What did you do today? Did you have breakfast, brush your teeth, put your clothes on, drive your car, read an assignment, text a friend? Whatever you did, we are sure of one thing: It required a whole lot of memory. You could not send a text message without knowing how to spell, read, and use a cell phone—all things you had to learn and remember. Likewise, you could not drive without remembering how to unlock your car, start the engine, use the pedals. Memory is involved in virtually everything you do.

If memory is behind all your daily activities, important processes must be occurring in the brain to make this happen: both on the macro (large) and micro (small) scale. But as we learned from Clive’s example, these processes are fragile and can be profoundly disrupted. Exploring the causes of memory failure can help us understand the biological basis of memory.

LO 13 Compare and contrast anterograde and retrograde amnesia.

Amnesia, or memory loss, can result from either a physical or psychological condition. There are different types and degrees of amnesia, ranging from extreme (losing decades of autobiographical memories) to mild (temporarily forgetting people’s names after a concussion).

ANTEROGRADE AMNESIA According to researchers, Clive suffers from “a more severe anterograde amnesia than any other patient previously reported” (Wilson et al., 1995, p. 680). Anterograde amnesia (an-tə-ˌrō-ˌgrād) is the inability to “lay down” or create new long-term memories (Figure 6.12), and it is generally caused by damage or injury to the brain, resulting from surgery, alcohol, head trauma, or illness. Someone with anterograde amnesia cannot form memories of events and experiences that occur following the brain damage, regardless of its cause. People affected by anterograde amnesia may be incapable of holding down a job, as their inability to lay down new memories affects their capacity to remember daily tasks. For Clive, his short-term memory still functioned to a certain extent, but he could only absorb and process information for several seconds before it was lost. From his perspective, every experience was fresh, and every person (with the exception of some he knew well from the past) a total stranger.

RETROGRADE AMNESIA A second type of memory loss is retrograde amnesia, an inability to access memories created before a brain injury or surgery (Brandt & Benedict, 1993; Figure 6.12). With retrograde amnesia, a person has difficulty retrieving old memories, though how “old” depends on the extent of trauma to the brain. People with retrograde amnesia generally remember who they are and the most important events of their earlier lives (Manns, Hopkins, & Squire, 2003; Squire & Wixted, 2011). Remember that retrograde refers to the inability to access old memories, and anterograde refers to the inability to create new memories.

Clive suffered from retrograde amnesia in addition to his anterograde amnesia. While he appeared to retain a vague outline of his past (hazy information about his childhood, the fact that he had been a choral scholar at Clare College, Cambridge, and so on), he could not retrieve the names of his children unless prompted. And although Clive’s children were all adults when he developed encephalitis, he came out of the illness thinking they were young children. The retrograde amnesia has improved, but only minimally. In 2005, for example, Clive asked his 40-something son what subjects he was studying in grammar school (equivalent to American high school). Nowadays when inquiring about his children, Clive simply asks, “What are they doing?” (D. Wearing, personal communication, June 18 and 25, July 11, 2013).

In spite of the severe retrograde and anterograde amnesia, some of Clive’s memory functions continued to operate quite well. At one point, Deborah arranged for Clive to be reunited with the singers from the London Lassus Ensemble, a group he had conducted for more than a decade before his illness. At first Clive paused and looked at the musicians with uncertainty, but then he raised his hands and began conducting, leading them through the music with precision and grace. Remembering the piece (which he had edited himself), Clive mouthed its words in Latin and employed the same tempo and conducting style he had used in the past (D. Wearing, personal communication, July 11, 2013). After the performance, the musicians left and Clive sat in the empty chapel wondering what had gone on there earlier (Wearing, 2005). When shown a video of himself leading the chorus, he remarked, “I wasn’t conscious then” (Wilson et al., 2008). Clive’s explicit memory of the event vanished in seconds, but his implicit memory—knowing how to conduct—was intact.

How is it possible that some of Clive’s long-term memories were blotted out, while others, such as how to conduct music, remained fairly clear? The evidence suggests that different types of long-term memories have distinct processing routes in the brain. Thus, damage to one area of the brain may impair some types of memory but not others. Let’s take a closer look at where memories seem to be stored in the brain.

LO 14 Identify the brain structures involved in memory.

A few years after the onset of Clive’s illness, doctors evaluated his brain using an MRI scan. A troubling picture emerged; the virus had destroyed many parts of his brain, notably the hippocampus, which plays a vital role in the creation of new memories (Wilson et al., 2008).

Only in the last 50 years have scientists come to appreciate the role of the hippocampus in memory (Infographic 6.3). Back in the 1920s, psychologist Karl Lashley set out to find a memory trace: the physical spot where memories are etched in the brain, also called an engram. Lashley selected a group of rats that had learned the layout of specific mazes, and then made large cuts at different places in their cortices to see how this affected their memory of the mazes. No matter where Lashley sliced, the rats still managed to maneuver their way through the mazes (Costandi, 2009, February 10; Lashley, 1950). These findings led Lashley and other scientists to believe that memory is spread throughout the brain rather than localized in a particular region (Costandi, 2009, February 10; Kandel & Pittenger, 1999). Connectionism is a model that suggests our memories are distributed throughout the brain in a network of interlinked neurons.

INFOGRAPHIC 6.3

INFOGRAPHIC 6.3

Credit: Lashley’s sketches showing where he made incisions in rat brains, Journal of Comparative Neurology, K. S. Lashley, L. E. Wiley. Copyright © 1933 The Wistar Institute of Anatomy and Biology

THE CASE OF H.M. Henry Molaison (better known as “H.M.”) forced scientists to completely reevaluate their understanding of the brain’s memory system. From the onset of his amnesia in 1953 until his death in 2008, H.M. served as a research participant for some 100 scientists (Corkin, 2002), making him the most extensively studied amnesic patient.

H.M.’s brain troubles began at the age of 10, a year or so after being knocked unconscious in a bicycle accident. He began to experience seizures, which worsened with age and eventually became so debilitating that he could no longer hold a steady job. Antiseizure medications were unsuccessful in controlling his seizures, so at the age of 27, H.M. opted for an experimental surgery to remove parts of his brain: the temporal lobes (just beneath the temples), including the hippocampus (Scoville & Milner, 1957).

H.M.’s surgery succeeded in reining in his epilepsy but left his memory in shambles. Upon waking from the operation, he could no longer find his way to the bathroom or recognize the hospital workers caring for him. He played with the same jigsaw puzzles and read the same magazines day after day as if he were seeing them for the first time (Scoville & Milner, 1957). Like Clive, H.M. suffered from profound anterograde amnesia, the inability to encode new long-term memories, and a milder form of retrograde amnesia, trouble retrieving existing memories from storage. Although H.M. had difficulty recalling what occurred during the few years leading up to his surgery (Scoville & Milner, 1957), he did remember events from the more distant past, for example, the 1929 stock market crash and the events of World War II (Carey, 2008).

H.M. maintained a working implicit memory, which he demonstrated in an experiment involving the complex task of tracing a pattern reflected in a mirror. With repeated practice sessions (none of which he remembered), H.M. improved his performance on the drawing task, learning it as well as someone without amnesia (Gabrieli, Corkin, Mickel, & Growdon, 1993). Clive can also acquire new implicit memories, but his ability is very limited. According to Deborah, it took years for Clive to learn how to get to his bedroom in the small community residence where he moved after leaving the hospital (Wearing, 2005).

THE ROLE OF THE HIPPOCAMPUS Imagine you are a scientist trying to figure out exactly what role the hippocampus plays in memory. Consider the facts you know about H.M.: (1) He has virtually no hippocampus; (2) he has lost the ability to make new explicit memories, yet can create implicit memories; and (3) he can still tap into memories of the distant past. So what do you think the hippocampus does? Evidence suggests that the hippocampus is essential for creating new explicit memories but not implicit memories. Researchers have also shown that explicit memories are processed and stored in other parts of the brain, including the temporal lobes and areas of the frontal cortex (García-Lázaro, Ramirez-Carmona, Lara-Romero, & Roldan-Valadez, 2012).

As in H.M.’s case, Clive’s ability to form explicit memories is profoundly compromised, largely a result of the destruction of his hippocampus. Yet Clive also struggles with the creation of implicit memories—not surprising given the extensive damage to other regions of his brain, such as the amygdala and temporal lobes (Wilson et al., 2008). Studies have zeroed in on other brain areas, such as the cerebellum and amygdala, as processing hubs for implicit memory (Thompson & Kim, 1996; Thompson & Steinmetz, 2009). The amygdala plays a central role in the processing of emotional memories (García-Lázaro et al., 2012). See Infographic 6.3 for more information about memory processing in the brain.

So although the hippocampus plays a central role in laying down new memories, it does not appear to serve as their ultimate destination. This process of memory formation, which moves a memory from the hippocampus to other areas of the brain, is called memory consolidation (Squire & Bayley, 2007). The consolidation that begins in the hippocampus allows for the long-term storage of memories. According to Kandel and Pittenger (1999): “The final locus of storage of memory is widely assumed to be the cerebral cortex, though this is a difficult assertion to prove” (p. 2041). As for retrieval, the hippocampus appears to be in charge of accessing young memories, but then passes on that responsibility to other brain regions as memories grow older (Smith & Squire, 2009).

This idea that the hippocampus is essential for creating explicit memories (as opposed to implicit memories) is supported by what we know about infantile amnesia, that is, the inability to remember events from our earliest years. Most adults cannot remember events before the age of 3, though it is not clear why. Some researchers suggest that it is because the hippocampus and frontal cortex, both important for the creation of long-term explicit memories, are not fully developed in children (Bauer, 2006; Willoughby, Desrocher, Levine, & Rovet, 2012).

This macrolevel perspective allows us to see the “big picture” of memory, but what’s going on microscopically? The next section focuses on the important changes occurring in and between neurons.

LO 15 Describe long-term potentiation.

How does your brain change when you learn a new driving route to school? If we could peer into your skull, we might see a change in your hippocampus. As one study found, London taxicab drivers with greater time spent on the job had structural changes in some regions of the hippocampus, particularly to an area that processes “spatial knowledge” (Maguire, Woollett, & Spiers, 2006). Zooming in for a closer look, we might actually see changes at the level of the neuron. If you are looking for a memory imprint, the best place to look is the synapse.

LONG-TERM POTENTIATION As it turns out, the more neurons communicate with each other, the better the connections between them. Long-term potentiation occurs when sending neurons release neurotransmitters more effectively, and receiving neurons become more sensitive, boosting synaptic strength for days or even weeks (Lynch, 2002; Malenka & Nicoll, 1999; Whitlock, Heynen, Shuler, & Bear, 2006). In other words, long-term potentiation refers to the increased efficiency of neural communication over time, resulting in learning and the formation of memories. Researchers suggest long-term potentiation may be the biological basis of many kinds of learning. As you learn a new skill, for example, the neurons involved in performing that skill increase their communication with each other. It might start with a somewhat random firing of neurons, but eventually the neurons responsible for the new skill develop pathways through which they communicate more efficiently. Having trouble visualizing the process? Imagine this scenario: Your college has opened a new campus with an array of brand-new buildings, but it has yet to construct the sidewalks connecting them. In order to go from one class to the next, students have to wade through tall grass and weeds. All the trampling eventually gives way to a system of paths linking the buildings, including a multitude of efficient paths that develop among them. Long-term potentiation of neural connections occurs in a similar fashion: over time, the communication among neurons improves and strengthens, allowing for the skill to develop and become more natural (Whitlock et al., 2006). These paths represent how a skill, whether tying your shoes or driving a stick shift, is learned and thus becomes a memory.

APLYSIA Amazingly, we have learned much about long-term potentiation from the sea slug Aplysia. Why the sea slug? One reason is that Aplysia has only about 20,000 neurons (Kandel, 2009)—a little easier to work with than the 100 billion neurons of a human brain. The sea slug’s neural simplicity, that is, the fact that the synapses are relatively easy to examine individually, also allows for the intensive study of habituation and other processes involved in classical conditioning. Studies using sea slugs as their subjects indicate that long-term potentiation, or increases in synaptic “strength,” is associated with learning and memory. What can a sea slug learn? They can be classically conditioned to retract their gills in response to being squirted with water. Researchers report that when the sea slugs are conditioned in this way, there are structural changes in both presynaptic and postsynaptic cells, including changes to connections between neurons (Kandel, 2009)—evidence of long-term potentiation. So never, ever complain to your instructor that you cannot learn: If a sea slug can do it, so can you!

ALZHEIMER’S DISEASE On a less positive note, disruptions in long-term potentiation appear to be at work in Alzheimer’s disease, a progressive, devastating brain illness that causes cognitive decline, including memory, language, and thinking problems. Alzheimer’s affects as many as 5.1 million Americans (National Institute on Aging, 2013). The disease was first discovered by Alois Alzheimer, a German neuropathologist, in the early 1900s. He had a patient with severe memory problems whose autopsy revealed that neurons in her brain were tangled like the wires of your earbud headphones. These neurofibrillary tangles, as they came to be called, were eventually shown to result from twisted protein fibers accumulating inside brain cells. In addition to the tangles, the other distinctive sign of Alzheimer’s is the presence of amyloid plaques, protein clumps that build up between neurons, blocking their lines of communication (Vingtdeux, Davies, Dickson, & Marambaud, 2011).

There is no cure for Alzheimer’s disease, and current treatments focus only on reducing the severity of symptoms rather than correcting the brain damage responsible. But there is also reason to be hopeful. Promising new drugs are coming down the pipeline, and there is some preliminary evidence suggesting that simple lifestyle changes, like becoming more physically active and pursuing intellectually and socially stimulating activities, may actually decrease the speed and severity of cognitive decline (Hertzog, Kramer, Wilson, & Lindenberger, 2009, July/August; Wilson & Bennett, 2003). Additional good news comes from research suggesting that we should not think of cognitive decline as inevitable in aging. We have more control of aging than previously thought, especially when we focus on the lifelong possibilities of learning and autonomy (Hertzog et al., 2009). Furthermore, it’s not only the strengthening of synapses that makes for enduring memories, but also the activation of new ones (Yu, Ponomarev, & Davis, 2004), and this process could offset cognitive decline (Table 6.1).

Like many topics psychologists study, the biological mechanisms that give rise to memory remain somewhat mysterious. We know we have memories; we know they are formed in the brain; and we know the brain is a physical entity, yet we still don’t know exactly how we go from a bunch of firing neurons to a vivid recollection of your 21st birthday bash, your high school prom, or the image of Bruno Mars banging on his drums at the Super Bowl halftime show. Studies attempting to test the various theories of memory formation are inconclusive, often generating more questions than answers. But one thing seems certain: Memory researchers have plenty of exciting work ahead.

Question 1

1. Anterograde amnesia

2. Retrograde amnesia

3. Infantile amnesia

4. Long-term potentiation

Question 2

1. engram

2. temporal lobe

3. hippocampus

4. aplysia

Question 3

1. Long-term potentiation

2. Memory consolidation

3. Priming

4. The memory trace

Question 4