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Prenatal restraint stress: an in vivo microdialysis study on catecholamine release in the rat prefrontal cortex
E Carboni1, V G Barros, M Ibba
1Department of Toxicology, University of Cagliari and CNR Institute of Neuroscience, Via Ospedale 72, 09124 Cagliari, Italy. ecarboni@unica.it
Insights
Prenatal stress in rats alters prefrontal cortex catecholamine transmission, impacting neurotransmitter levels. This may contribute to psychiatric disorders and increase vulnerability to drug addiction.
Area of Science:
- Neuroscience
- Psychiatry
- Environmental Health
Background:
- Prenatal exposure to adverse conditions is linked to psychiatric disorders and drug addiction.
- Altered catecholamine transmission in the prefrontal cortex is implicated in psychiatric disorders.
Purpose of the Study:
- To investigate the effects of prenatal stress on catecholamine transmission in the medial prefrontal cortex.
- To determine if prenatal stress influences dopamine and noradrenaline levels in adolescent and adult offspring.
Main Methods:
- Microdialysis was used to measure basal and stimulated dopamine and noradrenaline extracellular concentrations.
- Offspring were exposed to restraint stress during the last week of pregnancy.
- Stimulation was achieved using amphetamine or nicotine.
Main Results:
- Prenatal stress decreased basal noradrenaline output but did not alter basal dopamine output.
- Prenatal stress reduced amphetamine-stimulated dopamine output and increased amphetamine-stimulated noradrenaline output.
- Nicotine-stimulated noradrenaline output was decreased in adult offspring exposed to prenatal stress.
Conclusions:
- Prenatal stress significantly modifies prefrontal cortex catecholamine transmission in an age-dependent manner.
- These neurochemical alterations may underlie the increased risk for psychiatric disorders and drug addiction vulnerability.
- The findings highlight the long-term impact of prenatal environmental factors on brain development and behavior.
Abstract:
There is substantial evidence that prenatal exposure to adverse environmental conditions might lead to the psychiatric disorders that can appear in adolescence or in adulthood; vulnerability to drug addiction may increase as well. It is currently accepted that the alteration of catecholamine transmission in the prefrontal cortex plays a prominent role in the etiology of psychiatric disorders. We assessed basal and stimulated dopamine and noradrenaline extracellular concentration in the medial prefrontal cortex by means of microdialysis in awake male adolescent and young adult offspring of rats exposed to restraint stress in the last week of pregnancy. Catecholamine stimulation was obtained by amphetamine or nicotine. We observed that prenatal stress (PNS) did not change dopamine but decreased noradrenaline basal output in both adolescents and adults. Moreover, it decreased amphetamine stimulated dopamine output and increased amphetamine stimulated noradrenaline output. PNS decreased nicotine stimulated noradrenaline (but not dopamine output) in adults, though not in adolescents. These data show that PNS stress modifies prefrontal cortex catecholamine transmission in a complex and age dependent manner. Our results support the view that prenatal stress may be a contributing factor for the development of psychiatric disorders and that its effect may augment drug addiction vulnerability.
