Age-related changes of structures in cerebellar cortex of cat

Abstract

We studied the structures of the cerebellar cortex of young adult and old cats for age-related changes, which were statistically analysed. Nissl staining was used to visualize the cortical neurons. The immunohistochemical method was used to display glial fibrillary acidic protein (GFAP)-immunoreactive (IR) astrocytes and neurofilament-immunoreactive (NF-IR) neurons. Under the microscope, the thickness of the cerebellar cortex was measured; and the density of neurons in all the layers as well as that of GFAP-IR cells in the granular layer was analysed. Compared with young adult cats, the thickness of the molecular layer and total cerebellar cortex was significantly decreased in old cats, and that of the granular layer increased. The density of neurons in each layer was significantly lower in old cats than in young adult ones. Astrocytes in old cats were significantly denser than in young adult ones, and accom-panied by evident hypertrophy of the cell bodies and enhanced immunoreaction of GFAP substance. Purkinje cells (PCs) in old cats showed much fewer NF-IR dendrites than those in young adults. The above findings indicate a loss of neurons and decrease in the number of dendrites of the PCs in the aged cerebellar cortex, which might underlie the functional decline of afferent efficacy and information integration in the senescent cerebellum. An age-dependent enhancement of activity of the astrocytes may exert a protective effect on neurons in the aged cerebellum.

Aging of cerebellar Purkinje cells

“…PCs are among the most vulnerable neurons in the brain (Patrick and Anderson 2000;Woodruff-Pak 2006;Servais et al 2007;Dhar et al 2007;Woodruff-Pak et al 2010) and are prone to aging insult (Quackenbush et al 1990;HadjSahraoui et al 2001;Andersen et al 2003;Zhang et al 2006). A complicated and disputed issue is whether the quantity of PCs decreases or remains constant during the normal aging process.…”

“…PC dendritic arborizations are profuse and approach the pial surface in young cerebellum, whereas old dendrites appear significantly atrophied (Quackenbush et al 1990;HadjSahraoui et al 2001;Zhang et al 2006). The height of PC dendrites (measured from the maximal point in the arbors perpendicularly to the PC layer) accounts for a large percentage of the molecular layer thickness in younger cerebellum, whereas that of the old PC dendrites occupies significantly less of the molecular layer thickness, despite a significant atrophy in the molecular layer during cerebellar aging (Hadj-Sahraoui et al 2001).…”

“…The parallel fibers arise from granule cells in the cerebellar cortex and form synapses onto the dendrites of Purkinje cells. Thus, loss of parallel fibers (Huang et al 1999) or granule cells (Pentney et al 2002;Zhang et al 2006) may trigger the dendritic loss in aging PCs. In addition, since specific trophic factors, such as insulin-like growth factor-1 (IGF-1) and brain-derived neurotrophic factor (BDNF), can promote dendritic growth (Niblock et al 2000;Binder 2007), but exhibit age-related reduction in aging brain (Markowska et al 1998;Erickson et al 2010), it is reasonable to propose that age-related declines of PC dendrites might also be associated with such reduced trophic support during cerebellar aging.…”

“…Age-related loss of PC arborizations could directly reduce the amount of information input, reduce afferent efficacy, and affect information integration and signal transmission in the aged cerebellum, consequently leading to a reduction in cerebellar function. In addition, loss of PC dendritic arborizations might also contribute to the decline in the thickness of the molecular layer in the aged cerebellum (Zhang et al 2006).…”

“…Agerelated hyperplasia and hypertrophy of astrocytes (Sabbatini et al 1999;Zhang et al 2006) have been reported to provide neuroprotective effects on aging neurons, and might also exert protection for the aging PCs. Some compensatory mechanisms might be invoked by the aging brain.…”