Table 1.

Alterations of glutamate receptors during PD and anti-Parkinsonian process.

Types	Changes during PD Process	Antiparkinsonian Treatment and Compounds	References
NMDA	GluN1, GluN2A, B, D: increase	NAMs: MK-801, dextrorphan, L-701324, SDZ220-581, MDL100,453, et al. GluN2B-selective NAMs: Ifenprodil, traxoprodil, Radiprodil Effects: improve PD motor symptoms, synergistically increase the anti-Parkinsonian efficiency of dopaminergic agents, reduce LIDs	[15,16,17,60,61,62,63,64,72,73,74,75]
AMPA	Increase	NAMs: NBQX, talampanel Effects: improve motor deficits, reduce LIDs	[23,77,78,79]
KA	GluK2: increase	NAMs: NBQX and CNQX (share with AMPA receptor), LU97175, LY382884, LY377770 Effects: no direct anti-Parkinsonian study targeting KAR	[32,83,84,85]
mGluR1/5	mGluR1: dynamically changed mGluR5: increase	NAMs of mGluR5: MPEP, MTEP, AFQ056, ADX48621 Effects: limite the extent of nigrostriatal damage, alleviate LIDs	[35,38,88,89,90,92,93,94]
mGluR2/3	mGluR2/3: decrease	PAMs: LY379268, (2R, 4R)-APDC, DCG-IV Effects: reduce the extent toxicity and corticostriatal transmission of 6-OHDA	[46,99,100]
mGluR4,6,7,8	lacking mGluR4 impairs learning ability of complex motor tasks	PAMs of mGluR4: PHCCC, ADX88178, VU0364770, Lu AF21934 Effects: reduce the extent nigrostriatal toxicity and dosage of L-DOPA	[101,102,120,121]

NAMs: Negative allosteric modulators; PAMs: Positive allosteric modulators.