Prenatal restraint stress: an in vivo microdialysis study on catecholamine release in the rat prefrontal cortex

• Published in: Neuroscience 2010-06, Vol.168 (1), p.156-166
• Main Authors: Carboni, E, Barros, V.G, Ibba, M, Silvagni, A, Mura, C, Antonelli, M.C
• Format: Article
• Language: English
• Subjects: Adolescence; Age Factors; Amphetamine - pharmacology; Animals; Biological and medical sciences; Catecholamines - metabolism; Central Nervous System Stimulants - pharmacology; Dopamine - metabolism; Extracellular Space - metabolism; Female; Fundamental and applied biological sciences. Psychology; Male; Medical sciences; Neurology; Neuropharmacology; Nicotine - pharmacology; Norepinephrine - metabolism; Pharmacology. Drug treatments; Prefrontal Cortex - drug effects; Prefrontal Cortex - metabolism; Pregnancy; Prenatal Exposure Delayed Effects - etiology; Prenatal Exposure Delayed Effects - metabolism; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease); Psychology. Psychoanalysis. Psychiatry; Psychopharmacology; Rats; Rats, Wistar; Restraint, Physical; Stress, Psychological - complications; Vertebrates: nervous system and sense organs
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2010.03.046

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.