Chandelier cell axons identified by parvalbumin-immunoreactivity in the normal human temporal cortex and in Alzheimer's disease

Abstract

Parvalbumin is a calcium-binding protein which is thought to play a role in neuronal excitability. In the cerebral cortex parvalbumin is largely found in two subsets of GABAergic neurons, the chandelier and basket cells. A distinguishing characteristic of the chandelier cell is that the terminal portions of its axon form short vertical strings of boutons resembling candlesticks, which embrace the initial segment of pyramidal cell axon. In the present study, the terminals of chandelier cells in the human temporal cortex were immunostained with an antibody against parvalbumin. These terminals were found more abundantly in layers II and VI, less frequently in layers III and V, were hardly identified in layer IV, and absent in layer I. The relationship of parvalbumin-immunoreactive terminals and axon initial segments was further evidenced by re-sectioning identified rows of boutons into semithin sections. Electron microscopy of both temporal cortex and the somatosensory region of a biopsy sample revealed that these parvalbumin-positive boutons indeed form symmetric synaptic contacts on the axon initial segments of pyramidal cells. As part of an enquiry into the possibility that these specialized interneurons may be involved in degenerative neurological diseases, the temporal lobes from seven patients with Alzheimer's disease were immunostained for parvalbumin. As in the control brains, the specific terminal portions of chandelier cells were recognized and identified in the temporal cortex by parvalbumin-immunocytochemistry. No major difference from normal brains was found, excepting for a lower density of candlesticks (30–35%) in layer II–III. Since we showed in a previous study [Ferrer et al. (1991) J. neurol. Sci. 106, 135–141] that the number of parvalbumin-immunoreactive somata in the same Alzheimer's disease cases was not decreased, the observed reduction of terminals in layer II suggest that only the terminals of chandelier cells, but not the parent neurons, are decreased in Alzheimer's disease.