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Firing properties of Renshaw cells defined by Chrna2 are modulated by hyperpolarizing and small conductance ion currents I h and I SK
Author(s) -
Perry Sharn,
Gezelius Henrik,
Larhammar Martin,
Hilscher Markus M.,
Lamotte d'Incamps Boris,
Leao Katarina E.,
Kullander Klas
Publication year - 2015
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12852
Subject(s) - renshaw cell , neuroscience , electrophysiology , apamin , chemistry , membrane potential , patch clamp , spinal cord , interneuron , cholinergic , hyperpolarization (physics) , potassium channel , biophysics , microbiology and biotechnology , biology , inhibitory postsynaptic potential , organic chemistry , nuclear magnetic resonance spectroscopy
Renshaw cells in the spinal cord ventral horn regulate motoneuron output through recurrent inhibition. Renshaw cells can be identified in vitro using anatomical and cellular criteria; however, their functional role in locomotion remains poorly defined because of the difficulty of functionally isolating Renshaw cells from surrounding motor circuits. Here we aimed to investigate whether the cholinergic nicotinic receptor alpha2 ( Chrna2 ) can be used to identify Renshaw cells ( RC s α2 ) in the mouse spinal cord. Immunohistochemistry and electrophysiological characterization of passive and active RC s α2 properties confirmed that neurons genetically marked by the Chrna2 ‐Cre mouse line together with a fluorescent reporter mouse line are Renshaw cells. Whole‐cell patch‐clamp recordings revealed that RC s α2 constitute an electrophysiologically stereotyped population with a resting membrane potential of −50.5 ± 0.4 mV and an input resistance of 233.1 ± 11 MΩ. We identified a ZD 7288‐sensitive hyperpolarization‐activated cation current ( I h ) in all RC s α2 , contributing to membrane repolarization but not to the resting membrane potential in neonatal mice. Additionally, we found RC s α2 to express small calcium‐activated potassium currents ( I SK ) that, when blocked by apamin, resulted in a complete attenuation of the afterhyperpolarisation potential, increasing cellular firing frequency. We conclude that RC s α2 can be genetically targeted through their selective Chrna2 expression and that they display currents known to modulate rebound excitation and firing frequency. The genetic identification of Renshaw cells and their electrophysiological profile is required for genetic and pharmacological manipulation as well as computational simulations with the aim to understand their functional role.