Spatial memory decline after masticatory deprivation and aging is associated with altered laminar distribution of CA1 astrocytes
1 Universidade Federal do Pará-UFPA, Instituto de Ciências Biológicas, Laboratório de Investigações em Neurodegeneração e Infecção, Hospital Universitário João de Barros Barreto, Belém, PA, Brazil
2 Departamento de Arbovirologia e Febres Hemorrágicas, Instituto Evandro Chagas, IEC, Ananindeua, PA, Brazil
3 Southampton Neuroscience Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
4 Laboratório de Investigações em Neurodegeneração e Infecção, ICB/HUJBB/UFPA, Rua dos Mundurucus, 4487, Guamá, Belém, PA CEP:66073-000, Brazil
BMC Neuroscience 2012, 13:23 doi:10.1186/1471-2202-13-23Published: 29 February 2012
Chewing imbalances are associated with neurodegeneration and are risk factors for senile dementia in humans and memory deficits in experimental animals. We investigated the impact of long-term reduced mastication on spatial memory in young, mature and aged female albino Swiss mice by stereological analysis of the laminar distribution of CA1 astrocytes. A soft diet (SD) was used to reduce mastication in the experimental group, whereas the control group was fed a hard diet (HD). Assays were performed in 3-, 6- and 18-month-old SD and HD mice.
Eating a SD variably affected the number of astrocytes in the CA1 hippocampal field, and SD mice performed worse on water maze memory tests than HD mice. Three-month-old mice in both groups could remember/find a hidden platform in the water maze. However, 6-month-old SD mice, but not HD mice, exhibited significant spatial memory dysfunction. Both SD and HD 18-month-old mice showed spatial memory decline. Older SD mice had astrocyte hyperplasia in the strata pyramidale and oriens compared to 6-month-old mice. Aging induced astrocyte hypoplasia at 18 months in the lacunosum-moleculare layer of HD mice.
Taken together, these results suggest that the impaired spatial learning and memory induced by masticatory deprivation and aging may be associated with altered astrocyte laminar distribution and number in the CA1 hippocampal field. The underlying molecular mechanisms are unknown and merit further investigation.