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Voltage Dependence of a Neuromodulator-Activated Ionic Current.

Michael Gray¹, Jorge Golowasch²

¹Behavioral and Neural Science Graduate Program, Rutgers University-Newark, Newark, New Jersey 07102; Federated Department of Biological Sciences, New Jersey Institute of Technology, Newark, New Jersey 07102.

|June 4, 2016

Summary

The voltage dependence of a key neuronal current (IMI) in crabs is regulated by intracellular signaling pathways. This regulation involves calcium-sensing receptors and calmodulin, crucial for neural network oscillations.

Keywords:

activity calcium sensing receptor calcium-dependence central pattern generation crustacean stomatogastric

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Area of Science:

Neuroscience
Cellular Neuroscience
Computational Neuroscience

Background:

The neuromodulatory inward current (IMI) is vital for the oscillatory activity of the crab Cancer borealis stomatogastric ganglion's pyloric network.
IMI's voltage dependence is critical for this network function but is lost in low extracellular calcium.
Intracellular calmodulin has been implicated in regulating this calcium-dependent effect.

Purpose of the Study:

To investigate the hypothesis that intracellular signaling pathways activated by extracellular calcium mediate IMI's voltage dependence.
To elucidate the specific roles of calmodulin, CaMKII, and calcium-sensing receptors (CaSR) in regulating IMI voltage dependence.

Main Methods:

Utilized pharmacological inhibitors and activators targeting calmodulin, ryanodine receptors, CaMKII, endocytosis, and G-protein-coupled receptors.
Manipulated extracellular calcium concentrations to observe effects on IMI voltage dependence in crab neurons.
Investigated the downstream effects of CaSR activation, including myosin light chain kinase and Gβγ-subunits.

Main Results:

Calmodulin inhibitors and a ryanodine antagonist reduced IMI voltage dependence in normal calcium conditions.
Calmodulin activators failed to restore IMI voltage dependence in low calcium conditions, suggesting calmodulin is necessary but not sufficient.
Evidence suggests CaSR activation, G-protein signaling, and myosin light chain kinase are involved in maintaining IMI voltage dependence.

Conclusions:

The voltage dependence of IMI is actively regulated by intracellular signaling pathways initiated by extracellular calcium.
A G-protein-coupled calcium-sensing receptor (CaSR) likely plays a central role, with calmodulin and downstream effectors like myosin light chain kinase contributing.
These findings reveal a novel mechanism for regulating neuronal network activity through extracellular calcium sensing.