| First Author | Wan K | Year | 1999 |
| Journal | Biochem Biophys Res Commun | Volume | 266 |
| Issue | 2 | Pages | 588-92 |
| PubMed ID | 10600547 | Mgi Jnum | J:59072 |
| Mgi Id | MGI:1350866 | Doi | 10.1006/bbrc.1999.1871 |
| Citation | Wan K, et al. (1999) Involvement of ryanodine receptor type 3 in dopamine release from the striatum: evidence from mutant mice lacking this receptor. Biochem Biophys Res Commun 266(2):588-92 |
| abstractText | Although it is known that ryanodine receptor type 3 is expressed in the striatum, the function of this receptor has not been elucidated. Therefore, we examined whether caffeine- and ryanodine-induced dopamine release in striatal slices is affected in mice lacking ryanodine receptor type 3. Pretreatment with thapsigargin, an inhibitor of the Ca(2+) ATPase pump of the endoplasmic reticulum, abolished caffeine- or ryanodine-induced dopamine release in slices from normal mice. Dopamine concentration in the striatum and KCl-induced dopamine release were unaffected by a ryanodine receptor type 3 deficiency. Ryanodine-induced dopamine release was significantly attenuated in mice lacking ryanodine receptor type 3, whereas caffeine-induced dopamine release was partially attenuated. Caffeine produced a similar hyper-motor activity in both wild and homozygous mice. The present results suggest the involvement of ryanodine receptor type 3 in dopamine release from the striatum. Copyright 1999 Academic Press. |
