Abstract
The present study was aimed at evaluating cognitive changes following neonatal methamphetamine exposure in combination with repeated treatment in adulthood of female Wistar rats. Pregnant dams and their pups were used in this study. One half of the offspring were treated indirectly via the breast milk of injected mothers, and the other half of pups were treated directly by methamphetamine injection. In the group with indirect exposure, mothers received methamphetamine (5 mg/ml/kg) or saline (1 ml/kg) between postnatal days (PD) 1–11. In the group with direct exposure, none of the mothers were treated. Instead, progeny were either: (1) treated with injected methamphetamine (5 mg/ml/kg); or (2) served as controls and received sham injections (no saline, just a needle stick) on PD 1–11. Learning ability and memory consolidation were tested on PD 70–90 in the Morris Water Maze (MWM) using three tests: Place Navigation Test, Probe Test, and Memory Recall Test. Adult female progeny were injected daily, after completion of the last trial of MWM tests, with saline or methamphetamine (1 mg/ml/kg). The effects of indirect/direct neonatal methamphetamine exposure combined with acute adult methamphetamine treatment on cognitive functions in female rats were compared. Statistical analyses showed that neonatal drug exposure worsened spatial learning and the ability to remember the position of a hidden platform. The study also demonstrated that direct methamphetamine exposure has a more significant impact on learning and memory than indirect exposure. The acute dose of the drug did not produce any changes in cognitive ability. Analyses of search strategies (thigmotaxis, scanning) used by females during the Place Navigation Test and Memory Recall Test confirmed all these results. Results from the present study suggested extensive deficits in learning skills and memory of female rats that may be linked to the negative impact of neonatal methamphetamine exposure.
Highlights
Molecular mechanisms underlying memory formation include many specific signaling pathways involving neurotransmitter release, calcium influx, and second messenger activation, transcription of genes, de novo protein synthesis, and histone modification of gene expression (Keiser and Tronson, 2016)
Our results suggested that the most serious impact of MA exposure was on hippocampaldependent spatial learning [Morris Water Maze (MWM)] was associated with neonatal administration
The aim of this study is to examine the potential interaction of neonatal MA exposure during postnatal days (PD) 1–11 and an acute dose of the same drug (1 mg/kg) in adulthood
Summary
Molecular mechanisms underlying memory formation include many specific signaling pathways involving neurotransmitter release, calcium influx, and second messenger activation, transcription of genes, de novo protein synthesis, and histone modification of gene expression (Keiser and Tronson, 2016). Each of these transduction pathways may be disrupted with methamphetamine (MA), a psychostimulant drug that primarily blocks dopaminergic and serotonergic systems (Sulzer et al, 2005). The study compared the effect of MA exposure during different stages of rat brain development (i.e., the first half of gestation, the second half of gestation, and early neonatal stage). Our results suggested that the most serious impact of MA exposure was on hippocampaldependent spatial learning [Morris Water Maze (MWM)] was associated with neonatal administration
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