Exam 4: Long-Term Memory

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The two-stage model suggested by Marr et al. (1991) and McClelland et al. (1995) posits that two systems affect memory: a temporary store (which relies on the hippocampus and adjacent temporal lobe structures) that learns quickly and holds on to information only briefly, and a long-term store (which relies on the neocortex) that learns slowly but holds on to information for long periods of time. Proponents of these two-stage models suggest that new information, which is gathered during wakefulness, is initially coded in both the temporary and the long-term stores. In subsequent periods of consolidation during sleep, the new information is reactivated repeatedly and is slowly organized and integrated into the long-term store. The two-stage model holds that because the same processes needed for reactivation are also used to process incoming stimuli, it is necessary to perform reactivation and redistribution processes during sleep, when there are no encoding demands from external stimuli. Plasticity is maintained because new information is constantly being incorporated into the long-term store, and stability is maintained because this consolidation doesn't disrupt existing memories. According to the two-stage model, the process of repeated reactivation and consolidation also serves to encourage the long-term consolidation of relevant information that integrates well with existing knowledge, and erases irrelevant details

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One important feature of hippocampal neurons is that they contain two types of glutamate receptors: AMPA receptors and NMDA receptors. Glutamate is the most prevalent neurotransmitter in the brain and thus hippocampal neurons are poised to respond to a wide variety of neuronal activity. When glutamate comes in contact with a dendrite of a hippocampal neuron, the glutamate binds with both the NMDA and AMPA receptors. The binding of the glutamate to the NMDA receptor initially does nothing because the receptor's calcium channel is blocked by a magnesium ion. However the binding of glutamate to the AMPA receptor opens a sodium channel allowing sodium ions to enter the neuron. The positively charged sodium ions that enter through the AMPA receptor sodium channel cause a moderate depolarization of the hippocampal neuron. This moderate depolarization of the hippocampal neuron dislodges the magnesium ion from the NMDA receptor and opens the NMDA calcium channel, allowing large numbers of calcium ions to enter. This influx of calcium causes the hippocampal neuron to create additional silent receptors along the postsynaptic membrane. This strengthens, or potentiates, the synapse because now the neuron can respond more rapidly to glutamate