Table 3.
AKAP150 transgenic mouse model studies.
| AKAP150 mutation | Phenotype | References |
|---|---|---|
| Knockout (two different lines) | Basal | Tunquist et al. (2008) |
| 2 weeks normal or slightly enhanced | ||
| 8 weeks normal | ||
| LTP (100 Hz, 1 s) | ||
| 8 weeks normal | ||
| LTD (1 Hz, 15 min) | ||
| 2 weeks normal | ||
| 8–16 weeks impaired (NMDAR vs. mGluR? Not determined) | Weisenhaus et al. (2010) | |
| Behavior | ||
| Modest deficits in spatial memory | ||
| Normal reversal learning | ||
| Impaired cerebellar behaviors | ||
| Reduced pilocarpine seizures | ||
| PTT-LTP (5 Hz, 3 min in presence of a β-adrenergic receptor agonist) CP-AMPAR dependent, 6–8 weeks impaired | Zhang et al. (2013) | |
| D36 (PKA anchoring-deficient) | Basal | Lu et al. (2007) |
| Normal | ||
| LTP (100 Hz, 1 s) | ||
| CP-AMPAR and PKA independent, 4–5 weeks normal | Lu et al. (2008) | |
| CP-AMPAR and PKA dependent, 8 weeks impaired | ||
| LTD (1 Hz, 15 min) | Weisenhaus et al. (2010) | |
| 2 weeks, impaired (retain ~10%) | ||
| Depotentiation (100 Hz, 1 s and 5 min later 1 Hz, 15 min) | ||
| Normal | ||
| Behavior | ||
| Impaired reversal learning | ||
| Normal spatial learning, working memory, and open field behaviors | ||
| PTT-LTP (5 Hz, 3 min in presence of a β-adrenergic receptor agonist) 6–8 weeks partially impaired | Zhang et al. (2013) | |
| ΔPKA (PKA anchoring-deficient) | Basal | Sanderson et al. (2016) |
| Normal | ||
| LTP (100 Hz, 1 s) | ||
| 2 weeks normal magnitude (but unlike WT is not CP-AMPAR dependent) | ||
| LTD (1 Hz, 15 min) | ||
| CP-AMPAR dependent, 2 weeks impaired (retain ~10%) | ||
| ΔPIX (CaN anchoring-deficient) | Basal | Sanderson et al. (2012) |
| Normal but increased CP-AMPARs | ||
| LTP (100 Hz, 1 s) | ||
| 2–3 weeks enhanced due to increased CP-AMPAR synaptic recruitment, but 50 Hz, 2 s normal | ||
| Depotentiation (100 Hz, 1 s and 30 min later 1 Hz, 15 min) | ||
| Impaired: de-potentiates to a similar amount but does not reach WT baseline levels | ||
| LTD (Fields 1 Hz, 15 min or Whole-cell 1 Hz, 6 min paired at −30 mV) | ||
| 2 weeks impaired due to decreased CP-AMPAR synaptic removal (1 Hz PP 900 pulses, 50 ms interval LTD and 10 Hz transient depression also impaired) | ||
| CS (palmitoylation-deficient) | Basal | Purkey et al. (2018) |
| Normal but increased CP-AMPARs | ||
| LTP (Fields 100 Hz, 1 s) | ||
| 2–3 weeks impaired | ||
| LTP (Whole-cell 2 × 100 Hz, 0 mV) | ||
| CP-AMPAR dependent, 2–3 weeks impaired | ||
| LTP (Whole-cell 3 Hz, 90 s, 0 mV) | ||
| CP-AMPAR independent, 2–3 weeks normal | ||
| LTD (Fields 1 Hz, 15 min) | ||
| 2 weeks normal | ||
| De-depression (Fields 1 Hz LTD, 15 min and 15 min later 100 Hz, 1 s LTP) | ||
| CP-AMPAR dependent, 2 weeks enhanced |