7.4 The Brain and Memory

Just as information is stored on digital media such as DVDs and flash drives, the information in LTM must be stored in the brain. The ability to maintain information in LTM involves a gradual strengthening of the connections among the neurons in the brain. When pathways in these neural networks are frequently and repeatedly fired, the synapses become more efficient in communicating with each other, and these changes create memory. As described in Chapter 5.1, this process, known as long-term potentiation (LTP), refers to the strengthening of the synaptic connections between neurons as result of frequent stimulation (Lynch, 2002). Drugs that block LTP reduce learning, whereas drugs that enhance LTP increase learning (Lynch et al., 1991). Because the new patterns of activation in the synapses take time to develop, LTP happens gradually. The period of time in which LTP occurs and in which memories are stored is known as the period of consolidation.

Memory is not confined to the cortex; it occurs through sophisticated interactions between new and old brain structures (Figure 7.12). One of the most important brain regions in explicit memory is the hippocampus, which serves as a preprocessor and elaborator of information (Squire, 1992). The hippocampus helps us encode information about spatial relationships, the context in which events were experienced, and the associations among memories (Eichenbaum, 1999). The hippocampus also serves in part as a switching point that holds the memory for a short time and then directs the information to other parts of the brain, such as the cortex, to actually do the rehearsing, elaboration, and long-term storage (Jonides, Lacey, & Nee, 2005). Without the hippocampus, which might be described as the brain’s “librarian,” our explicit memories would be inefficient and disorganized.

While the hippocampus is handling explicit memory, the cerebellum and the amygdala are concentrating on implicit and emotional memories, respectively. Research shows that the cerebellum is more active when we are learning associations and in priming tasks, and animals and humans with damage to the cerebellum have more difficulty in classical conditioning studies (Krupa, Thompson, & Thompson, 1993; Woodruff-Pak, Goldenberg, Downey-Lamb, Boyko, & Lemieux, 2000). The storage of many of our most important emotional memories, and particularly those related to fear, is initiated and controlled by the amygdala (Sigurdsson, Doyère, Cain, & LeDoux, 2007).

Evidence for the role of different brain structures in different types of memories comes in part from case studies of patients who suffer from amnesia, a memory disorder that involves the inability to remember information. As with memory interference effects, amnesia can work in either a forward or a backward direction, affecting retrieval or encoding. For people who suffer damage to the brain, for instance, as a result of a stroke or other trauma, the amnesia may work backward. The outcome is retrograde amnesia, a memory disorder that produces an inability to retrieve events that occurred before a given time. Demonstrating the fact that LTP takes time (the process of consolidation), retrograde amnesia is usually more severe for memories that occurred just prior to the trauma than it is for older memories, and events that occurred just before the event that caused memory loss may never be recovered because they were never completely encoded.

Organisms with damage to the hippocampus develop a type of amnesia that works in a forward direction to affect encoding, known as anterograde amnesia. Anterograde amnesia is the inability to transfer information from short-term into long-term memory, making it impossible to form new memories. One well-known case study was a man named Henry Gustav Molaison (before he died in 2008, he was referred to only as H. M.) who had parts of his hippocampus removed to reduce severe seizures (Corkin, Amaral, González, Johnson, & Hyman, 1997). Following the operation, Molaison developed virtually complete anterograde amnesia. Although he could remember most of what had happened before the operation, and particularly what had occurred early in his life, he could no longer create new memories. Molaison was said to have read the same magazines over and over again without any awareness of having seen them before.

Cases of anterograde amnesia also provide information about the brain structures involved in different types of memory (Bayley & Squire, 2005; Helmuth, 1999; Paller, 2004). Although Molaison’s explicit memory was compromised because his hippocampus was damaged, his implicit memory was not (because his cerebellum was intact). He could learn to trace shapes in a mirror, a task that requires procedural memory, but he never had any explicit recollection of having performed this task or of the people who administered the test to him.

Although some brain structures are particularly important in memory, this does not mean that all memories are stored in one place. The American psychologist Karl Lashley (1929) attempted to determine where memories were stored in the brain by teaching rats how to run mazes, and then lesioning different brain structures to see if they were still able to complete the maze. This idea seemed straightforward, and Lashley expected to find that memory was stored in certain parts of the brain. But he discovered that no matter where he removed brain tissue, the rats retained at least some memory of the maze, leading him to conclude that memory isn’t located in a single place in the brain, but rather is distributed around it.

Long-term potentiation occurs as a result of changes in the synapses, which suggests that chemicals, particularly neurotransmitters and hormones, must be involved in memory. There is quite a bit of evidence that this is true. Glutamate, a neurotransmitter and a form of the amino acid glutamic acid, is perhaps the most important neurotransmitter in memory (McEntee & Crook, 1993). When animals, including people, are under stress, more glutamate is secreted, and this glutamate can help them remember (McGaugh, 2003). The neurotransmitter serotoninis also secreted when animals learn, and epinephrine may also increase memory, particularly for stressful events (Maki & Resnick, 2000; Sherwin, 1998). Estrogen, a female sex hormone, also seems critical, because women who are experiencing menopause, along with a reduction in estrogen, frequently report memory difficulties (Chester, 2001).

Our knowledge of the role of biology in memory suggests that it might be possible to use drugs to improve our memories, and Americans spend several hundred million dollars per year on memory supplements with the hope of doing just that. Yet controlled studies comparing memory enhancers, including Ritalin, methylphenidate, ginkgo biloba, and amphetamines, with placebo drugs find very little evidence for their effectiveness (Gold, Cahill, & Wenk, 2002; McDaniel, Maier, & Einstein, 2002). Memory supplements are usually no more effective than drinking a sugared soft drink, which also releases glucose and thus improves memory slightly. This is not to say that we cannot someday create drugs that will significantly improve our memory. It is likely that this will occur in the future, but the implications of these advances are as yet unknown (Farah et al., 2004; Turner & Sahakian, 2006).

Although the most obvious potential use of drugs is to attempt to improve memory, drugs might also be used to help us forget. This might be desirable in some cases, such as for those suffering from posttraumatic stress disorder (PTSD) who are unable to forget disturbing memories. Although there are no existing therapies that involve using drugs to help people forget, it is possible that they will be available in the future. These possibilities will raise some important ethical issues: Is it ethical to erase memories, and if it is, is it desirable to do so? Perhaps the experience of emotional pain is a part of being a human being. And perhaps the experience of emotional pain may help us cope with the trauma.

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