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P0289 - Aging in C57B/6 mice is accompanied by a decrease of Purkinje cells and changes in open field motor activity

Published online by Cambridge University Press:  16 April 2020

E. Maloku
Affiliation:
University of Illinois, Chicago, IL, USA
I. Rivero-Covelo
Affiliation:
University of Illinois, Chicago, IL, USA
I. Hanbauer
Affiliation:
University of Illinois, Chicago, IL, USA
A. Guidotti
Affiliation:
University of Illinois, Chicago, IL, USA
E. Costa
Affiliation:
University of Illinois, Chicago, IL, USA

Abstract

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Purkinje cells are among the most vulnerable neurons, therefore during aging a decrease in these cells in the cerebellar cortex may have a functional impact.

Here we prepared cerebellar serial sections (10 micrometers) in the sagittal plane from adult (3-5 months) and old (25 months) C57BL/6 mice. After staining with 3% cresyl violet, the Purkinje cells were counted in every 40th section in various regions of the cerebellum (10X magnification, Olympus microscope).

The number of Purkinje cells in old mice was lower than in adult mice. In particular, the decrease was 41% in the flocculus (10.4±0.97 versus 17.6±1.8; p<0.005), 38% in the paraflocculus (10.0±0.48 versus 15.8±7.3; p<0.0001), and 26% in the ansiform lobule (10.2±0.65 versus 13.7±1.7; p<0.04).

Measurement of motor activity in adult and old mice showed no changes in horizontal or vertical activity. However, old mice moved a significantly shorter distance in the open field margin (141±13.2 cm/15 min) than adult mice (220± 20.7 cm/15 min; p<0.001). In addition, old mice spent less time in the open field margin (291±36.9 sec/15min) than adult mice (609±36.9 sec/15 min; p<0.0001). Consequently, the time spent in the center was significantly greater in old mice (525±29.9 sec/15min) than in adult mice (291±36.9 sec/15min; p<0.0001.

The present data suggest that abnormalities in cerebellar cortical–pontine circuitry may impair movement. However, the lack of anxiety, indicated by the increased time spent in the open field center, suggests that a defect in the cerebral cortical-hippocampal-amygdala circuitry of old mice should be investigated.

Type
Poster Session III: Miscellaneous
Copyright
Copyright © European Psychiatric Association 2008
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