Table 2.

AMPAR studies in transgenic mice.

Reference(s)	Mutation	Age	Result
Kim et al. (2005; PDZ ligand)	KI mutant mice lacking the last 7 a.a. GluA1; male	3 weeks–7 months	Unaffected: Basal localization and transmission, LTP (Fields: 1 TBS, whole-cell pairing: 2 Hz, 200 pulses at 0 mV) and LTD (Fields: 1 Hz, 900 pulses, whole-cell pairing: 0.5–1 Hz, 200–300 pulses at −40 mV).
Granger et al. (2013) and Granger and Nicoll (2014a)	Gria1–3fl/fl; replaced with different mutant receptors	P17–20	No single portion of the GluA1 C-terminal tail is required for LTP (2 Hz, 90 s at 0 mV), GluA2, GluA2(Q) or GluK1 replacement sufficient to rescue LTP. GluA1 and GluA2 conditional knockouts have normal LTD (1 Hz, 15 min), GluK1 replacement in GluA1–3 conditional knockout sufficient to rescue LTD.
Zamanillo et al. (1999), Hoffman et al. (2002), Reisel et al. (2002) and Jensen et al. (2003)	GluA1 knockout	3 months, P14–42, P41–56, Adult	LTP (Fields: 1 × 100 Hz, 1 s): impaired; normal spatial learning in Morris Water Maze; LTP (Fields: 1 × 100 Hz, 1 s/Whole-cell 0.67 Hz, 3 min at 0 mV): modest/normal amount of LTP at P14 disappears by P42; LTP (TBS): decreased initially but normalizes to WT after 25 min; Normal spatial memory; spatial working memory deficits.
Meng et al. (2003)	GluA3 knockout	2–3 weeks, 2–3 months	Normal basal transmission and pre-synaptic function; LTD (1 Hz, 15 min) 12–16 days: normal; Depotentiation 2–3 weeks: normal; Enhanced LTP (100 Hz, 1 s) in adults and enhanced level of LTP saturation (6 trains of 100 Hz, 1 s with 5 min interval) in adults.
Jia et al. (1996), Gerlai et al. (1998) and Meng et al. (2003)	GluA2 knockout	P16–30, 5–8 weeks, 2–3 weeks, 2–3 months	LTP (Fields: 5 × 100 Hz, 200 ms pulses): enhanced; growth retardation and motor deficits, normal brain anatomy, increased excitability, alterations in a number of behaviors across multiple brain areas; LTD (Fields: 1 Hz, 15 min): normal; Depotentiation (HFS 100 Hz 1 s followed by LFS 1 Hz, 15 min): impaired depotentiation but enhanced LTP (100 Hz, 1 s) in adults.
Meng et al. (2003)	GluA2/3 double knockout	2-3 weeks, 2-3 months	Reduced basal transmission in adults; Normal PPR in adults; Enhanced LTD and de-depression (12–16 days); Enhanced LTP and de-potentiation (2–3 weeks old); Enhanced LTP in adult mice.
Lee et al. (2003)	GluA1 S831/845A knock-in	Young (P21–P28) and old (3 months or older)	Normal basal transmission; LTP (Fields TBS) old mostly blocked, young normal; LTD (Fields: old PP 1 Hz, 15 min and young 1 Hz, 15 min): blocked likely due to lack of receptor internalization; MWM: learning normal, impaired retention of spatial memory (delayed sessions).
Lee et al. (2010)	GluA1 S831A knock-in	Young (3 weeks) and old (3 months+)	Young-Normal basal transmission; LTP (Fields: 4 × TBS) normal; LTD: (Fields: 1 Hz) slight decrease but not statistically significant. Old-Normal basal transmission; LTP: (Fields: 4 × TBS and 1 × TBS) normal; LTD: (Fields: PP-1 Hz) normal. Normal de-potentiation and de-depression.
Lee et al. (2010) and Qian et al. (2012)	GluA1 S845A knock-in	Young (3 weeks) and old (3 months+), 6–8 weeks	Young mice have normal basal transmission and normal LTP (Fields: 4 × TBS) but virtually absent LTD (Fields: 1 Hz). Old mice have normal basal transmission and normal LTP (Fields: 4× TBS and 1 × TBS) but mostly blocked LTD (Fields: PP 1 Hz) and normal de-potentiation. At 6–8 weeks, PTT-LTP (5 Hz, 3 min in presence of β-adrenergic receptor agonist) is impaired.
Zhou et al. (2018)	GluA1 and GluA2 C-terminal tail swap knock-ins	3–4 weeks for LTP; 13–15 days for LTD	Both show normal basal transmission GluA1-C2KI has normal NMDAR LTD, impaired LTP (1 × 100 Hz, 4 × 100 Hz); GluA2-C1KI has normal mGluR LTD (100 μM (RS)-3,5-DHPG for 10 min), no NMDAR LTD (900 pulses at 1 Hz), enhanced LTP (4 × 100 Hz). With the double replacement, LTP and LTD are normal. Behavior: GluA1-C2KI impaired spatial learning and memory, GluA2-C1KI impaired contextual fear memory.