Characterization of a Rat Neuronal Nicotinic Acetylcholine Receptor α7 Promoter

Nagavarapu, Usha; Danthi, Sanjay; Boyd, Ryan L.

doi:10.1074/jbc.m009712200

Cited by 24 publications

(16 citation statements)

References 53 publications

(54 reference statements)

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“…This transient developmental upregulation in cortical structures has also been reported for α3, β4, α5 and α7 subunits (Adams et al, 2002, WinzerSerhan and Leslie, 1997, suggesting a general pattern of nAChR subunit mRNA regulation, despite different transcriptional elements controlling their expression (Boyd, 1994, Bessis et al, 1993, Yang et al, 1997, Nagavarapu et al, 2001). …”

Section: Expression Of Nachr α2 Mrna During Developmentsupporting

confidence: 56%

Postnatal expression of α2 nicotinic acetylcholine receptor subunit mRNA in developing cortex and hippocampus

Son

Winzer‐Serhan

2006

Journal of Chemical Neuroanatomy

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Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated cation channels composed of α and β subunits. nAChR subunit expression is highly regulated during development. Previous studies have revealed increased expression of α3, α5, α7, and β4 subunit mRNAs and α7 binding sites during hippocampal and cortical development. Here, we examined the expression of α2 subunit mRNA in rat cortex and hippocampus using highly sensitive radioactive in situ hybridization. α2 subunit mRNA expression was first detected at P3 in cortex and hippocampus. During postnatal development the distribution of α2 subunit mRNA expression was spatially similar to the one found in adult, exhibiting highly restricted expression in scattered cells mostly in cortical layer V and retrosplenial cortex, and in scattered cells in CA1/CA3 stratum oriens and CA3 stratum radiatum. However, the expression intensity and number of α2 positive cells strongly increased to reach peak levels in both cortex and hippocampus at P7 and decreased thereafter to moderate to low to levels. Double in situ hybridization revealed that most, but not all, α2 mRNA expression was located in nonpyramidal GAD-positive cortical and hippocampal interneurons. Thus, similar to other nAChR subunits, α2 mRNA expression is transiently upregulated during postnatal development and nAChRs containing α2 subunits could regulate GABAergic activity during a critical period of network formation.

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Section: Expression Of Nachr α2 Mrna During Developmentsupporting

confidence: 56%

Postnatal expression of α2 nicotinic acetylcholine receptor subunit mRNA in developing cortex and hippocampus

Son

Winzer‐Serhan

2006

Journal of Chemical Neuroanatomy

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“…A number of GC-rich TATA-less promoters regulated by Sp1 and Sp3 have previously been shown to contain sequence elements that confer tissue-specific expression (33,34). Additionally, the CBS 5Ј-flanking sequence contains numerous binding sites for delta EF1 and HNF-3 beta, which have previously been shown to regulate gene expression in a tissue-specific manner (35,36).…”

Section: Figmentioning

confidence: 99%

The Dominant Role of Sp1 in Regulating the Cystathionine β-Synthase –1a and –1b Promoters Facilitates Potential Tissue-specific Regulation by Kruppel-like Factors

Maclean

Kraus

2004

Journal of Biological Chemistry

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Cystathionine ␤-synthase (CBS) catalyzes the condensation of serine with homocysteine to form cystathionine and occupies a crucial regulatory position between the methionine cycle and transsulfuration. The human cystathionine ␤-synthase gene promoters ؊1a and ؊1b are expressed in a limited number of tissues and are coordinately regulated with proliferation through a redox-sensitive mechanism. Site-directed mutagenesis, DNase I footprinting and deletion analysis of 5276 bp of 5 proximal ؊1b flanking sequence revealed that this region does not confer tissue-specific expression and that 210 bp of proximal sequence is sufficient for maximal promoter activity. As little as 32 bp of the ؊1b proximal promoter region is capable of driving transcription in HepG2 cells, and this activity is entirely dependent upon the presence of a single overlapping Sp1/Egr1 binding site. Co-transfection studies in Drosophila SL2 cells indicated that both promoters are transactivated by Sp1 and Sp3 but only the ؊1b promoter is subject to a site-specific synergistic regulatory interaction between Sp1 and Sp3. Sp1-deficient fibroblasts expressing both Sp3 and NF-Y were negative for CBS activity. Transfection of these cells with a mammalian Sp1 expression construct induced high levels of CBS activity indicating that Sp1 has a critical and indispensable role in the regulation of cystathionine ␤-synthase. Sp1 binding to both CBS promoters is sensitive to proliferation status and is negatively regulated by Kruppel-like factors in co-transfection experiments suggesting a possible mechanism for the tissue specific regulation of cystathionine ␤-synthase.

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“…Without experimental data, however, it is difficult to judge the significance of these transcription factors as direct regulators. Here, it should be noted that binding sites for Egr-1, Sp1, and Sp3, transcription factors not associated with BDNF-trkB signaling, are thought to regulate the activity of the rat ␣7-nAChR promoter (Nagavarapu et al, 2001). …”

Section: Detection Of Trkb and Bdnfmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor and trkB Signaling in Parasympathetic Neurons: Relevance to Regulating α7-Containing Nicotinic Receptors and Synaptic Function

Zhou¹,

Nai²,

Chen³

et al. 2004

J. Neurosci.

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Parasympathetic neurons do not require neurotrophins for survival and are thought to lack high-affinity neurotrophin receptors (i.e., trks). We report here, however, that mRNAs encoding both brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin-related kinase B (trkB) are expressed in the parasympathetic chick ciliary ganglion (CG) and that BDNF-like protein is present in the ganglion and in the iris, an important peripheral target of ciliary neurons. Moreover, CG neurons express surface trkB and exogenous BDNF not only initiates trk-dependent signaling, but also alters nicotinic acetylcholine receptor (nAChR) expression and synaptic transmission. In particular, BDNF applied to CG neurons rapidly activates cAMP-dependent response element-binding protein (CREB), and over the long-term selectively upregulates expression of ␣7-subunit-containing, homomeric nAChRs (␣7-nAChRs), increasing ␣7-subunit mRNA levels, ␣7-nAChR surface sites, and ␣7-nAChR-mediated whole-cell currents. At nicotinic synapses formed on CG neurons in culture, brief and long-term BDNF treatments also increase the frequency of spontaneous EPSCs, most of which are mediated by heteromeric nAChRs containing ␣3, ␣5, ␤4, and ␤2 subunits (␣3*-nAChRs) with a minor contribution from ␣7-nAChRs. Our findings demonstrate unexpected roles for BDNF-induced, trk-dependent signaling in CG neurons, both in regulating expression of ␣7-nAChRs and in enhancing transmission at ␣3*-nAChR-mediated synapses. The presence of BDNF-like protein in CG and iris target coupled with that of functional trkB on CG neurons raise the possibility that signals generated by endogenous BDNF similarly influence ␣7-nAChRs and nicotinic synapses in vivo.

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Characterization of a Rat Neuronal Nicotinic Acetylcholine Receptor α7 Promoter

Cited by 24 publications

References 53 publications

Postnatal expression of α2 nicotinic acetylcholine receptor subunit mRNA in developing cortex and hippocampus

Postnatal expression of α2 nicotinic acetylcholine receptor subunit mRNA in developing cortex and hippocampus

The Dominant Role of Sp1 in Regulating the Cystathionine β-Synthase –1a and –1b Promoters Facilitates Potential Tissue-specific Regulation by Kruppel-like Factors

Brain-Derived Neurotrophic Factor and trkB Signaling in Parasympathetic Neurons: Relevance to Regulating α7-Containing Nicotinic Receptors and Synaptic Function

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