Involvement of α7 Nicotinic Acetylcholine Receptors in Activation of Tyrosine Hydroxylase and Dopamine β‐Hydroxylase Gene Expression in PC12 Cells

Gueorguiev, Volodia D.; Zeman, Richard J.; Meyer, Edwin M.; Sabban, Esther L.

doi:10.1046/j.1471-4159.2000.0751997.x

Cited by 53 publications

(50 citation statements)

References 53 publications

(75 reference statements)

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“…There are three types of cytoplasmic calcium signals initiated by neuronal nAChR activation; (1) direct calcium influx through the nAChR [6,11] , (2) indirect calcium influx through voltage-dependent calcium channels (VDCCs) which are activated by the nAChR-mediated depolarization [6,11] , and (3) calcium-induced calcium release (CICR) (triggered by the two sources listed above) from the endoplasmic reticulum (ER) through the ryanodine receptors [12][13][14] and inositol (1,4,5)-triphosphate receptors (IP 3 Rs) [13][14][15] .…”

Section: Cytoplasmic Calcium Signals Initiated By Neuronal Nachr Actimentioning

confidence: 99%

“…The involvement of IP 3 R-dependent calcium stores in neuronal nAChR signaling was shown when nAChRinduced calcium responses were reduced with IP 3 R-selective antagonists [13][14][15] . The functional interaction between IP 3 and ryanodine receptor-dependent calcium signals is considered to be a key signaling mechanism [28] .…”

Section: Cytoplasmic Calcium Signals Initiated By Neuronal Nachr Actimentioning

confidence: 99%

“…Regulation of neurotransmitter release The activation of nAChRs can influence gene expression for immediate early genes and genes involved in transmitter synthesis [15,52,59,60] . In the chick ciliary ganglion [61] , the nAChR-mediated control of transcription relies on calcium influx and calcium release from internal stores to activate first CaMKII/IV, and then ERK/MAPK.…”

Section: Instantaneous Effectsmentioning

confidence: 99%

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Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system

2009

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Based on the composition of the five sub units forming functional neuronal nicotinic acetylcholine receptors (nAChRs), they are grouped into either heteromeric (comprising both α and β subunits) or homomeric (comprising only α subunits) receptors. The nAChRs are known to be differentially permeable to calcium ions, with the α7 nAChR subtype having one of the highest permeabilities to calcium. Calcium influx through nAChRs, particularly through the α-bungarotoxin-sensitive α7-containing nAChRs, is a very efficient way to raise cytoplasmic calcium levels. The activation of nAChRs can mediate three types of cytoplasmic calcium signals: (1) direct calcium influx through the nAChRs, (2) indirect calcium influx through voltage-dependent calcium channels (VDCCs) which are activated by the nAChR-mediated depolarization, and (3) calciuminduced calcium release (CICR) (triggered by the first two sources) from the endoplasmic reticulum (ER) through the ryanodine receptors and inositol (1,4,5)-triphosphate receptors (IP 3 Rs). Downstream signaling events mediated by nAChRmediated calcium responses can be grouped into instantaneous effects (such as neurotransmitter release, which can occur in milliseconds after nAChR activation), short-term effects (such as the recovery of nAChR desensitization through cellular signaling cascades), and long-term effects (such as neuroprotection via gene expression). In addition, nAChR activity can be regulated by cytoplasmic calcium levels, suggesting a complex reciprocal relationship. Further advances in imaging techniques, animal models, and more potent and subtype-selective ligands for neuronal nAChRs would help in understanding the neuronal nAChR-mediated calcium signaling, and lead to the development of improved therapeutic treatments.

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Section: Cytoplasmic Calcium Signals Initiated By Neuronal Nachr Actimentioning

confidence: 99%

Section: Cytoplasmic Calcium Signals Initiated By Neuronal Nachr Actimentioning

confidence: 99%

Section: Instantaneous Effectsmentioning

confidence: 99%

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Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system

2009

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“…Nicotinic transmission can also influence gene expression as originally shown for immediate early genes and genes involved in transmitter synthesis (Chalazonitis and Zigmond, 1980;Greenberg et al, 1986;Pelto-Huikko et al, 1995;Salminen et al, 1999;Gueorguiev et al, 2000). The underlying mechanisms have been examined in some detail in the chick ciliary ganglion .…”

Section: Long-term Consequencesmentioning

confidence: 99%

Nicotinic α7 receptors: Synaptic options and downstream signaling in neurons

2002

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Nicotinic receptors are cation-ion selective ligand-gated ion channels that are expressed throughout the nervous system. Most have significant calcium permeabilities, enabling them to regulate calcium-dependent events. One of the most abundant is a species composed of the ␣7 gene product and having a relative calcium permeability equivalent to that of NMDA receptors. The ␣7-containing receptors can be found presynaptically where they modulate transmitter release, and postsynaptically where they generate excitatory responses. They can also be found in perisynaptic locations where they modulate other inputs to the neuron and can activate a variety of downstream signaling pathways. The effects the receptors produce depend critically on the sites at which they are clustered. Instructive preparations for examining ␣7-containing receptors are the rat hippocampus, where they are thought to play a modulatory role, and the chick ciliary ganglion, where they participate in throughput transmission as well as regulatory signaling. Relatively high levels of ␣7-containing receptors are found in the two preparations, and the receptors display a variety of synaptic options and functions in the two cases. Progress is starting to be made in understanding the mechanisms responsible for localizing the receptors at specific sites and in identifying components tethered in the vicinity of the receptors that may facilitate signal transduction and downstream signaling.

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“…Previously, we found that the ␣7 nAChR subtype is required for the nicotine-elicited elevation of TH mRNA in PC12 cells. Moreover, ␣7 receptor agonists were at least as effective as nicotine in triggering these effects (Gueorguiev et al, 2000). The ␣7 subunits can form a homopentameric receptor, which is reported to desensitize rapidly compared with other nAChR subtypes.…”

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confidence: 99%

Involvement of α7 Nicotinic Acetylcholine Receptors in Gene Expression of Dopamine Biosynthetic Enzymes in Rat Brain

Serova

Sabban

2002

J Pharmacol Exp Ther

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Brain dopaminergic systems are critical in mediating the physiological responses to nicotine. The effects of several concentrations of nicotine (0.08, 0.17, or 0.33 mg/kg body weight) and involvement of ␣7 nicotinic acetylcholine receptors (nAChRs) in gene expression of key enzymes in dopamine biosynthesis were evaluated in the ventral tegmental area (VTA) and substantia nigra (SN), cell bodies of the mesocorticolimbic and nigrostriatal pathways. Nicotine elicited a dose-dependent elevation of mRNA for tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis in VTA and SN. The VTA was more sensitive to lower concentrations of nicotine with maximal response observed with the lowest dose of nicotine. Nicotine also elevated mRNA levels of GTP cyclohydrolase I (GTPCH), rate limiting in biosynthesis of TH's essential cofactor tetrahydrobiopterin in both dopaminergic locations. The changes in TH and GTPCH mRNAs were correlated. Pretreatment with the ␣7 nAChR antagonist methyllycaconitine prevented the nicotine-induced rise in TH or GTPCH mRNA in VTA and SN. Administration of ␣7 nAChR agonist 3-[2,4-dimethoxybenzilidene]anabaseine at 1 to 10 mg/kg or (E,E-3-(cinnamylidene)anabaseine at 0.3 to 1 mg/kg increased TH mRNA in VTA and SN, but not in peripheral catecholaminergic cells. Thus, agonists of ␣7 nAChRs have therapeutic potential for increasing TH gene expression in dopaminergic regions without some of nicotine's disadvantages, such as its harmful effects on the cardiovascular system. The findings indicate that nicotine may regulate dopamine biosynthesis by alterations in gene expression of TH and its cofactor. The ␣7 nAChRs are involved in mediating these effects of nicotine.Catecholaminergic systems are critical in mediating the physiological effects of nicotine. The self-administering and reinforcing properties of nicotine seem to arise from direct action on the mesocorticolimbic dopamine system. This system, with cell bodies in VTA, plays a key role in mediating the reinforcing effects of natural rewards as well as of drugs of abuse, including nicotine, through increased dopaminergic transmission in the nucleus accumbens. The nigrostriatal dopaminergic system, with cell bodies in the SN, innervates the caudate nucleus and putamen of the corpus striatum. Activation of striatal neuronal acetylcholine receptors (nAChRs) triggers release of dopamine. These receptors are also involved in mediating nicotine's effects on locomotion.

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Involvement of α7 Nicotinic Acetylcholine Receptors in Activation of Tyrosine Hydroxylase and Dopamine β‐Hydroxylase Gene Expression in PC12 Cells

Cited by 53 publications

References 53 publications

Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system

Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system

Nicotinic α7 receptors: Synaptic options and downstream signaling in neurons

Involvement of α7 Nicotinic Acetylcholine Receptors in Gene Expression of Dopamine Biosynthetic Enzymes in Rat Brain

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