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Calmodulin and calmodulin kinase II mediate emergent bursting activity in the brainstem respiratory network
1Department of Neuro- and Sensory Physiology, Georg-August-University, Humboldtallee 23, 37073 Göttingen, Germany. smirono@gwdg.de
The Journal of Physiology
|December 5, 2012
Summary
Intracellular signaling pathways, including calmodulin (CaM) and CaM kinase (CaMKII), regulate respiratory network activity. CaMKII enhances synaptic transmission, strengthening rhythmic bursting in the preBötzinger complex.
Area of Science:
- Neuroscience
- Respiratory Physiology
- Cellular Signaling
Background:
- Persistent network activity is crucial for respiratory motor output.
- Intracellular signaling pathways controlling this activity are not fully understood.
- The preBötzinger complex (preBötC) is a key respiratory network.
Purpose of the Study:
- To investigate the role of intracellular signaling, specifically calmodulin (CaM) and CaM kinase (CaMKII), in regulating preBötC rhythmic activity.
- To elucidate the mechanisms by which these pathways influence bursting activity and synaptic transmission.
Main Methods:
- Utilized calcium imaging and patch-clamp electrophysiology in acute and organotypic brainstem slices.
- Applied stimuli such as hypoxia, electrical stimulation, and AMPA receptor activation.
- Employed pharmacological agents to chelate calcium, block channels, and inhibit CaM and CaMKII.
Main Results:
- Hypoxia, stimulation, and AMPA receptor activation transiently depressed, then augmented, preBötC bursting activity.
- These effects were dependent on intracellular calcium, CaM, and CaMKII.
- CaMKII augmented glutamatergic synaptic drive currents, indicating postsynaptic potentiation.
Conclusions:
- CaMKII-mediated facilitation of glutamatergic transmission strengthens emergent synchronous activity in the preBötC.
- This activity is maintained by calcium surges during bursts, modulated by ADP and TRPM4 channels.
- Findings suggest potential therapeutic implications for respiratory disorders involving autonomous activity deficits.
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