Neurophysiological abnormalities in cultured dorsal root ganglion neurons from the trisomy-16 mouse fetus, a model for Down syndrome

B Ault; P Caviedes; S I Rapoport

doi:10.1016/0006-8993(89)90678-1

Neurophysiological abnormalities in cultured dorsal root ganglion neurons from the trisomy-16 mouse fetus, a model for Down syndrome

Brain Res. 1989 Apr 17;485(1):165-70. doi: 10.1016/0006-8993(89)90678-1.

Authors

B Ault¹, P Caviedes, S I Rapoport

Affiliation

¹ Laboratory of Neurosciences, National Institute on Aging, Bethesda, MD 20892.

PMID: 2524240
DOI: 10.1016/0006-8993(89)90678-1

Abstract

The trisomy-16 mouse is considered to be a model of human trisomy-21 (Down syndrome). We have examined the electrical membrane properties of cultured dorsal root ganglion (DRG) neurons from normal and trisomy-16 fetuses. Trisomy-16 neurons had significantly accelerated rates of action potential depolarization and repolarization compared to diploid neurons, resulting in decreased spike duration. These changes match those reported in human trisomy-21 DRG neurons. Such abnormalities may contribute to the mental retardation characteristic of Down syndrome.

MeSH terms

Action Potentials
Animals
Cells, Cultured
Disease Models, Animal
Down Syndrome / physiopathology*
Ganglia, Spinal / cytology
Ganglia, Spinal / physiopathology*
Membrane Potentials
Mice