Calbindin-D-28K like immunoreactivity in superficial dorsal horn neurons and effects of sciatic chronic constriction injury. (2nd June 2016)

• Record Type: Journal Article
• Authors: Stebbing, M.J.; Balasubramanyan, S.; Smith, P.A.
• Is Part Of: Neuroscience. Volume 324(2016)
• Page Start: 330
• Page End: 343
• Publication Date: 2016-06-02
• Subjects: Cal− not displaying calbindin-D-28K immunoreactivity -- Cal+ displaying calbindin-D-28K immunoreactivity -- CCI chronic constriction injury (of sciatic nerve) -- EGTA (ethylene glycol tetraacetic acid -- HEPES 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid -- K–S Kolmogorov-Smirnoff (statistics) -- Lamina IIi inner portion of substantia gelatinosa -- Lamina IIo outer portion of substantia gelatinosa -- NHS Normal Horse Serum -- PBS phosphate-buffered saline -- sEPSC spontaneous excitatory postsynaptic current; substantia gelatinosa -- nerve injury -- electrophysiology -- neuropathic pain -- neuronal morphology -- calcium-binding protein; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2016.03.016
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: Calbindin D-28K is found in 30% of neurons in spinal dorsal laminae I and II. Calbindin does not associate with specific electrophysiological phenotype. Calbindin may associate with putative excitatory neurons and is found in some radial, vertical and central neurons. Calbindin containing neurons receive relatively weak excitatory synaptic drive. Altered synaptic drive to calbindin neurons does not contribute to central sensitization in neuropathic pain. 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.