| First Author | Ohgake S | Year | 2009 |
| Journal | Prog Neuropsychopharmacol Biol Psychiatry | Volume | 33 |
| Issue | 3 | Pages | 541-6 |
| PubMed ID | 19217924 | Mgi Jnum | J:151029 |
| Mgi Id | MGI:4352624 | Doi | 10.1016/j.pnpbp.2009.02.005 |
| Citation | Ohgake S, et al. (2009) Dopaminergic hypofunctions and prepulse inhibition deficits in mice lacking midkine. Prog Neuropsychopharmacol Biol Psychiatry 33(3):541-6 |
| abstractText | Midkine is a 13-kDa retinoic acid-induced heparin-binding growth factor involved in various biological phenomena such as cell migration, neurogenesis, and tissue repair. We previously demonstrated that midkine-deficient (Mdk(-/-)) mice exhibited a delayed hippocampal development with impaired working memory and increased anxiety only at the age of 4 weeks. To assess whether midkine gene could play important roles in development and maintenance of central nervous system, we investigated biochemical and behavioral parameters in dopamine and glutamate neurotransmission of Mdk(-/-) mice. The Mdk(-/-) mice exhibited a hypodopaminergic state (i.e., decreased levels of dopamine and its receptors in the striatum) with no alterations of glutamatergic system (i.e., normal level of glutamate, glutamine, glycine, d-serine, l-serine, and NMDA receptors in the frontal cortex and hippocampus). We also found prepulse inhibition deficits reversed by clozapine and haloperidol in the Mdk(-/-) mice. Our results suggested that midkine deficiency may be related to neurochemical and behavioral dysfunctions in dopaminergic system. |
