Glazewski S, Bejar R, Mayford M, Fox K
Cardiff School of Biosciences, Cardiff University, Museum Avenue, CF10 3US, Cardiff, UK.
Neuropharmacology. 2001 Nov;41(6):771-8. doi: 10.1016/s0028-3908(01)00097-1.
The calcium/calmodulin kinase II (CaMKII) autophosphorylation site is thought to be important for plasticity, learning and memory. If autophosphorylation is prevented by a point mutation (T286A) LTP is blocked in the hippocampus and cortex. Conversely, if the point mutation mimics autophosphorylation (T286D) a range of frequencies that normally produce LTP in wild types cause LTD instead. In order to test whether the alphaCaMKII-T286D mutation increases levels of depression in vivo, we examined the effect of the alphaCaMKII-T286D transgene on plasticity induced in the barrel cortex by whisker deprivation. Surprisingly, the mutation did not affect depression or potentiation. However, in animals reared with the transgene turned on from birth, the surround receptive field responses were greater than normal. This effect may be due to the potentiating action of autophosphorylated CaMKII during early development.
钙/钙调蛋白激酶II（CaMKII）的自磷酸化位点被认为对可塑性、学习和记忆很重要。如果通过点突变（T286A）阻止自磷酸化，海马体和皮层中的长时程增强（LTP）就会被阻断。相反，如果点突变模拟自磷酸化（T286D），那么一系列通常在野生型中产生LTP的频率反而会导致长时程抑制（LTD）。为了测试αCaMKII - T286D突变是否会增加体内的抑郁水平，我们研究了αCaMKII - T286D转基因对由触须剥夺在桶状皮层中诱导的可塑性的影响。令人惊讶的是，该突变并未影响抑制或增强。然而，在从出生就开启转基因饲养的动物中，周围感受野反应比正常情况更大。这种效应可能是由于自磷酸化的CaMKII在早期发育过程中的增强作用。
