GRIN2A and schizophrenia: DTNBP1 null mutant mice, which do not express dysbindin protein, display cellular and functional abnormalities in the brain of relevance to schizophrenia, such as decreased GRIN1 mRNA expression [83], increased surface GluN2A protein expression [84], altered prepulse inhibition [85, 86], decreased hippocampal long-term potentiation [84, 87], and impaired working memory [83, 85].