ArticleBritish journal of pharmacology2001
Involvement of protein kinase C in the presynaptic nicotinic modulation of [(3)H]-dopamine release from rat striatal synaptosomes..
Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 35 citations in OpenAlex.
- Translational Research in Nicotine Addiction.Cold Spring Harbor perspectives in medicine · 2021Review
- Cellular responses and functions of α7 nicotinic acetylcholine receptor activation in the brain: a narrative review.Annals of translational medicine · 2021Review
- Translational research in nicotine dependence.Cold Spring Harbor perspectives in medicine · 2013Review
- Neurotransmitter receptors and cognitive dysfunction in Alzheimer's disease and Parkinson's disease.Progress in neurobiology · 2012Review
- Dihydrotestosterone activates CREB signaling in cultured hippocampal neurons.Brain research · 2009Article
- Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system.Acta pharmacologica Sinica · 2009Review
- In vivo neurochemical characterization of anatoxin-a evoked dopamine release from striatum.Journal of neural transmission (Vienna, Austria : 1996) · 2007Article
- In vivo effects of the anatoxin-a on striatal dopamine release.Neurochemical research · 2006Article
- Nifedipine facilitates neurotransmitter release independently of calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Internalization and recycling of 5-HT2A receptors activated by serotonin and protein kinase C-mediated mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Presynaptic nicotinic ACh receptors modulate transmitter release in the brain. Here we report their interactions with protein kinase C (PKC) with respect to [(3)H]-dopamine release from rat striatal synaptosomes, monitored by superfusion. 2. Two specific PKC inhibitors, Ro 31-8220 (1 microM) and D-erythro-sphingosine (10 microM) significantly reduced (by 51 and 26% respectively) [(3)H]-dopamine release stimulated by anatoxin-a (AnTx), a potent and selective agonist of nicotinic ACh receptors. The inactive structural analogue of Ro 31-8220, bisindolylmaleimide V (1 microM) had no effect. 3. Two phorbol esters, PDBu (1 microM) and PMA (1 microM) potentiated AnTx-evoked [(3)H]-dopamine release by 50 - 80%. This was Ca(2+)-dependent and prevented by PKC inhibitors. In the absence of nicotinic agonist, phorbol esters enhanced basal release through a PKC-independent mechanism. 4. A (86)Rb(+) efflux assay of nicotinic ACh receptor function confirmed that Ro 31-8220 has no nonspecific effect on presynaptic nicotinic ACh receptors. 5. These results suggest that PKC is activated by nicotinic ACh receptor stimulation and mediates a component of AnTx-evoked [(3)H]-dopamine release. In addition, independent activation of PKC can further amplify the response, offering a potential mechanism for receptor crosstalk.
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