The Effect of Calcium Ions on Mechanosensation and Neuronal Activity in Proprioceptive Neurons

Author:

Atkins Devan E.,Bosh Kimberly L.,Breakfield Grace W.,Daniels Sydney E.,Devore Makayla J.,Fite Hailey E.,Guo Landys Z.,Henry Danielle K. J.,Kaffenberger Alana K.,Manning Katherine S.,Mowery Tatum E.,Pankau Cecilia L.ORCID,Parker Nyla,Serrano Malina E.,Shakhashiro Yamaan,Tanner Hannah N.,Ward Ruth. A.,Wehry Aubrey. H.,Cooper Robin L.ORCID

Abstract

Proprioception of all animals is important in being able to have coordinated locomotion. Stretch activated ion channels (SACs) transduce the mechanical force into electrical signals in the proprioceptive sensory endings. The types of SACs vary among sensory neurons in animals as defined by pharmacological, physiological and molecular identification. The chordotonal organs within insects and crustaceans offer a unique ability to investigate proprioceptive function. The effects of the extracellular environment on neuronal activity, as well as the function of associated SACs are easily accessible and viable in minimal saline for ease in experimentation. The effect of extracellular [Ca2+] on membrane properties which affect voltage-sensitivity of ion channels, threshold of action potentials and SACs can be readily addressed in the chordotonal organ in crab limbs. It is of interest to understand how low extracellular [Ca2+] enhances neural activity considering the SACs in the sensory endings could possibly be Ca2+ channels and that all neural activity is blocked with Mn2+. It is suggested that axonal excitability might be affected independent from the SAC activity due to potential presence of calcium activated potassium channels (K(Ca)) and the ability of Ca2+ to block voltage gated Na+ channels in the axons. Separating the role of Ca2+ on the function of the SACs and the excitability of the axons in the nerves associated with chordotonal organs is addressed. These experiments may aid in understanding the mechanisms of neuronal hyperexcitability during hypocalcemia within mammals.

Funder

National Institutes of Health Clinical Center

Publisher

MDPI AG

Subject

General Medicine

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