|Short-Term Memory Molecule: AMPAR||Memory|
Figure 3-1. The Brain. [Source: NIH]
In the brain, fear memory is stored in the amygdala while most of other memories are formed in the hippocampus first and then transferred to the cerebral cortex. An event (e.g, a birthday party) is recalled whenever a group of neurons representing the event fire at that moment. Different groups of neurons represent different events. The easier a group of neurons can fire synchronously, the more likely their represented event will be remembered.
As discussed in the previous chapter, neuronal firing is determined by the summation of EPSPs and IPSPs at the axon hillock. A larger EPSP facilitates neuronal firing. Glutamate is a major neurotransmitter that can induce EPSPs. It has been well established that two of its receptors, NMDAR and AMPAR, play crucial roles in learning and memory.
Long-term potentiation (LTP) is an enhancement of synaptic connection. During the Hebbian type of learning, Ca2+ ions enter the spine through NMDARs and activate CaMKII, resulting in the insertion of AMPARs into the postsynaptic membrane. Since the opening of AMPARs allows Na+ ions to enter the neuron, more AMPARs on the postsynaptic membrane should generate larger EPSP when glutamates are released from the presynaptic axon terminal. In this manner, the connection between the two neurons is enhanced. The increase of AMPARs at the postsynaptic membrane is a memory trace left by the learning process.
Figure 3-2. LTP arises from the increase of AMPARs at the postsynaptic membrane.
Author: Frank Lee