Utility of the Hebb-Williams Maze Paradigm for Translational Research in Fragile X Syndrome: A Direct Comparison of Mice and Humans.

To generate meaningful information, translational research must employ paradigms that allow extrapolation from animal models to humans. However, few studies have evaluated translational paradigms on the basis of defined validation criteria. We outline three criteria for validating translational paradigms.

Visual-spatial learning impairments are associated with hippocampal PSD-95 protein dysregulation in a mouse model of fragile X syndrome.

Fragile X syndrome is the most common cause of inherited intellectual disability and is caused by the lack of fragile X mental retardation protein (FMRP) expression. In-vitro findings in mice and post-mortem autopsies in humans are characterized by dendritic spine abnormalities in the absence of Fmrp/FMRP. Biochemical and electrophysiological studies have identified postsynaptic density protein (PSD)-95 as having an established role in dendritic morphology as well as a molecular target of Fmrp.

Comparison of nafadotride, CNQX, and haloperidol on acquisition versus expression of amphetamine-conditioned place preference in rats.

Neurotransmission at dopamine (DA) and glutamate synapses has been implicated in conditioning place preference (CPP) in rats, but different receptor subtypes may be differentially involved in acquisition and expression. A balanced CPP was used to study the role of DA D2 and D3 and glutamatergic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors in acquisition and expression of amphetamine (2.0 mg/kg) CPP.