data available), 25 percent of pregnant women entering drug treatment reported
methamphetamine as her primary drug of abuse. This is compared with 8 percent
in 1994. Given the steady upward trend use may be even higher today.
These data underestimate
the prevalence of this problem for several reasons: the majority of drug users
do not enter treatment, and methamphetamine has become more widely available since
2006. Yet little is known about how methamphetamine affects brain development.
The lab investigates how methamphetamine
affects brain development, finding that it results in enduring learning and
memory impairments. We also investigate
what treatments might be developed to ameliorate such deficits.
To do this we expose
laboratory rats to methamphetamine during selected stages of brain
development. During exposure, methamphetamine
causes ACTH release from the anterior pituitary and corticosterone release from
the adrenals, and reductions in brain 5-HT. After exposure ends, methamphetamine
results in long-term dopamine reductions, alters dopamine D1 receptor function and changes dopamine utilization.
More recently we found
evidence that developmental methamphetamine exposure causes changes to dopamine
D1, D2, and NMDA receptors. We are currently testing several hypotheses
about the mechanisms of methamphetamine’s effects on brain development,
including whether the drug induces reactive oxygen species (ROS) that may
damage neuronal membranes, or cause overstimulation of dopamine receptors. We are measuring markers of ROS during and
shortly after drug exposure and whether ROS scavenging drugs (spin-trapping
agents) can block the adverse effects of early methamphetamine exposure.
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