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Updated: Sep 8, 2025
Moderate Prenatal Alcohol Exposure and Quantification of Social Behavior in Adult Rats
Published on: December 14, 2014
Effects of prenatal methamphetamine exposure on spatial cognition and hippocampal synaptic plasticity in adolescent
Razieh Aghazadeh1, Shiva Roshan-Milani1,2, Leila Derafshpour2
1Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Insights
Prenatal methamphetamine exposure (PME) impairs learning and memory in adolescent rats. Early adolescent rats showed greater cognitive deficits, with impaired hippocampal synaptic plasticity contributing to these effects.
Area of Science:
- Neuroscience
- Developmental Psychology
- Toxicology
Background:
- Methamphetamine abuse during pregnancy poses risks to children.
- Prenatal methamphetamine exposure (PME) effects on adolescent behavior and neurobiology are understudied.
- Research on sex- and dose-dependent PME effects and mechanisms is limited.
Purpose of the Study:
- To investigate the cognitive and synaptic plasticity effects of PME in adolescent male and female rats.
- To examine dose- and age-dependent impacts of PME.
- To explore the role of hippocampal synaptic plasticity in PME-induced cognitive deficits.
Main Methods:
- Pregnant rats received low or high doses of methamphetamine (MA) orally.
- Offspring were assessed for cognitive function using the Morris water maze (MWM) at early (PND 21) and mid-adolescence (PND 33).
- Hippocampal long-term potentiation (LTP) in the Schaffer collateral-CA1 pathway was measured in vitro.
Main Results:
- PME significantly impaired learning and memory in both male and female rat offspring.
- Early adolescent rats (PND 21) exhibited more severe cognitive impairments than mid-adolescent rats (PND 33).
- PME depressed hippocampal LTP in most exposed groups, suggesting impaired synaptic plasticity.
Conclusions:
- PME negatively impacts cognitive performance in prepubertal rats.
- Impaired hippocampal synaptic function is a likely contributor to PME-induced cognitive deficits.
- No sex-dependent differences were observed in PME's effects on cognition or synaptic plasticity.
Abstract:
Global rise in methamphetamine (MA) abuse during pregnancy has placed a large number of children at risk for the adverse consequences of prenatal methamphetamine exposure (PME). While behavioral and neurocognitive deficits of PME have been extensively studied in humans and adult rodents, far less is known regarding the sex- and dose-dependent effects of PME as well as the underlying mechanisms. Adolescence in nonhuman primates is also a less explored territory. In the present study, PME was inducted by oral treatment to pregnant rats on gestational days 15-19 with either low dose (0.1 mg/ml) or high dose (0.6 mg/ml) of MA. The cognitive effects of PME were then evaluated in two adolescence age-intervals: early adolescent (started on postnatal day [PND] 21) and mid-adolescent (started on PND 33), among male and female rat offspring using Morris water maze (MWM) test. Alterations in hippocampal synaptic plasticity in Schaffer collaterals-CA1 pathway were also measured in vitro. Results of behavioral test showed that PME led to serious deficits of learning and memory abilities in both male and female rat offspring. PME also depressed LTP in most of the PME subgroups. Moreover, 21-day-old rats were more sensitive to PME-induced cognitive impairment in MWM tasks, but not in hippocampal synaptic plasticity, than 33-day-old rats. No sex-dependent effects of PME were found on the cognitive function and synaptic plasticity. These findings confirmed that PME impacted negatively on cognitive performance in prepubertal male and female rats, and the impairment of hippocampal synaptic functions might partly play a significant role in these effects.
