Prenatal protein deficiency causes age-specific alteration in number and distribution of inhibitory neurons in the somatosensory cortex during early postnatal development.

Abstract

Prenatal protein deficiency causes behavioral and cognitive dysfunctions in children. The deficits could be caused by altered acquisition and processing of sensory information in the brain. Although GABAergic neurons are the key regulators of neuronal activity, the effect of prenatal protein deficiency on GABA neurons in the brain is largely unknown. We fed pregnant mice diets with one-third (7%) or half (10%) the normal protein requirement (20% protein). After birth, the pups were fostered with normally fed lactating females. We used transgenic mice to show that protein deficiency in pregnant dams fed a 7% protein diet affected the number and distribution of GABA neurons in the somatosensory barrel cortex and individual cortical layers during early postnatal development of pups. If the mothers were fed a 10% protein diet, the effects on GABA neurons were much less. Development of barrels was also affected in pups born to mothers fed the 7% protein diet, but not the 10% group. In addition, high protein deficiency, i.e., the 7% protein diet, affected conception, hampered gestational weight gain, induced resorption of embryos, reduced litter sizes, and increased cannibalism, which was not observed in females on 10% protein diet.