Research Article

Experimental Brain Research

, Volume 187, Issue 3, pp 459-465

First online:

Distribution of parvalbumin and calretinin immunoreactive interneurons in motor cortex from multiple sclerosis post-mortem tissue

  • Robert J. ClementsAffiliated withDepartment of Biological/Biomedical Sciences, A330 Cunningham Hall, Kent State University Email author 
  • , Jennifer McDonoughAffiliated withOak Clinic for Multiple Sclerosis Research, School of Biomedical Sciences, Kent State University
  • , Ernest J. FreemanAffiliated withOak Clinic for Multiple Sclerosis Research, School of Biomedical Sciences, Kent State University

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access


Parvalbumin (PV) and calretinin (CR) are calcium binding proteins (CBP’s) expressed in discrete GABAergic interneuron populations in the human cortex. CBP’s are known to buffer calcium concentrations and protect neurons from increases in intracellular calcium. Perturbations in intracellular calcium can activate proteolytic enzymes including calpain, leading to deleterious effects to axons. Ca++-mediated mechanisms have been found to be associated with axonal pathology in MS and the restructuring of calcium channels has been shown to occur in experimental autoimmune encephalomyelitis (EAE) as well as multiple sclerosis tissue. Previous data indicates a reduction in the expression of the parvalbumin gene as well as reduced extension of neurites on parvalbumin expressing interneurons within multiple sclerosis normal appearing grey matter (NAGM). Modifications in interneuron parvalbumin or calretinin levels could change calcium buffering capacity, as well as the way these cells respond to neuronal insults. The present study was designed to compare CBP immunoreactive neurons in normal and multiple sclerosis post-mortem NAGM. To this end, we utilized immunofluorescent staining and high resolution confocal microscopy to map regions of the human motor cortex, and characterize layer specific CBP distribution in the normal and multiple sclerosis motor cortex. Our results indicate a significant reduction in the number of PV interneurons within layer 2 of the multiple sclerosis primary motor cortex with no concurrent change in number of calretinin positive neurons.