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Activation mechanism of a neuromodulator-gated pacemaker ionic current
Michael Gray1,2, Daniel H Daudelin2, Jorge Golowasch3
1Behavioral and Neural Science Graduate Program, Rutgers University-Newark, Newark, New Jersey; and.
Journal of Neurophysiology
|April 28, 2017
Summary
Neuromodulator-gated currents (IMI) crucial for rhythmic activity in crab neural networks are activated by G proteins. This activation depends on calcium and calmodulin, not PLC or cyclic nucleotides.
Area of Science:
- Neuroscience
- Cellular Electrophysiology
- Signal Transduction
Background:
- Neuromodulator-gated currents (IMI) are essential for rhythmic activity in the crustacean pyloric network.
- Understanding IMI activation provides insights into neural oscillations and regulation of other ionic currents.
Purpose of the Study:
- To elucidate the specific signaling molecules involved in neuromodulator receptor activation of IMI.
- To investigate the roles of G proteins, calcium, calmodulin, and other pathways in IMI activation.
Main Methods:
- Utilized a battery of agonists and antagonists for common signal transduction pathways.
- Applied G protein inhibitors (GDPβS) and activators (GTPγS).
- Used pertussis toxin and antagonists for calcium- and calmodulin-associated signaling.
Main Results:
- G protein modulators GDPβS and GTPγS significantly affected IMI amplitude.
- Pertussis toxin inhibited IMI amplitude in a calcium-dependent manner.
- Calcium- and calmodulin-associated signaling antagonists reduced IMI amplitude; PLC and cyclic nucleotide signaling showed minimal involvement.
Conclusions:
- Proctolin-induced IMI is mediated by a G protein sensitive to pertussis toxin, with calcium-dependent regulation.
- Intracellular calcium, calmodulin, and calmodulin-activated kinases are critical for IMI activation.
- Phospholipase C (PLC) signaling and cyclic nucleotides do not appear to mediate IMI.
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