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