Table 4.

Summary of literature supporting increase in specific synaptic weights with the advance of Parkinson's disease

Weight	Literature supporting weight increase in Parkinson's disease
wSG	Dopamine reduces the effect of glutamate on GPe neurons (Johnson and Napier, 1997; Kita, 2007)
	D2 receptors are present in GPe (Hoover and Marshall, 2004; Kita, 2007)
wGS	In the parkinsonian state, GABA agonists in GPe evokes greater currents in STN (Shen and Johnson, 2005)
	Dopamine reduces the effect of GABA on STN neurons (Cragg et al., 2004)
	D2 receptors are present in STN (Shen and Johnson, 2000)
wGG	Increased ambient GABA in GPe in animal models of Parkinson's disease (Robertson et al., 1991; Ochi et al., 2000; Schroeder and Schneider, 2002)
	D2 receptors are present in GPe (Hoover and Marshall, 2004; Kita, 2007)
wCS	In the parkinsonian state, STN neurons are excited to a greater extent by cortex (Magill et al., 2001)
	In the parkinsonian state, AMPA and NMDA currents are greater in the STN (Shen and Johnson, 2005)
	D2 receptors are present in STN (Shen and Johnson, 2000)
wXG	Striatal neurons activity is increased after dopamine depletion (Kish et al., 1999; Tseng et al., 2001; O'Donnell, 2003)
	D2 receptors reduce the excitability of striatopallidal neurons (Obeso et al., 2000; Surmeier et al., 2007)
	Increased GPe ambient GABA in animal models of Parkinson's disease (Robertson et al., 1991; Ochi et al., 2000; Schroeder and Schneider, 2002)
	D2 receptors are present in GPe (Hoover and Marshall, 2004; Kita, 2007)
	Striatopallidal neurons are activated by dopamine lesion (Mallet et al., 2006)

The indexes of the weights refer to the origin and target nuclei of the connection they describe, and these can be C (cortex), X (striatum), S (STN), or G (GPe).