Abstract
The piriform cortex is involved in olfactory information processing, that is altered in Down Syndrome. Moreover, piriform cortex has a crucial involvement in epilepsy generation and is one of the first regions affected in Alzheimer's Disease, both maladies being prevalent among Down Syndrome individuals. In this work, we studied the alterations in neuronal morphology, synaptology and structural plasticity in the piriform cortex of the Ts65Dn mouse model, which is the most used model for the study of this syndrome and mimics some of their alterations. We have observed that Ts65Dn piriform cortex displays: a reduction in dendritic arborisation, a higher density of inhibitory synapses (GAD67), a lower density of excitatory synapses (vGLUT1) and a higher density of inhibitory postsynaptic puncta (gephyrin). Under electron microscopy the excitatory presynaptic and postsynaptic elements were larger in trisomic mice than in controls. Similar results were obtained using confocal microscopy. There were less immature neurons in piriform cortex layer II in addition to a reduction in the expression of PSA-NCAM in the neuropil that subsequently can reflect impairment in structural plasticity. These data support the idea of an impaired environment with altered ratio of inhibition and excitation that involves a reduction in plasticity and dendritic atrophy, providing a possible substrate for the olfactory processing impairment observed in DS individuals.