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Neuroscience. 2016 Jun 2;324:330-43. doi: 10.1016/j.neuroscience.2016.03.016. Epub 2016 Mar 11.

Calbindin-D-28K like immunoreactivity in superficial dorsal horn neurons and effects of sciatic chronic constriction injury.

Author information

1
School of Medical Sciences and Health Innovations Research Institute, RMIT University, Bundoora 3083, Victoria, Australia.
2
Department of Pharmacology, University of Alberta, Edmonton, T6G 2H7 Alberta, Canada.
3
Department of Pharmacology, University of Alberta, Edmonton, T6G 2H7 Alberta, Canada; Neuroscience and Mental Health Institute, University of Alberta, Edmonton, T6G 2H7 Alberta, Canada. Electronic address: pas3@ualberta.ca.

Abstract

The neuropathic pain that results from peripheral nerve injury is associated with alterations in the properties of neurons in the superficial spinal laminae. Chronic constriction injury (CCI) of the rat sciatic nerve increases excitatory synaptic drive to excitatory neurons in the substantia gelatinosa while limiting that to inhibitory neurons. Since the calcium-binding protein calbindin D-28K has been associated with excitatory neurons, we examined whether CCI altered the properties of neurons expressing calbindin-like immunoreactivity (Cal+). These account for 30% of the neurons in lamina I and II. Calbindin did not co-localize with any particular electrophysiological phenotype of neuron; in substantia gelatinosa, it was found in some tonic, delay, irregular, phasic and transient firing neurons and in some cells that displayed central, radial or vertical morphology. When neuronal phenotype was defined more precisely in terms of both morphology and electrophysiological properties, no strong correlation with calbindin expression was found. The frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSC) in calbindin negative (Cal-) neurons was greater than that in Cal+ neurons. CCI did not alter the proportion of Cal+ neurons in the dorsal horn. Although CCI promoted a fourfold increase in sEPSC frequency in Cal+ neurons, sEPSC amplitude was reduced by 22% and charge transfer per second was unchanged. Since synaptic drive to Cal+ neurons is weak and there is no firm correlation between neuronal phenotype and calbindin expression, it is doubtful whether these neurons play a major role in the generation of central sensitization.

KEYWORDS:

calcium-binding protein; electrophysiology; nerve injury; neuronal morphology; neuropathic pain; substantia gelatinosa

[Indexed for MEDLINE]

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