Lesion-induced synaptic plasticity in the somatosensory cortex of prenatally stressed rats

Prenatal stress exposure causes long-lasting impairments of the behavioral and neuroendocrine responses to later stressors of the offspring. Although mechanisms underlying these effects remain largely unknown, abnormalities in the neuronal plasticity might be responsible for neurobiological alterations. This study used the whisker-to-barrel pathway as a model system to investigate the effects of prenatal stress on lesion-induced plasticity of neurons. Pregnant rats were subjected to immobilization stress during the trigeminal neurogenesis period, corresponding to gestational days 12 to 17, for three hours a day. After birth, the middle row (C) whisker follicles of pups from the control and stressed groups were electrocauterized. Ten days later, tangentially sectioned cortical hemispheres were stained with cytochrome oxidase histochemistry to calculate the volumes of each barrel row (A-E) in both lesioned and intact sides of the cortex, using stereological methods. The adrenal to body weight ratios were significantly increased in stressed animals, when compared to the controls. The pattern and total volume of the barrel subfield remained unaltered, but the lesion-induced map plasticity index, calculated as the D/C ratio, decreased in stressed animals. In addition, the BDNF (Brain Derived Neurotrophic Factor), NT-3 (neurotrophin-3) and the cyclic AMP response element binding protein (CREB) phosphorylation levels in tissue homogenates of the barrel cortices were measured using the ELISA method. In prenatally stressed animals, the BDNF and NT-3 levels were reduced on the lesioned side, but significant CREB activation was observed on the intact side of the barrel cortex. Taken together, the results show that prenatal stress exposure negatively affects critical period plasticity by reducing the expansion of active barrels following peripheral whisker lesion. These changes arise independent of CREB phosphorylation and appear to be mediated by reduced levels of neurotrophins.