Homozygous neurogranin-deficient (Ng-/-) mice are viable and fertile (although the donating investigator reports that homozygous females do not nurse their pups as well as wildtype or heterozygous mothers). Homozygotes have no mRNA or protein from the targeted gene observed in brain tissues. Expression of lacZ is observed in a manner consistent with the endogenous gene. Ng-/- mice exhibit impaired spatial learning, altered hippocampal short- and long-term plasticity (including long-term potentiation induction), and decreased activated CaMKII. Heterozygotes show similar, yet milder, effects. These neurogranin- (Ng or RC3)-mutant mice may be useful for neurological studies involving memory and learning, neuronal signaling pathways (including calmodulin, alpha-CaMKII, protein kinase A, protein kinase C, MAPK, and CREB), attention deficit-hyperactivity disorder (ADHD), and schizophrenia.
