Nicotine and epibatidine triggered prolonged rise in calcium and TH gene transcription in PC12 cells

Gueorguiev, Volodia D.; Frenz, Christopher M.; Ronald, Kimberly M.; Sabban, Esther L.

doi:10.1016/j.ejphar.2004.10.045

Cited by 7 publications

(10 citation statements)

References 54 publications

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“…The relative potencies of the PKA and CaMKII pathways for mediating Ca 2+ ‐dependent TH gene expression in PC12 cells are unclear because co‐treatments that elevate Ca 2+ and cAMP together have been reported to have either additive (Kilbourne et al. 1992) or no additive effects on TH (Gueorguiev et al. 2004) compared with either treatment alone.…”

Section: Ca2+‐sensitive Regulatory Elements In the Th Gene Promoter Amentioning

confidence: 99%

“…Another Ca 2+ -dependent kinase, PKC, has also been implicated (Raymond and Millhorn 1997), but see (Kilbourne et al 1992), which may act through the AP-1 site (Sabban 1997). The relative potencies of the PKA and CaMKII pathways for mediating Ca 2+ -dependent TH gene expression in PC12 cells are unclear because co-treatments that elevate Ca 2+ and cAMP together have been reported to have either additive (Kilbourne et al 1992) or no additive effects on TH (Gueorguiev et al 2004) compared with either treatment alone. However, using selective inhibitors, Gueorguiev et al (2006) conclude they are equally potent.…”

Section: Evidence For Activity-and Ca 2+ -Dependent Regulation Of Th mentioning

confidence: 99%

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Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Aumann

Horne

2012

Journal of Neurochemistry

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The impetus behind this review is the question of whether the dopamine (DA) phenotype of neurons in the substantia nigra pars compacta (SNc) is activity-dependent. SNc DA neurons control movement through their projections to, and DA signaling in the dorsal striatum (the nigrostriatal pathway). Abnormal reduction of nigrostriatal DA signaling causes the motor symptoms of Parkinson's disease (PD), and abnormal DA signaling originating from the ventral midbrain generally (i.e. the nigrostriatal and mesocorticolimbic pathways) is thought to underlie symptoms of schizophrenia, drug addiction, and depression. The possibility that the DA phenotype of SNc neurons is activity-dependent is therefore intriguing from the viewpoints of neurobiology, behavior, and neurological disorders.Gene expression in neurons is activity-and Ca 2+ -dependent. More specifically, gene expression is sensitive to

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Section: Ca2+‐sensitive Regulatory Elements In the Th Gene Promoter Amentioning

confidence: 99%

Section: Evidence For Activity-and Ca 2+ -Dependent Regulation Of Th mentioning

confidence: 99%

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Aumann

Horne

2012

Journal of Neurochemistry

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“…The immediate early genes regulate the transcription of downstream targets that have diverse roles in signalling, cell growth and cell maintenance. Recently, Gene-array technology indicates that nicotine administration might affect numerous genes, including those involved in intracellular signalling, transcription, translation, CREB phosphorylation (Gueorguiev et al, 2004), transmitter receptors, ion channel signalling pathways (Sun et al, 2004) and proteins associated with RNA binding and the plasma membrane (Dunckley and Lukas, 2003). We used Rat Genome U34A Affymetrix GeneChip arrays to find in the rat parietal cortex new genes responsive to acute intermittent nicotine treatment and linked to neuroprotection .…”

Section: Molecular Mechanisms Mediating Neurotrophic Effects Of Nachrmentioning

confidence: 99%

Nicotinic receptor agonists as neuroprotective/neurotrophic drugs. Progress in molecular mechanisms

2006

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Summary In the present work we reviewed recent advances concerning neuroprotective=neurotrophic effects of acute or chronic nicotine exposure, and the signalling pathways mediating these effects, including mechanisms implicated in nicotine addiction and nAChR desensitization. Experimental and clinical data largely indicate long-lasting effects of nicotine and nicotinic agonists that imply a neuroprotective=neurotrophic role of nAChR activation, involving mainly a7 and a4b2 nAChR subtypes, as evidenced using selective nAChR agonists. Compounds interacting with neuronal nAChRs have the potential to be neuroprotective and treatment with nAChR agonists elicits long-lasting neurotrophic effects, e.g. improvement of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Nicotine addiction, which is mediated by interaction with nACh receptors, is believed to involve the modification of signalling cascades that modulate synaptic plasticity and gene expression. Desensitization, in addition to protecting cells from uncontrolled excitation, is recently considered as a form of signal plasticity. nAChR can generate these longe-lasting effects by elaboration of complex intracellular signals that mediate medium to long-term events crucial for neuronal maintenance, survival and regeneration. Although a comprehensive survey of the gene-based molecular mechanisms that underlie nicotine effects has yet not been performed a growing amount of data is beginning to improve our understanding of signalling mechanisms that lead to neurotrophic=neuroprotective responses. Evidence for an involvement of the fibroblast growth factor-2 gene in nAChR mechanisms mediating neuronal survival, trophism and plasticity has been obtained. However, more work is needed to establish the mechanisms involved in the effects of nicotinic receptor subtype activation from cognition-enhancing and neurotrophic effects to smoking behaviour and to determine more precisely the therapeutic objectives in potential nicotinic drug treatments of neurodegenerative diseases.

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“…2000), hippocampal mossy fibre terminals (Sharma and Vijayaraghavan 2003), neuronal cell lines (Dajas‐Bailador et al . 2002; Gueorguiev et al . 2004), hippocampal astrocytes (Sharma and Vijayaraghavan 2001) and nerve terminals innervating the mouse vas deferens (Brain et al .…”

mentioning

confidence: 99%

Differential coupling of α7 and non‐α7 nicotinic acetylcholine receptors to calcium‐induced calcium release and voltage‐operated calcium channels in PC12 cells

Dickinson

Hanrott

Mok

et al. 2006

Journal of Neurochemistry

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Neuronal nicotinic acetylcholine receptors (nAChRs) are ligand-gated cation channels that can modulate various neuronal processes by altering intracellular Ca 2+ levels. Following nAChR stimulation Ca 2+ can enter cells either directly, through the intrinsic ion channel, or indirectly following voltage-operated Ca 2+ channel (VOCC) activation; Ca 2+ levels can subsequently be amplified via Ca 2+ -induced Ca 2+ release from intracellular stores. We have used subtype-selective nAChR agonists to investigate the Ca 2+ sources contributing to a7 and non-a7 nAChR-mediated increases in intracellular Ca 2+ in PC12 cells. Application of the a7 nAChR positive allosteric modulator PNU 120596 (10 lM), in conjunction with the a7 nAChR agonist, compound A [(R)-N-(1-azabicyclo [2.2.2]oct-3-yl)(5-(2-pyridyl)thiophene-2-carboxamide), 10 nM], produces a rapid increase in fluo-3 fluorescence that is prevented by the selective a7 nAChR antagonist a-bungarotoxin. The non-a7 nAChR agonist 5-Iodo-A-85380 produces a-bungarotoxin-insensitive increases in intracellular Ca 2+ (EC 50 ¼ 11.2 lM). Using these selective agonists or KCl in conjunction with general and selective VOCC inhibitors, we demonstrate that the primary route of Ca 2+ entry following either non-a7 nAChR activation or KCl stimulation is via L-type VOCCs. In contrast, the a7 nAChR-mediated response is unaffected by VOCC blockers but is inhibited by modulators of intracellular Ca 2+ stores. These results indicate that a7 and non-a7 nAChRs are differentially coupled to Ca 2+ -induced Ca 2+ release and VOCCs, respectively.

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Nicotine and epibatidine triggered prolonged rise in calcium and TH gene transcription in PC12 cells

Cited by 7 publications

References 54 publications

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Nicotinic receptor agonists as neuroprotective/neurotrophic drugs. Progress in molecular mechanisms

Differential coupling of α7 and non‐α7 nicotinic acetylcholine receptors to calcium‐induced calcium release and voltage‐operated calcium channels in PC12 cells

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