Effects of maternal LPS and developmental exposure to an environmentally relevant phthalate mixture on neuron number in the rat medial prefrontal cortex.

The brain is especially vulnerable to environmental influences during the perinatal period. While the effects of environmental factors are usually studied in isolation, it is more typical to be exposed to multiple influences during early development, necessitating study of synergistic actions on the developing brain. Both maternal infection and endocrine disrupting phthalates can decrease cell number in the medial prefrontal cortex (mPFC), a region critical for executive functioning.

Timing of methamphetamine exposure during adolescence differentially influences parvalbumin and perineuronal net immunoreactivity in the medial prefrontal cortex of female, but not male, rats.

Adolescence involves significant reorganization within the medial prefrontal cortex (mPFC), including modifications to inhibitory neurotransmission mediated through parvalbumin (PV) interneurons and their surrounding perineuronal nets (PNNs). These developmental changes, which result in increased PV neuron activity in adulthood, may be disrupted by drug use resulting in lasting changes in mPFC function and behavior. Methamphetamine (METH), which is a readily available drug used by some adolescents, increases PV neuron activity and could influence the activity-dependent maturational process of these neurons.

The last stage of development: The restructuring and plasticity of the cortex during adolescence especially at puberty.

There is considerable evidence of reorganization in the prefrontal cortex during adolescence in humans, as well as in rodents, where the cellular basis can be explored. Studies from my laboratory in the rat medial prefrontal cortex are reviewed here. In general, growth predominates before puberty.

Region- and age-specific effects of perinatal phthalate exposure on developmental cell death and adult anatomy of dorsal and ventral hippocampus and associated cognitive behaviors.

Humans are exposed to phthalates, a class of endocrine-disrupting chemicals used in food packaging/processing, PVC plastics, and personal care products. Gestational exposure may lead to adverse neurodevelopmental outcomes. In a rat model, perinatal exposure to an environmentally relevant mixture and dose of phthalates leads to increased developmental apoptosis in the medial prefrontal cortex (mPFC) and a subsequent reduction in neurons and in cognitive flexibility measured in adults of both sexes (Sellinger et al.