Prenatal lipopolysaccharide increases maternal behavior, decreases maternal odor preference, and induces lipopolysaccharide hyporesponsiveness.

Abstract

The present study investigated whether late maternal inflammation disrupts the mother/pup interaction, resulting in longlasting effects on pup behavior and alterations in biological pathways, thereby programming prepubertal behavior and the pups' inflammatory responses after bacterial endotoxin treatment. Female rats received 100 μg/kg lipopolysaccharide (LPS) or .9% saline solution on gestation day 18. Reproductive performance was observed at birth. On lactation days (LD) 5 and LD 6, respectively, maternal behavior and maternal aggressive behavior were assessed. In pups, maternal odor preference on LD 7, open field behavior on LD 21, and serum tumor necrosis factor α (TNF-α) levels after LPS challenge on LD 21 were investigated. The results showed that prenatal LPS exposure improved maternal care and reduced maternal aggressive behavior but did not alter maternal reproductive performance. Male offspring exhibited increased body weights at birth and reduced maternal odor preference. Lipopolysaccharide challenge increased the duration of immobility in the open field and induced a slight increase in serum TNF-α levels. Prenatal exposure to LPS during late pregnancy improved maternal care, reduced maternal olfactory preference, and induced TNF-α hyporesponsiveness to a single dose of LPS in pups.

Prenatal lipopolysaccharide disrupts maternal behavior, reduces nest odor preference in pups, and induces anxiety: Studies of F1 and F2 generations

“…In the present study, a reduced pup-mother interaction was observed in the F2 generation in rats whose F1 generation was prenatally exposed to LPS, showing a transgenerational effect of LPS. Interestingly, we previously found that prenatal LPS exposure on GD18 also reduced nest odor preference, suggesting a reduction of maternal recognition in the F1 generation (Penteado et al, 2013). Thus, epigenetic inheritance could explain this transgenerational transmission.…”

“…We previously found that maternal exposure to LPS in late pregnancy (GD18) improved maternal care but reduced nest odor preference in pups of the F1 generation, suggesting a decreased in maternal-pups interaction (Penteado et al, 2013).…”

“…Viral and bacterial infections, including those caused by prenatal LPS exposure, induce short-and long-term changes in behavior and central nervous system activity Boksa, 2010;Golan et al, 2005;Kirsten et al, 2012Kirsten et al, , 2010aKirsten et al, , 2010bMeyer et al, 2009;Penteado et al, 2013;Soto et al, 2013). Previous investigations by our group showed that prenatal LPS exposure (100 μg/kg, intraperitoneally, on gestational day [GD] 9.5) reduced social behavior in F1 males in both infancy and adulthood and decreased striatal dopamine (DA) and DA metabolite levels in the absence of signs that indicate neuroinflammation (Kirsten et al, 2010b).…”

Lipopolysaccharide-Induced Sickness Behavior in Lactating Rats Decreases Ultrasonic Vocalizations and Exacerbates Immune System Activity in Male Offspring

“…These findings are in agreement with Bussière et al [57] who observed in experimental Mg-deficient rats an increase in activity of phagocytosis and an oxidative burst of neutrophils. Interestingly, we previously observed that prenatal exposure to LPS during late pregnancy decreased TNF-α levels of pups challenged with the same endotoxin [26]. …”

“…Late maternal inflammation disrupts mother/pup interactions, resulting in long-lasting effects on pup behavior and alterations in biological pathways, thereby programming prepubertal behavior and the pups' inflammatory responses after bacterial endotoxin treatment [26]. Single early prenatal LPS exposure also impairs striatal monoamines and maternal care in female rats [27].…”