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Cyclic ADP-ribose as a potential second messenger for neuronal Ca2+ signaling
H Higashida1, M Hashii, S Yokoyama
1Department of Biophysical Genetics, Molecular Medicine and Bioinformatics, Kanazawa University Graduate School of Medicine, Japan. haruhiro@med.kanazawa-u.ac.jp
Journal of Neurochemistry
|February 24, 2001
Summary
Cyclic ADP-ribose (cADPR) acts as a second messenger in the nervous system, modulating calcium signaling and acetylcholine release. Its synthesis and activity are regulated by various cellular mechanisms, suggesting a key role in neuronal function.
Area of Science:
- Neuroscience
- Cellular Signaling
- Biochemistry
Background:
- Cyclic ADP-ribose (cADPR) is an endogenous modulator of ryanodine receptor Ca2+ channels found in the nervous system.
- cADPR influences intracellular Ca2+ concentration ([Ca2+]i) and potentiates depolarization-induced Ca2+ influx.
- It also facilitates acetylcholine release from cholinergic neurons and modulates ion currents.
Purpose of the Study:
- To investigate the role of cADPR as a second messenger in neuronal Ca2+ signaling.
- To elucidate the synthesis, regulation, and functional effects of cADPR in the nervous system.
Main Methods:
- Injection of cADPR into neuronal cells.
- Analysis of cADPR synthesis and hydrolase activity in membrane and cytosolic fractions.
- Investigation of ADP-ribosyl cyclase activation via receptor stimulation.
Main Results:
- cADPR induces transient elevations in [Ca2+]i and potentiates depolarization-induced Ca2+ increases.
- Both membrane-bound and cytosolic ADP-ribosyl cyclase synthesize cADPR in neurons.
- Cytosolic cyclase activity is upregulated by NO/cGMP-dependent phosphorylation, while membrane-bound cyclase is activated by G protein-coupled receptors.
Conclusions:
- cADPR functions as a second messenger in neuronal Ca2+ signaling.
- Its synthesis and regulation involve complex enzymatic and signaling pathways.
- Further research is needed to fully confirm its identity and role in the nervous system.