A novel approach to the assessment of higher-order rule learning in male mice.

Historically, the development of valid and reliable methods for assessing higher-order cognitive abilities (e.g., rule learning and transfer) has been difficult in rodent models.

Rapid auditory processing and medial geniculate nucleus anomalies in Kiaa0319 knockout mice.

Developmental dyslexia is a common neurodevelopmental disorder characterized by difficulties in reading and writing. Although underlying biological and genetic mechanisms remain unclear, anomalies in phonological processing and auditory processing have been associated with dyslexia. Several candidate risk genes have also been identified, with KIAA0319 as a main candidate.

Peripheral Anomalies in USH2A Cause Central Auditory Anomalies in a Mouse Model of Usher Syndrome and CAPD.

Central auditory processing disorder (CAPD) is associated with difficulties hearing and processing acoustic information, as well as subsequent impacts on the development of higher-order cognitive processes (i.e., attention and language).

Communication-related assessments in an Angelman syndrome mouse model.

Introduction: Angelman syndrome (AS) is a neurodevelopmental disorder characterized by motor deficits, seizures, some autistic-like behaviors, and severe impairment of speech. A dysfunction of the maternally imprinted UBE3A gene, coupled with a functional yet silenced paternal copy, results in AS. Although studies of transgenic mouse models have revealed a great deal about neural populations and rescue timeframes for specific features of AS, these studies have largely failed to examine intermediate phenotypes that contribute to the profound communicative disabilities associated with AS.

Effort-related decision making in humanized COMT mice: Effects of ValMet polymorphisms and possible implications for negative symptoms in humans.

Catechol-o-methyltransferase (COMT) is an enzyme that metabolizes catecholamines, and is crucial for clearance of dopamine (DA) in prefrontal cortex. ValMet polymorphism, which causes a valine (Val) to methionine (Met) substitution at codon 158, is reported to be associated with human psychopathologies in some studies. The Val/Val variant of the enzyme results in higher dopamine metabolism, which results in reduced dopamine transmission.