Mice hemizygous for the S-SCAM allele are viable and fertile. Expression of myc-tagged Magi2 is regulated by a calcium/calmodulin-dependent protein kinase II alpha (CaMKII&alpha;) promoter, which leads to overexpression of Magi2 (Synaptic Scaffolding Molecule; S-SCAM) in the excitatory neurons of the forebrain from postnatal stages to the adult stage. S-SCAM encodes a postsynaptic scaffolding protein involved in the synaptic protein organization and maintenance of synaptic AMPA receptor levels. Mutations and duplications (rare copy number variations (CNVs)) of S-SCAM have been associated with the pathogenesis of the psychiatric disorder Schizophrenia (SZ). 

S-SCAM mice express myc-S-SCAM specifically in the forebrain, no expression is seen in the cerebellum. These Tg mice show a 1.5-fold increase in the expression of S-SCAM protein. They exhibit morphological features and sex-dependent selective behavioral deficits, similar to those seen in individuals with SZ. S-SCAM Tg mice have an increased size of lateral ventricles and a reduced number of parvalbumin-stained neurons. They show enhanced excitatory synaptic transmission and elevated synaptic strength, which is detrimental to the induction of normal synaptic plasticity in males. As such, male S-SCAM Tg mice showed significantly impaired long term potential (LTP) hyperglutamatergic function due to a partial saturation of synaptic AMPA receptors. Mice exhibit hyperlocomotor activity, deficits in prepulse inhibition, increased anxiety, impaired social interaction, and working memory deficit.

S-SCAM transgenic mice may be useful for studying the morphological features and sex-dependent behavioral defects associated with Schizophrenia.

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