Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

被引:18
作者
Anderson, NJ
Seif, I
Nutt, DJ
Hudson, AL
Robinson, ESJ
机构
[1] Univ Bristol, Sch Med Sci, Dept Pharmacol, Bristol BS8 1TD, Avon, England
[2] Univ Paris Sud, Fac Pharm, Orsay, France
[3] Univ Bristol, Henry Wellcome LINE, Psychopharmacol Unit, Bristol, Avon, England
关键词
brain; imidazoline-binding sites; kidney; knockout mice; monoamine oxidase; receptor autoradiography;
D O I
10.1111/j.1471-4159.2006.03662.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
This study has used receptor autoradiography to characterize imidazoline binding sites (I-BS) in monoamine oxidase (MAO) A knockout and wild-type mice. A comparison between MAO-A and MAO-B, binding of the endogenous beta-carboline [H-3]harmane, and I-BS, has been made using sections from brain and kidney. The loss of binding to MAO-A in the knockout animals was confirmed using the selective radioligand [H-3]Ro41-1049, with labelling reduced to background levels. The binding of [H-3]Ro19-6327 to MAO-B was unaffected, indicating no change in this isoform in response to the loss of MAO-A. A reduction in binding to the I-2-BS, as labelled by both [H-3]idazoxan and [H-3]2-BFI (2-(2-benzofuranyl)-2-imidazoline), was seen in the MAO-A knockout animals in both brain and kidney sections, whereas binding to the I-1-BS in kidney sections remained unchanged. The loss of I-2 binding was found to be regionally dependent and was positively correlated with the relative expression of MAO-A in specific regions in the wild-type animals. Using the MAO-A knockout mice it was also possible to demonstrate a non-MAO-A population of binding sites labelled by the putative I-BS endogenous ligand, harmane.(2)
引用
收藏
页码:1551 / 1559
页数:9
相关论文
共 47 条
[1]
Characterization of [3H]harmane binding to rat whole brain membranes [J].
Anderson, NJ ;
Robinson, ESJ ;
Husbands, SM ;
Delagrange, P ;
Nutt, DJ ;
Hudson, AL .
AGMATINE AND IMIDAZOLINES: THEIR NOVEL RECEPTORS AND ENZYMES, 2003, 1009 :175-179
[2]
ANDERSON NJ, 2004, BR J PHARM BATH M
[3]
ANDERSON NJ, 2004, 457 SOC NEUR
[4]
ATLAS D, 1984, EUR J BIOCHEM, V144, P287, DOI 10.1111/j.1432-1033.1984.tb08462.x
[5]
I1 receptors, cardiovascular function, and metabolism [J].
Bousquet, P .
AMERICAN JOURNAL OF HYPERTENSION, 2001, 14 (11) :317S-321S
[6]
AGGRESSIVE-BEHAVIOR AND ALTERED AMOUNTS OF BRAIN-SEROTONIN AND NOREPINEPHRINE IN MICE LACKING MAOA [J].
CASES, O ;
SEIF, I ;
GRIMSBY, J ;
GASPAR, P ;
CHEN, K ;
POURNIN, S ;
MULLER, U ;
AGUET, M ;
BABINET, C ;
SHIH, JC ;
DEMAEYER, E .
SCIENCE, 1995, 268 (5218) :1763-1766
[7]
CESURA AM, 1990, MOL PHARMACOL, V37, P358
[8]
THE ALPHA-2-ADRENOCEPTOR ANTAGONIST EFAROXAN MODULATES K+ATP CHANNELS IN INSULIN-SECRETING CELLS [J].
CHAN, SLF ;
DUNNE, MJ ;
STILLINGS, MR ;
MORGAN, NG .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1991, 204 (01) :41-48
[9]
A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior [J].
Chen, K ;
Holschneider, DP ;
Wu, WH ;
Rebrin, I ;
Shih, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (38) :39645-39652
[10]
'Seeing through a glass darkly': casting light on imidazoline 'I' sites [J].
Eglen, RM ;
Hudson, AL ;
Kendall, DA ;
Nutt, DJ ;
Morgan, NG ;
Wilson, VG ;
Dillon, MP .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1998, 19 (09) :381-390