Differential expression and regulation of the high-affinity choline transporter CHT1 and choline acetyltransferase in neurons of superior cervical ganglia

Lecomte, Marie-José; Gois, Stéphanie De; Guerci, Aline; Ravassard, Philippe; Biguet, Nicole Faucon; Mallet, Jacques; Berrard, Sylvie

doi:10.1016/j.mcn.2004.09.014

Cited by 16 publications

(19 citation statements)

References 72 publications

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“…It has been shown that CHT and ChAT are coordinately upregulated in superior cervical ganglia when treated with LIF (Lecomte et al, 2005). We observed simultaneous upregulation of CHT and VAChT when primary septal cells were exposed to NGF .…”

Section: Introductionsupporting

confidence: 53%

“…However, there is also growing evidence that the regulation of CHT and the cholinergic locus are not identical. Treatment of superior cervical ganglia neurons with retinoic acid resulted in a significant downregulation of CHT, while ChAT expression was increased (Lecomte et al, 2005). Furthermore, treatment of primary septal cells with 0.1 μM retinoic acid had no effect on CHT mRNA expression, whereas VAChT expression was increased .…”

Section: Introductionmentioning

confidence: 88%

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Differential regulation of the high affinity choline transporter and the cholinergic locus by cAMP signaling pathways

Brock¹,

Nickel²,

Madziar³

et al. 2007

Brain Research

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Synthesis, storage and release of acetylcholine (ACh) require the expression of several specialized enzymes, including choline acetyltransferase (ChAT), vesicular acetylcholine transporter (VAChT) and the high-affinity choline transporter (CHT). Extracellular factors that regulate CHT expression and their signaling pathways remain poorly characterized. Using the NSC-19 cholinergic cell line, derived from embryonic spinal cord, we compared the effects of the second messenger cAMP on the expression of CHT and the cholinergic locus containing the ChAT and VAChT genes. Treatment of NSC-19 cells with dbcAMP and forskolin, thus increasing intracellular cAMP levels, significantly reduced CHT mRNA expression, while it upregulated ChAT/VAChT mRNA levels and ChAT activity. The cAMP-induced CHT downregulation was independent of PKA activity, as shown in treatments with the PKA inhibitor H-89. The alternative Epac-Rap pathway, when stimulated by a specific Epac activator, led to significant downregulation of CHT and ChAT, and, to a lesser extent, VAChT. In contrast, the PKA activator 6-BNZ-cAMP stimulated the expression of all three genes, but with varying concentration-dependence profiles. Our results indicate that elevations of intraneuronal cAMP concentration have differential effects on the cholinergic phenotype, depending on the involvement of different downstream effectors. Interestingly, although CHT is expressed predominantly in cholinergic cells, its regulation appears to be distinct from that of the cholinergic locus.

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Section: Introductionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 88%

Differential regulation of the high affinity choline transporter and the cholinergic locus by cAMP signaling pathways

Brock¹,

Nickel²,

Madziar³

et al. 2007

Brain Research

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“…On the other hand, it has been reported that regulation of CHT1 expression is independent of the cholinergic gene locus under some conditions. Treatment of superior cervical ganglia neurons with RA up-regulated ChAT expression but down-regulated CHT1 mRNA expression (41). Berse et al (34) also reported that all-trans-RA treatment increased VACHT expression in cultured mouse septal neurons, but that CHT1 expression was unaffected.…”

Section: Discussionmentioning

confidence: 97%

“…Many reports have demonstrated that the two genes encoding CHAT and VACHT are coordinately regulated by extracellular stimuli such as NGF, retinoic acids (RAs), and cytokines of the bone morphogenetic protein family (37)(38)(39)(40). Synergic up-regulation of CHT1 and ChAT is also observed when superior cervical ganglia are treated with leukemia inhibitory factor (41). It has been shown that simultaneous up-regulation of CHT1 and VACHT is induced when primary septal cells are stimulated with NGF (34).…”

Section: Discussionmentioning

confidence: 99%

Nuclear Choline Acetyltransferase Activates Transcription of a High-affinity Choline Transporter

Matsuo

Bellier

Nakagawa

et al. 2011

Journal of Biological Chemistry

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Choline acetyltransferase (ChAT) synthesizes the neurotransmitter, acetylcholine, at cholinergic nerve terminals. ChAT contains nuclear localization signals and is also localized in the nuclei of neural and non-neuronal cells. Nuclear ChAT might have an as yet unidentified function, such as transcriptional regulation. In this study, we investigated the alteration of candidate gene transcription by ChAT. We chose high affinity choline transporter (CHT1) and vesicular acetylcholine transporter (VACHT) as candidate genes, which function together with ChAT in acetylcholine production. Using SH-SY5Y human neuroblastoma cells stably expressing wild-type human ChAT, we found that overexpressed ChAT enhanced transcription of the CHT1 gene but not the VACHT gene. In contrast, nuclear localization signal disrupted, and catalytically inactive mutant ChATs could not induce, CHT1 expression. Additionally, ChAT did not alter CHT1 expression in non-neuronal HEK293 cells. Our results suggest that ChAT activates the transcription of selected target genes in neuronal cells. Both enzymatic activity and nuclear translocation of ChAT are required for its transcriptional enhancement.

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“…Recent studies indicate the CHT is expressed in some noradrenergic sympathetic neurons that do not contain detectable ChAT or VAChT (Lecomte et al, 2005). This raises the possibility that CHT is present in cholinergic sympathetic neurons prior to target contact, when they are still noradrenergic and do not express ChAT, VAChT, and VIP.…”

Section: Introductionmentioning

confidence: 99%

Developmental expression of the high affinity choline transporter in cholinergic sympathetic neurons

Guidry

Willison

Blakely

et al. 2005

Autonomic Neuroscience

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Choline uptake by the high affinity choline transporter (CHT) is the rate-limiting step in acetylcholine synthesis. Induction of CHT is therefore a critical step in cholinergic differentiation, and we examined the developmental expression of CHT in cholinergic sympathetic neurons that innervate rodent sweat glands. During postnatal development the earliest sympathetic axons in the rear footpads are noradrenergic, containing intense tyrosine hydroxylase immunoreactivity and lacking CHTimmunoreactivity (CHT-IR). By postnatal day 7 (P7) in mouse, and P10 in rat, weak CHT-IR appeared in axons associated with the sweat gland anlagen. CHT staining intensity increased during the following weeks in conjunction with plexus arborization and gland maturation. The pattern of CHT-immunoreactivity (CHT-IR) in the sweat gland innervation was similar to staining for the vesicular acetylcholine transporter and vasoactive intestinal peptide. Immunoblots of tissue from sympathectomized rats confirmed that most of the CHT in footpad was contained in sympathetic neurons. Although CHT expression has been reported in noradrenergic sympathetic neurons of the superior cervical ganglion, these data indicate that in the sympathetic neurons projecting to sweat glands CHT is present at detectable levels only after association with the glands.

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Differential expression and regulation of the high-affinity choline transporter CHT1 and choline acetyltransferase in neurons of superior cervical ganglia

Cited by 16 publications

References 72 publications

Differential regulation of the high affinity choline transporter and the cholinergic locus by cAMP signaling pathways

Differential regulation of the high affinity choline transporter and the cholinergic locus by cAMP signaling pathways

Nuclear Choline Acetyltransferase Activates Transcription of a High-affinity Choline Transporter

Developmental expression of the high affinity choline transporter in cholinergic sympathetic neurons

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