High expression of retinoic acid receptors and synthetic enzymes in the human hippocampus

Fragoso, Yára Dadalti; Shearer, Kirsty; Sementilli, Ângelo; Carvalho, Leda Viegas de; McCaffery, Peter

doi:10.1007/s00429-011-0359-0

Cited by 38 publications

(33 citation statements)

References 69 publications

(87 reference statements)

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“…RNA extraction and quantitative PCR (qPCR) analysis followed our previously published protocols (Fragoso et al, 2012). The following primers were used.…”

Section: Methodsmentioning

confidence: 99%

The expression and roles of Nde1 and Ndel1 in the adult mammalian central nervous system

Pei¹,

Lang²,

Fragoso³

et al. 2014

Neuroscience

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“…RNA extraction and quantitative PCR (qPCR) analysis followed our previously published protocols (Fragoso et al, 2012). The following primers were used.…”

Section: Methodsmentioning

confidence: 99%

The expression and roles of Nde1 and Ndel1 in the adult mammalian central nervous system

Pei¹,

Lang²,

Fragoso³

et al. 2014

Neuroscience

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“…Both RA and its ligand-activated nuclear retinoic acid receptors (RARs) are particularly abundantly present in the hippocampal dentate gyrus (DG) of adult mice and humans (Misner et al, 2001;Sakai et al, 2004;Fragoso et al, 2012;Goodman et al, 2012). The adult DG is a unique brain region where stem cells reside that continue to undergo division and proliferation into adulthood.…”

Section: Introductionmentioning

confidence: 99%

Chronic retinoic acid treatment suppresses adult hippocampal neurogenesis, in close correlation with depressive-like behavior

Wang

Liu

et al. 2016

Hippocampus

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Clinical studies have highlighted an association between retinoid treatment and depressive symptoms. As we had shown before that chronic application of all-trans retinoic acid (RA) potently activated the hypothalamus-pituitary-adrenal (HPA) stress axis, we here questioned whether RA also induced changes in adult hippocampal neurogenesis, a form of structural plasticity sensitive to stress and implicated in aspects of depression and hippocampal function. RA was applied intracerebroventricularly (i.c.v.) to adult rats for 19 days after which animals were subjected to tests for depressive-like behavior (sucrose preference) and spatial learning and memory (water maze) performance. On day 27, adult hippocampal neurogenesis and astrogliosis was quantified using BrdU (newborn cell survival), PCNA (proliferation), doublecortin (DCX; neuronal differentiation), and GFAP (astrocytes) as markers. RA was found to increase retinoic acid receptor-α (RAR-α) protein expression in the hippocampus, suggesting an activation of RA-induced signaling mechanisms. RA further potently suppressed cell proliferation, newborn cell survival as well as neurogenesis, but not astrogliosis. These structural plasticity changes were significantly correlated with scores for anhedonia, a core symptom of depression, but not with water maze performance. Our results suggest that RA-induced impairments in hippocampal neurogenesis correlate with depression-like symptoms but not with spatial learning and memory in this design. Thus, manipulations aimed to enhance neurogenesis may help ameliorate emotional aspects of RA-associated mood disorders. © 2016 Wiley Periodicals, Inc.

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“…In mouse hippocampal neurons, dendritic RARα is required to mediate RA's non-genomic effects on synaptic homeostasis by modulating local protein translation and AMPA receptor insertion (Aoto et al, 2008; Arendt et al, 2015; Chen et al, 2014; Maghsoodi et al, 2008). In adult human hippocampal neurons it is predominantly the RARβ isoform that is cytoplasmic (Fragoso et al, 2012). …”

Section: Discussionmentioning

confidence: 99%

Optic nerve injury upregulates retinoic acid signaling in the adult frog visual system

Duprey‐Díaz

Blagburn

Blanco

2016

Journal of Chemical Neuroanatomy

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Retinoic acid (RA) is important during development, in neuronal plasticity, and also in peripheral nervous system regeneration. Here we use the frog visual system as a model to investigate the changes in RA signaling that take place after axonal injury to the central nervous system. Immunocytochemistry was used to localize different components of RA signaling within sections of the retina and optic tectum, namely, the synthetic enzyme retinaldehyde dehydrogenase (RALDH), the RA binding proteins CRABPI and II, the retinoic acid receptors RARα, β and (, and finally the catabolic enzyme CYP26A1. The levels of these proteins were quantified in extracts of retina and tectum using Western blotting. Animals were studied at 1 week, 3 weeks and 6 weeks after optic nerve transection. At the latter time point the RGC axons were re-entering the optic tectum. All the components of RA signaling were present at low to moderate levels in retinas and tecta of control, unoperated animals. In retina, soon after optic nerve injury there was a large increase in RALDH, some increase in the CRABPs, and a large increase in RGC RARβ and ( expression. These increases continued as the RGC axons were regenerating, with the addition of later RARα expression at 6 weeks. At no stage did CYP26A1 expression significantly change. In the tectum the levels of RALDH increased after axotomy and during regrowth of axons (3 weeks), then decreased at 6 weeks, at which time the levels of CYP26A1 increased. Axotomy did not cause an immediate increase in tectal RAR levels but RARα and RARβ increased after 3 weeks and RAR( only after 6 weeks. These results are consistent with RA signaling playing an important role in the survival and regeneration of frog RGCs.

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High expression of retinoic acid receptors and synthetic enzymes in the human hippocampus

Cited by 38 publications

References 69 publications

The expression and roles of Nde1 and Ndel1 in the adult mammalian central nervous system

The expression and roles of Nde1 and Ndel1 in the adult mammalian central nervous system

Chronic retinoic acid treatment suppresses adult hippocampal neurogenesis, in close correlation with depressive-like behavior

Optic nerve injury upregulates retinoic acid signaling in the adult frog visual system

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