Reduced dysbindin expression mediates N-methyl-D-aspartate receptor hypofunction and impaired working memory performance.
|Title||Reduced dysbindin expression mediates N-methyl-D-aspartate receptor hypofunction and impaired working memory performance.|
|Publication Type||Journal Article|
|Year of Publication||2011|
|Authors||Karlsgodt, KH, Robleto K, Trantham-Davidson H, Jairl C, Cannon TD, Lavin A, Jentsch DJ|
|Date Published||2011 Jan 1|
|Keywords||Animals, Carrier Proteins, Down-Regulation, Female, Male, Memory, Short-Term, Mice, Mice, Inbred C57BL, Mice, Knockout, Patch-Clamp Techniques, Prefrontal Cortex, Pyramidal Cells, Receptors, AMPA, Receptors, N-Methyl-D-Aspartate|
Schizophrenia is a heritable disorder associated with disrupted neural transmission and dysfunction of brain systems involved in higher cognition. The gene encoding dystrobrevin-binding-protein-1 (dysbindin) is a putative candidate gene associated with cognitive impairments, including memory deficits, in both schizophrenia patients and unaffected individuals. The underlying mechanism is thought to be based in changes in glutamatergic and dopaminergic function within the corticostriatal networks known to be critical for schizophrenia. This hypothesis derives support from studies of mice with a null mutation in the dysbindin gene that exhibit memory dysfunction and excitatory neurotransmission abnormalities in prefrontal and hippocampal networks. At a cellular level, dysbindin is thought to mediate presynaptic glutamatergic transmission.
|Alternate Journal||Biol. Psychiatry|