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Auditory false perceptions are mediated by psychosis risk factors
TLDR
Younger participants seem most vulnerable to the effects of positive schizotypal traits in terms of a signal detection deficit that underlies auditory hallucinations, andSchizotypy may have greatest impact closer to the risk period for development of psychotic disorders.
Contribution of Hippocampal and Extra-Hippocampal NR2B-Containing NMDA Receptors to Performance on Spatial Learning Tasks
TLDR
Genetically modified mice in which the NR2B subunit is selectively ablated in principal neurons of the entire postnatal forebrain or only the hippocampus were impaired on a range of memory tasks, presenting both spatial and nonspatial phenotypes.
Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP
Wiseman et al. show that triplication of genes other than APP is sufficient to exacerbate Aβ deposition and associated cognitive changes in a mouse model of Down syndrome – Alzheimer’s disease. This
Aversive Prediction Error Signals in the Amygdala
TLDR
It is shown that aversive prediction signals are found in the hemodynamic responses and theta oscillations recorded from the basolateral amygdala and that amygdala activity conforms to temporal difference models of aversive learning.
Knockout of NMDA-receptors from parvalbumin interneurons sensitizes to schizophrenia-related deficits induced by MK-801
TLDR
It is shown here that Grin1ΔPV mice are not protected against the effects of MK-801, but are in fact sensitized to many of them, which argues against PV-specific NMDAR hypofunction as a key starting point of schizophrenia pathophysiology, but support a model where N MDAR hyp ofunction in multiple cell types contribute to the disease.
What causes aberrant salience in schizophrenia? A role for impaired short-term habituation and the GRIA1 (GluA1) AMPA receptor subunit
TLDR
The model supports the view that the dopaminergic abnormalities can be downstream of a glutamatergic aetiology and suggests that the real value of genetically modified mice is not as ‘models of schizophrenia’ but as experimental tools that can link genomic discoveries with psychological processes and help elucidate the underlying neural mechanisms.
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