Minocycline alleviates behavioral deficits and inhibits microglial activation in the offspring of pregnant mice after administration of polyriboinosinic–polyribocytidilic acid

Jul 22, 2014Psychiatry research

Minocycline reduces behavior problems and brain immune cell activation in offspring of pregnant mice exposed to a viral mimic

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Abstract

Pregnant mice treated with 20 mg/kg of Poly I:C showed behavioral changes in their offspring at postnatal day 42.

Maternal infection during pregnancy may increase the risk of schizophrenia in offspring.
Offspring exposed to Poly I:C exhibited hyperlocomotion, social interaction deficits, and prepulse inhibition impairments.
Microglial activation was significantly observed in the brains of offspring from the Poly I:C group.
Minocycline treatment in adult offspring reduced behavioral deficits and inhibited microglial activation.
These findings indicate a potential link between maternal infection and neurodevelopmental changes in offspring.

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Epidemiological studies have indicated that maternal infection during pregnancy may lead to a higher incidence of schizophrenia in the offspring. Activation of microglia is a key event in the reaction of the cerebral immune system to pathological changes. It can be hypothesized that microglia contribute to the neuropathology of schizophrenia. In this study, at embryonic day (ED) 9 pregnant mice were treated with intraperitoneal injection of polyriboinosinic-polyribocytidilic acid (Poly I:C) at a single dose of 20 mg/kg. At postnatal day 42, descendants were treated with minocycline (40 mg/kg) or saline for consecutive 14 days. Behavioral changes (locomotor activity, social interaction, and prepulse inhibition) were examined and the number of microglia was assessed after the treatment. The adult offspring exposed to Poly I:C at ED 9 showed behavioral changes (hyperlocomotion, deficits in social interaction and prepulse inhibition) and significant microglial activation in these brain areas (hippocampus, thalamus, and cerebral cortex) compared to those in saline-injected group. Moreover, minocycline attenuated the behavioral deficits and inhibited the activated microglia. These findings suggest that maternal infection may contribute to microglial activation in the offspring. In addition, the effect of minocycline in this immune model may be related to the inhibition of microglial activation.

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Minocycline alleviates behavioral deficits and inhibits microglial activation in the offspring of pregnant mice after administration of polyriboinosinic–polyribocytidilic acid

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