Fragile X syndrome (FXS) and diabetic retinopathy are poorly treated conditions that dramatically affect patient's and family members' life style. FXS is the most common known form of inherited mental retardation. FXS is caused by a genetic mutation leading to decreased fragile X mental retardation protein (FMRP) production. The absence of FMRP leads to alterations in synaptic plasticity, which are dependent on activation of metabotropic glutamate receptor (mGluR) activation. In this study, short term activation of group I and II mGluRs is not altered between an animal model of FXS, Fmr1 knock out mice and wild-type mice. These negative findings suggest that short-lasting actions of mGluR activation in the neocortex may not contribute to the cognitive or sensory processing alterations associated with FXS. Diabetic retinopathy is a common complication of diabetes and is the leading cause for blindness in US working age adults. In this experiment, intraocular injection of the proinflammatory cytokine, interleukin 1-β, was used to mimic inflammation similar to that which occurs during diabetic retinopathy. We used electrophysiological recording techniques to determine the impact of this manipulation on the excitability of thalamocortical neurons in the dorsal lateral geniculate nucleus. We found alterations in excitability, which could lead to altered visual processing as identified in diabetic retinopathy.
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