TY - JOUR
T1 - Expression analysis of P/Q-type Ca2+ channel α1A subunit mRNA in olfactory mitral cell in N-type Ca 2+ channel α1B subunit gene-deficient mice
AU - Takahashi, Eiki
AU - Ino, Mitsuhiro
AU - Miyamoto, Norimasa
AU - Nagasu, Takeshi
PY - 2004/4/8
Y1 - 2004/4/8
N2 - N-type and P/Q-type Ca2+ channels play an important role in the processing of olfactory information. However, N-type Ca2+ channel α1B-deficient mice show normal behavior, presumably owing to compensation by other Ca2+ channels. P/Q-type Ca2+ channel α1A mRNA was expressed at a higher level in olfactory bulb of homozygous α1B-deficient mice than wild-type or heterozygous mice. LacZ expression in olfactory mitral cells of homozygous α1B-deficient x α1A1.5-lacZ mice, carrying a 1.5-kb 5′-upstream fragment of the α1A 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 α1B-deficient mice is compensation by the α1A gene and that the 1.5-kb 5′-upstream region of this gene contains an enhancer cis-element for compensation in olfactory mitral cells.
AB - N-type and P/Q-type Ca2+ channels play an important role in the processing of olfactory information. However, N-type Ca2+ channel α1B-deficient mice show normal behavior, presumably owing to compensation by other Ca2+ channels. P/Q-type Ca2+ channel α1A mRNA was expressed at a higher level in olfactory bulb of homozygous α1B-deficient mice than wild-type or heterozygous mice. LacZ expression in olfactory mitral cells of homozygous α1B-deficient x α1A1.5-lacZ mice, carrying a 1.5-kb 5′-upstream fragment of the α1A 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 α1B-deficient mice is compensation by the α1A gene and that the 1.5-kb 5′-upstream region of this gene contains an enhancer cis-element for compensation in olfactory mitral cells.
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U2 - 10.1016/j.neulet.2004.01.066
DO - 10.1016/j.neulet.2004.01.066
M3 - Article
C2 - 15050706
AN - SCOPUS:1842608903
SN - 0304-3940
VL - 359
SP - 37
EP - 40
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1-2
ER -