Review Article
Mouse Models of Down Syndrome as a Tool to Unravel the Causes of Mental Disabilities
Table 4
Neurotransmitter and receptor alterations in DS and in the Ts65Dn mouse model of Down syndrome.
| | DS | Ts65Dn |
| GABA | (i) Reduced in fetuses | (i) Increased number of GABAergic interneurons |
| Excitatory transmitters | (i) Decreased levels of glutamate and aspartate in adults | (i) Alterations in the composition of the AMPA and NMDA receptor (ii) Alterations in the signalling mechanisms downstream the NMDA receptor |
| 5-HT | (i) Deficits of 5-HT in the frontal cortex (ii) Reduced levels of the 5-HT1A receptor | (i) Unchanged levels of 5-HT (ii) Reduced levels of the 5-HT1A receptor |
| Ach | (i) Deficits in the cholinergic system and in ChAT activity | (i) Reduced levels of markers for Ach (ii) Increased ChAT activity |
| NA | (i) Reduced levels in adult brains (ii) Altered β-adrenoceptor function in aged brains | (i) Loss of locus coeruleus neurons starting at 6 months of age (ii) Altered β-adrenoceptor function |
| Neurotrophins | | | (i) BDNF (ii) NT3 (iii) NGF | (i) Reduced levels in fetuses | (i) Reduced levels (ii) Increased levels (iii) Reduced levels |
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