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Malformations of neocortical development such as microgyria (MG) and periventricular nodular heterotopia (PNH) have been observed in the brains of language learning impaired (LLI) humans. Rats with MG have shown rapid auditory processing (RAP) deficits similar to acoustic deficits observed in some human LLI populations. Threlkeld et al., (2009) previously reported RAP and other learning impairments in rats with PNH resulting from disruption to embryonic neuronal cell division by way of Methylazoxymethanol (MAM) treatment on embryonic day 15 (E15). The thalamus and its subnuclei may be vulnerable to neurodevelopmental disruptions. Studies of MG rats have shown changes in cell size within the auditory thalamus, medial geniculate nucleus (MGN). Similar findings have also been observed in human dyslexic brains, providing further evidence that thalamic disruption may play a major role in behavioral pathology associated with neurodevelopmental disorders. In this study, a stereological assessment was performed on 11 MAM and 5 control brains of rats from a previous behavioral study showing RAP deficits in MAM treated subjects, specifically looking for effects of treatment on nuclear volume, and estimated cell number, area, and volume within the dorsal lateral geniculate nucleus (dLGN) and the MGN. Results showed no significant treatment effects on the MGN in any measure, although a trend was seen in nuclear volume. Significant treatment effects were seen, however, in the dLGN in all measures except for a trend found in cell area. This study further supports E15 MAM treatment in rats as a model for teratogen mediated pervasive developmental disorders. Future studies are suggested to examine the effects of E15 MAM exposure on dLGN dependent behaviors in rats and explore the relationship between pathological severity and general sensory processing deficits.