Inhibitory Interneurons of The Human Neocortex after Clinical Death

Abstract

Objective: to analyze the human neocortex interneurons (areas 4, 10, 17 and 21 by Brodmann) after cardiac arrest (clinical death).Materials and methods. The main group included patients (n=7, men) who survived 7—10 days and 70—90 days after cardiac arrest and later died due to heart failure. The control group (n=4, men) included individuals after sudden fatal accidents. The morphometric and histological analysis of 420 neocortical fields (Nissl#staining,calbindin D28k, neuropeptide Y) was performed using light and confocal microscopy.Results. We verified all main types of interneurons (Basket, Martinotti, and neurogliaform interneurons) in neocortex based on the morphology of their bodies and dendritic processes in both groups. The number of calbindin- and NPY-positive neurons in the neocortex was similar in the control and in the postoperative period.However, calbindin- and NPY-immunopositive structure fields including neuronal cell bodies and their dendrites were significantly more represented in neocortex of patients from the main group. Maximum increase in common square in the relative areas of calbindin-immunopositive structures was observed 90 days after ischemia. The squares of NPY#immunopositive fields became larger seven days after resuscitation and remained increased on 90th day post-resuscitation.Conclusion. Our findings demonstrate an increase of calbindin and NPY expression in human neocortex after clinical death, which can be explained by a compensatory eaction of undamaged inhibitory cortical interneurons directed to protectbrain from ischemia.

Keywords

• clinical death
• man
• neocortex
• inhibitory interneurons
• calbindin d28k
• neuropeptide y