Differential Regulation of Type I and Type VIII Ca2+-stimulated Adenylyl Cyclases by Gi-coupled Receptors in Vivo
Open accessAbstract
Coupling of intracellular Ca2+ to cAMP increases may be important for some forms of synaptic plasticity. The type I adenylyl cyclase (I-AC) is a neural-specific, Ca2+-stimulated enzyme that couples intracellular Ca2+ to cAMP increases. Since optimal cAMP levels may be crucial for some types of synaptic plasticity, mechanisms for inhibition of Ca2+-stimulated adenylyl cyclases may also be important for neuroplasticity. Here we report that Ca2+ stimulation of I-AC is inhibited by activation of Gi-coupled somatostatin and dopamine D2L receptors. This inhibition is due primarily to Gialpha and not betagamma subunits since coexpression of betagamma-binding proteins with I-AC did not affect somatostatin inhibition. However, betagamma released from Gs did inhibit I-AC, indicating that the enzyme can be inhibited by betagamma in vivo. Interestingly, type VIII adenylyl cyclase (VIII-AC), another Ca2+-stimulated adenylyl cyclase, was not inhibited by Gi-coupled receptors. These data indicate that I-AC and VIII-AC are differentially regulated by Gi-coupled receptors and provide distinct mechanisms for interactions between the Ca2+ and cAMP signal transduction systems. We propose that I-AC may be particularly important for synaptic plasticity that depends upon rapid and transient cAMP increases, whereas VIII-AC may contribute to transcriptional-dependent synaptic plasticity that is dependent upon prolonged, Ca2+-stimulated cAMP increases.
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AC8 is not stimulated by Gs-coupled receptors, even in the presence of Ca2+.
“The Ca 2ϩ sensitivity of AC8 is approximately five times lower than AC1 (Villacres et al., 1995), and it is not stimulated by G s -coupled receptors, even in the presence of Ca 2ϩ (Nielsen et al., 1996).”
From Type I Adenylyl Cyclase Mutant Mice Have Impaired Mossy Fiber Long-Term Potentiation (1998) · cites this paper as Nielsen et al., 1996
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Type I Adenylyl Cyclase Mutant Mice Have Impaired Mossy Fiber Long-Term Potentiation
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Self-citationCloning, Chromosomal Mapping, and Regulatory Properties of the Human Type 9 Adenylyl Cyclase (ADCY9)
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- Authors
- Nielsen, M. D., Chan, G. C. K., Poser, S. W., & Storm, D. R.
- Affiliations
- University of Washington (US)
- Corresponding author
- Storm, Daniel R.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1996-12
- Volume
- 271
- Issue
- 52
- Pages
- 33308-33316
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2066753814
- Cited by
- 88
- References
- 7
- Citations by year
- 2025: 1 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 3 · 2013: 5 · 2012: 3
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- Gi-coupled receptors, somatostatin receptors, G protein alpha subunit, cAMP signaling, intracellular calcium, synaptic plasticity, enzyme inhibition, signal transduction
- MeSH terms
- Calcimycin, Cyclic AMP, Adenylyl Cyclases, Calcium, Carbachol, Cell Line, Dopamine, Humans, Isoproterenol, Membrane Proteins, Nerve Tissue Proteins, Virulence Factors, Bordetella, Somatostatin, Transducin, GTP-Binding Protein alpha Subunits, Gi-Go, Adenylate Cyclase Toxin
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