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The postsynaptic terminal of vertebrate excitatory synapses contains a highly conserved multiprotein complex that comprises neurotransmitter receptors, cell‐adhesion molecules, scaffold proteins and enzymes, which are essential for brain signalling and plasticity underlying behaviour. Increasingly, mutations in genes that encode postsynaptic proteins belonging to the PSD‐95 protein complex, continue to be identified in neurodevelopmental disorders (NDDs) such as autism spectrum disorder, intellectual disability and epilepsy. These disorders are highly heterogeneous, sharing genetic aetiology and comorbid cognitive and behavioural symptoms. Here, by using genetically engineered mice and innovative touchscreen‐based cognitive testing, we sought to investigate whether loss‐of‐function mutations in genes encoding key interactors of the PSD‐95 protein complex display shared phenotypes in associative learning, updating of learned associations and reaction times. Our genetic dissection of mice with loss‐of‐function mutations in Syngap1, Nlgn3, Dlgap1, Dlgap2 and Shank2 showed that distinct components of the PSD‐95 protein complex differentially regulate learning, cognitive flexibility and reaction times in cognitive processing. These data provide insights for understanding how human mutations in these genes lead to the manifestation of diverse and complex phenotypes in NDDs. [ABSTRACT FROM AUTHOR]

In this brief review, we will highlight the ferret Mustela putorius furo as an increasingly utilized animal model for sensory systems and cognitive neuroscience research. In particular, the human like hearing range of the ferret, coupled with their amenability to training, make them an especially useful model for auditory and multisensory neuroscience. These factors, combined with the increasing availability of virally mediated circuit dissection methods, mean they occupy a unique niche as a versatile and valuable research model., Competing Interests: Declaration of competing interest We have nothing to declare., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)