Maternal immune activation increases the corticosterone response to acute stress without affecting the hypothalamic monoamine content and sleep patterns in male mice offspring.
OBJECTIVE
Early life experiences are homeostatic determinants for adult organisms. We evaluated the impact of prenatal immune activation during late gestation on the neuroimmune-endocrine function of adult offspring and its interaction with acute stress.


METHODS
Pregnant Swiss mice received saline or lipopolysaccharide (LPS) on gestational day 17. Adult male offspring were assigned to the control or restraint stress condition. We analyzed plasmatic corticosterone and catecholamine levels, the monoamine content in the hypothalamus, striatum and frontal cortex, and the sleep-wake cycle before and after acute restraint stress.


CONCLUSIONS
Offspring from LPS-treated dams had increased baseline norepinephrine levels and potentiated corticosterone secretion after the acute stressor, and no effect was observed on hypothalamic monoamine content or sleep behavior. The offspring of immune-activated dams exhibited impairments in stress-induced serotonergic and dopaminergic alterations in the striatum and frontal cortex. The data demonstrate a distinction between the plasmatic levels of corticosterone in response to acute stress and the hypothalamic monoamine content and sleep patterns. We provide new evidence regarding the influence of immune activation during late gestation on the neuroendocrine homeostasis of offspring.
Neuroimmunomodulation Research Group, Departamento de Patologia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo (FMVZ-USP), São Paulo (UNIFESP), Brazil.
Adriano
A
Zager
Monica L
ML
Andersen
Sergio
S
Tufik
João
J
Palermo-Neto
D000704:Analysis of Variance; D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood*; D004576:Electromyography; D005260:Female; D007031:Hypothalamus / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D051379:Mice; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000503:physiopathology*; D012727:Sex Characteristics; D012890:Sleep / Q000502:physiology*; D013315:Stress, Psychological / Q000097:blood / Q000150:complications / Q000473:pathology
D015306:Biogenic Monoamines; D008070:Lipopolysaccharides; D003345:Corticosterone