Localization of distinct monoamine oxidase a and monoamine oxidase b cell populations in human brainstem

Westlund, Karin N.; Denney, Richard M.; Rose, Robert M.; Abell, Creed W.

doi:10.1016/0306-4522(88)90250-3

Cited by 339 publications

(151 citation statements)

References 44 publications

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“…45 As does the MAOA enzyme, MAOB also degrades monoamines, but with a different substrate preference: MAOB has higher affinity for DA, 46,47 phenylethylamine 48,49 and benzylamine, 50 whereas MAOA displays higher affinity for NA and 5-HT. Further, both enzymes are expressed in the central nervous system (CNS) but with different distributions: MAOB is preferentially expressed on serotonergic 51 and histaminergic 52 neurons, while MAOA is mainly expressed in noradrenergic neurons. 51,53 Both genes are expressed in glia.…”

Section: Discussionmentioning

confidence: 99%

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Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

et al. 2007

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Women who have experienced childhood sexual abuse (CSA) have an increased risk of alcoholism and antisocial personality disorder (ASPD). Among male subjects, a functional polymorphism (MAOA-LPR, monoamine oxidase A linked polymorphic region) in the promoter region of the monoamine oxidase A gene (MAOA) appears to moderate the effect of childhood maltreatment on antisocial behavior. Our aim was to test whether MAOA-LPR influences the impact of CSA on alcoholism and ASPD in a sample of 291 women, 50% of whom have experienced CSA; we also tested whether haplotypes covering the region where both MAOA and monoamine oxidase B (MAOB) genes are located predict risk of alcoholism and ASPD better than the MAOA-LPR locus alone. Participants included 168 alcoholics (39 with ASPD (antisocial alcoholics) and 123 controls (no alcoholics, no ASPD). Antisocial behavior was also modeled as a continuous trait: ASPD symptoms count. The MAOA-LPR low activity allele was associated with alcoholism (P = 0.005), particularly antisocial alcoholism (P = 0.00009), only among sexually abused subjects. Sexually abused women who were homozygous for the low activity allele had higher rates of alcoholism and ASPD, and more ASPD symptoms, than abused women homozygous for the high activity allele. Heterozygous women displayed an intermediate risk pattern. In contrast, there was no relationship between alcoholism/antisocial behavior and MAOA-LPR genotype among non-abused women. The MAOA-LPR low activity allele was found on three different haplotypes. The most abundant MAOA haplotype containing the MAOA-LPR low activity allele was found in excess among alcoholics (P = 0.008) and antisocial alcoholics (P = 0.001). Finally, a MAOB haplotype, which we termed haplotype C, was significantly associated with alcoholism (P = 0.006), and to a lesser extent with antisocial alcoholism (P = 0.03). In conclusions, MAOA seems to moderate the impact of childhood trauma on adult psychopathology in female subjects in the same way as previously shown among male subjects. The MAOA-LPR low activity allele appears to confer increased vulnerability to the adverse psychosocial consequences of CSA. Haplotype-based analysis of the MAOA gene appeared to strengthen the association, as compared to the MAOA-LPR locus alone. A MAOB haplotype was associated with alcoholism independently from ASPD.

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Section: Discussionmentioning

confidence: 99%

“…51,53 Both genes are expressed in glia. 52 Since MAOB is a regulator of monoamine tone and is expressed in the brain, it is a logical candidate for susceptibility to neuropsychiatric diseases. Nevertheless, the role of MAOB in vulnerability to psychiatric disorders has been less investigated as compared to MAOA.…”

Section: Discussionmentioning

confidence: 99%

Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

et al. 2007

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“…MAO-A prefers serotonin, but the highest level of MAO-A expression has been found in noradrenergic neurons with low or moderate levels in dopamine or serotonin neurons, respectively. MAO-B prefers hydrophobic substrates such as phenylethylamine, but the expression of MAO-B is most abundant in serotonergic and histaminergic neurons (Westlund et al, 1985(Westlund et al, , 1988Arai et al, 1997;Abell and Kwan, 2001).…”

Section: Figurementioning

confidence: 99%

Effects of Ovarian Steroids and Raloxifene on Proteins that Synthesize, Transport, and Degrade Serotonin in the Raphe Region of Macaques

Smith

Henderson

Abell

et al. 2004

Neuropsychopharmacol

147

123

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In the monkey dorsal raphe, we reported that 1-month (mo) of estrogen replacement, with or without progesterone supplementation for 14 days, significantly increased tryptophan hydroxylase-1 (TPH-1) mRNA; decreased serotonin reuptake transporter (SERT) mRNA and decreased monoamine oxidase (MAO)-A mRNA, but had no effect on MAO-B mRNA. Here, we questioned what effect would 1 or 5 mo of ovarian hormones or the selective estrogen receptor modulator (SERM), raloxifene, have on TPH protein and phosphorylation, and on protein expression of SERT, MAO-A or MAO-B? Raloxifene antagonizes estrogen in breast or uterus, but estrogen-like activities in the brain have been reported. Cytoplasmic and membrane extracts of the dorsal raphe region were processed for Western blotting. TPH, phosphoserine, SERT, MAO-A, and MAO-B were detected with specific antibodies. The optical densities of the signals were measured with NIH image and analyzed by ANOVA. Both 1 and 5 mo of estrogen, with or without progesterone, and 5 mo of raloxifene significantly increased TPH protein. Administration for 5 mo of estrogen plus progesterone and raloxifene also increased TPH phosphorylation. Estrogen, with or without progesterone, for 1 mo had no effect on SERT protein. However, 5 mo of estrogen and 5 mo of raloxifene increased SERT protein. Estrogen alone or combined with progesterone for 1 mo caused a significant reduction in MAO-A. Yet, after 5 mo of the same treatments, MAO-A was not different from spayed controls. Estrogen alone had no effect on MAO-B. However, the addition of progesterone significantly increased MAO-B. Raloxifene for 5 mo had no effect on MAO-A or MAO-B. Thus, to various extents, estrogen, progesterone, and raloxifene may increase serotonin production and transport. The expression of the degradative enzymes suggests a complex combination of gene transcription, post-transcriptional processing, and substrate feedback mechanisms.

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“…The idazoxanpreferring subtype, the I2-imidazoline site (12-site), is expressed in several tissues (Langin & Lafontan, 1989;Coupry et al, 1989;Zonnenschein et al, 1990), including the brain (Mallard et al, 1992;Olmos et al, 1992;Miralles et al, 1993a) and, at the subcellular level, is located on the mitochondrial outer membrane Regunathan et al, 1993b). Recently, it has been shown that the density of I2-sites increases with age in the human brain and that the regional distribution of these sites correlates well with that of the B isoform of the enzyme monoamine oxidase (MAO-B) (Sastre & Garcia-Sevilla, 1993), which is mainly located in 5-hydroxytryptaminergic and glial cells (Westlund et al, 1988). Also in this context, it has been reported that cultured cortical astrocytes, but not cortical neurones, express I2-sites (Regunathan et al, 1993a).…”

Section: Introductionmentioning

confidence: 99%

The effects of chronic imidazoline drug treatment on glial fibrillary acidic protein concentrations in rat brain

Olmos

Alemany

Escribá

et al. 1994

British J Pharmacology

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1 The concentration of the astrocytic marker, glial fibrillary acidic protein (GFAP) was quantitated by immunoblotting (western blotting) in the rat brain after treatment with various imidazoline drugs and other agents. 2 Chronic (7 days) but not acute (1 day) treatment with the imidazoline drugs, cirazoline (1 mg kg-', i.p.) and idazoxan (1Omg kg', i.p.), but not with the structurally related a2-adrenoceptor antagonists, RX821002 (2-methoxy idazoxan) (1Omg kg', i.p.) and efaroxan (1O mg kg', i.p.), markedly increased (45%) GFAP immunoreactivity in the rat cerebral cortex. Chronic treatment (7 days) with yohimbine (10mg kg-', i.p.), a non-imidazoline a2-adrenoceptor antagonist, did not significantly modify GFAP immunoreactivity in the cerebral cortex. 3 Chronic treatment (7 days) with cirazoline and idazoxan did not alter the density of brain monoamine oxidase (MAO)-B sites labelled by [3H]-Ro 19-6327 (lazabemide), another relevant astroglial marker. Moreover, these imidazoline drug treatments did not modify the levels of a-tubulin in the cerebral cortex. These negative results reinforced the specificity of the effects of imidazoline drugs on GFAP. 4 Irreversible inactivation of brain x2-adrenoceptors (and other neurotransmitters receptors) after treatment with an optimal dose of the peptide-coupling agent EEDQ (1.6 mg kg-', i.p., for 6-24 h) did not alter GFAP immunoreactivity in the cerebral cortex. These results further disproved the involvement of these receptors on astroglial cells in the tonic control of GFAP levels. 5 The binding of [3H]-idazoxan in the presence of 10-6 M (-)-adrenaline was used to quantitate in parallel 12-imidazoline preferring sites in the rat brain after the same treatments. Chronic treatment (7 days) with cirazoline and idazoxan, but not with RX821002, efaroxan or yohimbine, significantly increased (25%) the density of I2-sites in the cerebral cortex. The up-regulation of I2-sites induced by cirazoline was not observed in the liver, a tissue that also expresses 12-sites but lacks glial cells. 6 A strong correlation (r = 0.97) was found when the mean percentage changes in GFAP immunoreactivity were related to the mean percentage changes in 12 imidazoline sites after the various drug treatments. 7 Together the results suggest a direct physiological function of glial I2-imidazoline preferring sites in the regulation of GFAP levels.

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Localization of distinct monoamine oxidase a and monoamine oxidase b cell populations in human brainstem

Cited by 339 publications

References 44 publications

Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism and antisocial personality disorder in adult women

Effects of Ovarian Steroids and Raloxifene on Proteins that Synthesize, Transport, and Degrade Serotonin in the Raphe Region of Macaques

The effects of chronic imidazoline drug treatment on glial fibrillary acidic protein concentrations in rat brain

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