Distribution of aromatic L‐amino acid decarboxylase mRNA in mouse brain by in situ hybridization histology

Eaton, Mary J.; Gudehithlu, Krishnamurthy P.; Quach, Tam; Silvia, Christopher; Hadjiconstantinou, Maria; Neff, Norton H.

doi:10.1002/cne.903370409

Cited by 33 publications

(26 citation statements)

References 50 publications

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“…It was then applied to recognize both catecholaminergic and serotoninergic neurons in the brainstem of different vertebrates (Beltramo et al, 1993). Our results on the principal pattern of this enzyme in the guinea pig diencephalon were consistent with those obtained by immunocytochemistry in the rat (Jaeger, 1986;Skagerberget al, 1988) in the cat (Ktahama et al, 1988) and by in situ hybridization in the mouse (Eaton et al, 1993). In spite of the close similarity in the general arrangement of AADC neurons in guinea pig and rat, the number of cells as well as areas occupied by AADC-IR cells seemed greater in the guinea pig than in the rat.…”

Section: Discussionsupporting

confidence: 92%

Progesterone receptor immunoreactivity in aromatic L-amino acid decarboxylase-containing neurons of the guinea pig hypothalamus and preoptic area

et al. 1996

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A double-labeling immunofluorescence procedure was used to determine whether progesterone receptor (PR)-immunoreactive (IR) neurons in the preoptic area and hypothalamus of female guinea pigs also contained aromatic L-amino acid decarboxylase (AADC), an enzyme involved in the synthesis of both catecholamines and serotonin. Immunostaining was performed on cryostat sections prepared from ovariectomized guinea pigs primed by estradiol to induce PR. The nuclear presence of PR was visualized by a red fluorescence while the AADC-containing perikarya showed a yellow-green fluorescence. The topographic distribution of AADC-IR neurons was investigated by using a specific antiserum obtained by immunization of rabbits with a recombinant protein beta-galactosidase-AADC in the two regions known to contain the densest populations of estradiol-induced PR-IR cells: the preoptic area and the mediobasal hypothalamus. The localization of PR-IR and AADC-IR cell populations showed considerable overlap in these areas, mainly in the medial and periventricular preoptic nuclei and in the arcuate nucleus. A quantitative analysis of double-labeled cells estimated that about 15% to 23% of AADC-IR cells in the preoptic area and about 11% to 21% of AADC-IR cells in the arcuate nucleus possessed PR. This colocalization persisted throughout the rostrocaudal extent of these areas and represented 3% to 9% of the population of PR-IR cells. These findings provide neuroanatomical evidence that a subset of AADC neurons is directly regulated by progesterone. The exact physiological role of this enzyme in target cells for progesterone is not understood. AADC may be involved in functions other than that for the synthesis of the classical neurotransmitters.

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Section: Discussionsupporting

confidence: 92%

Progesterone receptor immunoreactivity in aromatic L-amino acid decarboxylase-containing neurons of the guinea pig hypothalamus and preoptic area

et al. 1996

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“…S2). These findings were further confirmed by examining the expression of L-amino acid decarboxylase (L-AADC) (Eaton et al, 1993), monoamine oxidase type A (MaoA) (Arai et al, 1997), calcitonin gene related protein (CGRP) (Holm et al, 2003;Ma et al, 2003), vesicular glutamate transporter 1 (vGluT1) (Barr and Van Bockstaele, 2005), brainderived neurotrophic factor (BDNF) (Holm et al, 2003) and c-Ret (Holm et al, 2002) at E17.5 or P0 (supplementary material Fig. S2).…”

Section: Rbpj Inactivation Induces Overproduction Of Lc Neuronsmentioning

confidence: 74%

Notch-Rbpj signaling is required for the development of noradrenergic neurons in mouse locus coeruleus

Shi

Zheng

et al. 2012

Journal of Cell Science

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SummaryThe locus coeruleus (LC) is the main source of noradrenaline in the brain and is implicated in a broad spectrum of physiological and behavioral processes. However, genetic pathways controlling the development of noradrenergic neurons in the mammalian brain are largely unknown. We report here that Rbpj, a key nuclear effector in the Notch signaling pathway, plays an essential role in LC neuron development in the mouse. Conditional inactivation of Rbpj in the dorsal rhombomere (r) 1, where LC neurons are born, resulted in a dramatic increase in the number of Phox2a-and Phox2b-expressing early-differentiating LC neurons, and dopamine-b-hydroxylase-and tyrosine-hydroxylase-expressing late-differentiating LC neurons. In contrast, other neuronal populations derived from the dorsal r1 were either reduced or unchanged. In addition, a drastic upregulation of Ascl1, an essential factor for noradrenergic neurogenesis, was observed in dorsal r1 of conditional knockout mice. Through genomic sequence analysis and EMSA and ChIP assays, a conserved Rbpjbinding motif was identified within the Ascl1 promoter. A luciferase reporter assay revealed that Rbpj per se could induce Ascl1 transactivation but this effect was counteracted by its downstream-targeted gene Hes1. Moreover, our in vitro gene transfection and in ovo electroporation assays showed that Rbpj upregulated Ascl1 expression when Hes1 expression was knocked down, although it also exerted a repressive effect on Ascl1 expression in the presence of Hes1. Thus, our results provide the first evidence that Rbpj functions as a key modulator of LC neuron development by regulating Ascl1 expression directly, and indirectly through its target gene Hes1.

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“…Eighty percent of the striatal AAAD is located in dopaminergic neurons, and the remainder is in noradrenergic, serotonergic, and intrinsic AAADpositive neurons Eaton et al, 1993;Mura et al, 1995), all of which add to the AAAD activity assayed in striatum homogenates. Clozapine up-regulated the expression of AAAD mRNA in substantia nigra pars compacta and ventral tegmental area, indicating that enzyme activity is modulated in dopaminergic neurons.…”

Section: Discussionmentioning

confidence: 99%

“…35 S-Labeled (Amersham Biosciences) sense and antisense riboprobes were prepared from a 286-bp fragment of the mouse brain AAAD cDNA (Eaton et al, 1993). Sections were incubated with the probe for 20 h in 50% formamide, 10% dextran sulfate, 1ϫ Denhardt's solution, 0.3 M NaCl, 20 mM Tris HCl, 1 mM EDTA, 0.1 M dithiothreitol, and 0.3 g of tRNA.…”

Section: Aaad Modulation By Clozapine 481mentioning

confidence: 99%

Clozapine Modulates Aromatic l-Amino Acid Decarboxylase Activity in Mouse Striatum

Neff¹,

Wemlinger²,

Duchemin³

et al. 2006

J Pharmacol Exp Ther

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Clozapine is efficacious for treating dopaminergic psychosis in Parkinson's disease and ameliorates L-DOPA-induced motor complications. Based on its pharmacology and reported enhancing effects on dopamine metabolism and tyrosine hydroxylase activity, we investigated whether it could modulate the activity of aromatic L-amino acid decarboxylase (AAAD), the second enzyme for the biosynthesis of catecholamines and indoleamines. A single dose of clozapine increased AAAD activity of striatum in a dose-and time-dependent manner. At 1 h, enhanced enzyme activity was characterized by an increased V max for substrate and cofactor and was accompanied by elevated levels of protein in striatum and mRNA in substantia nigra, ventral tegmental area, locus coeruleus, and raphe nuclei. Acute clozapine increased tyrosine hydroxylase activity in striatum but with differing temporal patterns from AAAD and heightened dopamine metabolism. Interestingly, the response of the dopaminergic markers to clozapine was greater following a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesion. Chronically administered clozapine increased AAAD activity and protein and dopamine metabolism in striatum without affecting tyrosine hydroxylase. Exogenous L-DOPA decarboxylation was accelerated in the striatum of intact and MPTPlesioned mice following acute clozapine, and the effect was exaggerated in the MPTP mice. To identify receptors involved, antagonists of receptors occupied by clozapine were employed. D4, 5-HT1 A , and 5-HT2 A , in addition to D1, D2, and D3, antagonists, augmented AAAD activity in striatum, whereas 5-HT2 C , 5-HT3, muscarinic, and ␣-1 and ␣-2 adrenergic antagonists were ineffective. For the first time, these studies provide evidence that clozapine modulates AAAD activity in the brain and suggests that dopamine and serotonin receptors are involved.Aromatic L-amino acid decarboxylase (AAAD) is a ubiquitous enzyme essential for the formation of catecholamines, indoleamines, and trace amines (Berry et al., 1996). AAAD is not considered to be the rate-limiting enzyme for catecholamine or indoleamine synthesis; however, it is the rate-limiting step for the synthesis of trace amines and becomes rate-limiting for dopamine formation in Parkinson's disease patients treated with L-DOPA. AAAD is a regulated enzyme, and accumulated evidence suggests that its activity in the rodent brain is tuned by short-and long-term mechanisms that apparently involve enzyme activation and induction.Physiological stimuli (Hadjiconstantinou et al., 1988), neurotransmitter receptors (Rossetti et al., 1989(Rossetti et al., , 1990Zhu et al., 1992;Hadjiconstantinou et al., 1993Hadjiconstantinou et al., , 1995Cho et al., 1997;Fisher et al., 1998) and second messenger systems (Young et al., 1998) participate in the regulation of enzyme activity. In nigrostriatal neurons, dopamine appears to regulate AAAD via D1-and D2-like receptors. Indeed, acute blockade of dopamine D1-like receptors with SCH23390 and of dopamine D2-like receptors with haloperidol, ...

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Distribution of aromatic L‐amino acid decarboxylase mRNA in mouse brain by in situ hybridization histology

Cited by 33 publications

References 50 publications

Progesterone receptor immunoreactivity in aromatic L-amino acid decarboxylase-containing neurons of the guinea pig hypothalamus and preoptic area

Progesterone receptor immunoreactivity in aromatic L-amino acid decarboxylase-containing neurons of the guinea pig hypothalamus and preoptic area

Notch-Rbpj signaling is required for the development of noradrenergic neurons in mouse locus coeruleus

Clozapine Modulates Aromatic l-Amino Acid Decarboxylase Activity in Mouse Striatum

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