| First Author | Takahashi E | Year | 2004 |
| Journal | Neurosci Lett | Volume | 359 |
| Issue | 1-2 | Pages | 37-40 |
| PubMed ID | 15050706 | Mgi Jnum | J:121033 |
| Mgi Id | MGI:3709132 | Doi | 10.1016/j.neulet.2004.01.066 |
| Citation | Takahashi E, et al. (2004) Expression analysis of P/Q-type Ca2+ channel alpha 1A subunit mRNA in olfactory mitral cell in N-type Ca2+ channel alpha 1B subunit gene-deficient mice. Neurosci Lett 359(1-2):37-40 |
| abstractText | N-type and P/Q-type Ca2+ channels play an important role in the processing of olfactory information. However, N-type Ca2+ channel alpha1B-deficient mice show normal behavior, presumably owing to compensation by other Ca2+ channels. P/Q-type Ca2+ channel alpha1A mRNA was expressed at a higher level in olfactory bulb of homozygous alpha1B-deficient mice than wild-type or heterozygous mice. LacZ expression in olfactory mitral cells of homozygous alpha1B-deficient x alpha1A1.5-lacZ mice, carrying a 1.5-kb 5'-upstream fragment of the alpha1A gene fused to the lacZ reporter gene, was increased compared to that in wild-type or heterozygous mice. Therefore, a possible explanation for the normal behavior of alpha1B-deficient mice is compensation by the alpha1A gene and that the 1.5-kb 5'-upstream region of this gene contains an enhancer cis-element for compensation in olfactory mitral cells. |
