25-1 What is the capacity of long-term memory? Are our long-term memories processed and stored in specific locations?

In Arthur Conan Doyle’s A Study in Scarlet, Sherlock Holmes offers a popular theory of memory capacity:

I consider that a man’s brain originally is like a little empty attic, and you have to stock it with such furniture as you choose…. It is a mistake to think that that little room has elastic walls and can distend to any extent. Depend upon it, there comes a time when for every addition of knowledge you forget something that you knew before.

Contrary to Holmes’ “memory model,” our capacity for storing long-term memories is essentially limitless. Our brains are not like attics, which once filled can store more items only if we discard old ones.

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I [DM] marveled at my aging mother-in-law, a retired pianist and organist. At age 88, her blind eyes could no longer read music. But let her sit at a keyboard and she would flawlessly play any of hundreds of hymns, including ones she had not thought of for 20 years. Where did her brain store those thousands of sequenced notes?

For a time, some surgeons and memory researchers recorded patients’ seemingly vivid memories triggered by brain stimulation during surgery. Did this prove that our whole past, not just well-practiced music, is “in there,” in complete detail, just waiting to be relived? On closer analysis, the seeming flashbacks appeared to have been invented, not a vivid reliving of long-forgotten experiences (Loftus & Loftus, 1980). In a further demonstration that memories do not reside in single, specific spots, psychologist Karl Lashley (1950) trained rats to find their way out of a maze, then surgically removed pieces of their brain’s cortex and retested their memory. No matter which small brain section he removed, the rats retained at least a partial memory of how to navigate the maze. Memories are brain-based, but the brain distributes the components of a memory across a network of locations. These specific locations include some of the circuitry involved in the original experience: Some brain cells that fire when we experience something fire again when we recall it (G. Miller, 2012; J. F. Miller et al., 2013).

The point to remember: Despite the brain’s vast storage capacity, we do not store information as libraries store their books, in single, precise locations. Instead, brain networks encode, store, and retrieve the information that forms our complex memories.

Explicit Memory System: The Frontal Lobes and Hippocampus

25-2 What are the roles of the frontal lobes and hippocampus in memory processing?

The network that processes and stores your explicit memories for facts and episodes includes your frontal lobes and hippocampus. When you summon up a mental encore of a past experience, many brain regions send input to your frontal lobes for working memory processing (Fink et al., 1996; Gabrieli et al., 1996; Markowitsch, 1995). The left and right frontal lobes process different types of memories. Recalling a password and holding it in working memory, for example, would activate the left frontal lobe. Calling up a visual party scene would more likely activate the right frontal lobe.

Cognitive neuroscientists have found that the hippocampus, a temporal-lobe-neural center located in the limbic system, is the brain’s equivalent of a “save” button for explicit memories (FIGURE 25.1). The hippocampus and nearby brain networks are active as people form explicit memories of names, images, and events (Squire & Wixted, 2011).

Damage to this structure therefore disrupts recall of explicit memories. Chickadees and other birds can store food in hundreds of places and return to these unmarked caches months later—but not if their hippocampus has been removed (Kamil & Cheng, 2001; Sherry & Vaccarino, 1989). With left-hippocampus damage, people have trouble remembering verbal information, but they have no trouble recalling visual designs and locations. With right-hippocampus damage, the problem is reversed (Schacter, 1996).

Subregions of the hippocampus also serve different functions. One part is active as people learn to associate names with faces (Zeineh et al., 2003). Another part is active as memory champions engage in spatial mnemonics (Maguire et al., 2003b). The rear area, which processes spatial memory, grows bigger the longer a London cabbie has navigated the maze of streets (Woolett & Maguire, 2011).

Memories are not permanently stored in the hippocampus. Instead, this structure seems to act as a loading dock where the brain registers and temporarily holds the elements of a remembered episode—its smell, feel, sound, and location. Then, like older files shifted to a basement storeroom, memories migrate for storage elsewhere. This storage process is called memory consolidation. Removing a rat’s hippocampus 3 hours after it learns the location of some tasty new food disrupts this process and prevents long-term memory formation; removal 48 hours later does not (Tse et al., 2007).

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Sleep supports memory consolidation. During deep sleep, the hippocampus processes memories for later retrieval. After a training experience, the greater the hippocampus activity during sleep, the better the next day’s memory will be (Peigneux et al., 2004). Researchers have watched the hippocampus and brain cortex displaying simultaneous activity rhythms during sleep, as if they were having a dialogue (Euston et al., 2007; Mehta, 2007). They suspect that the brain is replaying the day’s experiences as it transfers them to the cortex for long-term storage. Cortex areas surrounding the hippocampus support the processing and storing of explicit memories (Squire & Zola-Morgan, 1991).

Implicit Memory System: The Cerebellum and Basal Ganglia

25-3 What roles do the cerebellum and basal ganglia play in memory processing?

Your hippocampus and frontal lobes are processing sites for your explicit memories. But you could lose those areas and still, thanks to automatic (not effortful) processing, lay down implicit memories for skills and newly conditioned associations. Joseph LeDoux (1996) recounted the story of a brain-damaged patient whose amnesia left her unable to recognize her physician as, each day, he shook her hand and introduced himself. One day, she yanked her hand back, for the physician had pricked her with a tack in his palm. The next time he returned, she refused to shake his hand but couldn’t explain why. Having been classically conditioned, she just wouldn’t do it. Intuitively (implicitly) she felt what she could not explain.

The cerebellum plays a key role in forming and storing the implicit memories created by classical conditioning. With a damaged cerebellum, people cannot develop certain conditioned reflexes, such as associating a tone with an impending puff of air—and thus do not blink in anticipation of the puff (Daum & Schugens, 1996; Green & Woodruff-Pak, 2000). When researchers surgically disrupted the function of different pathways in the cerebellum of rabbits, the rabbits became unable to learn a conditioned eyeblink response (Krupa et al., 1993; Steinmetz, 1999). Implicit memory formation needs the cerebellum.

The basal ganglia, deep brain structures involved in motor movement, facilitate formation of our procedural memories for skills (Mishkin, 1982; Mishkin et al., 1997). The basal ganglia receive input from the cortex but do not return the favor of sending information back to the cortex for conscious awareness of procedural learning. If you have learned how to ride a bike, thank your basal ganglia.

Our implicit memory system, enabled by the cerebellum and basal ganglia, helps explain why the reactions and skills we learned during infancy reach far into our future. Yet as adults, our conscious memory of our first three years is blank, an experience called infantile amnesia. In one study, events children experienced and discussed with their mothers at age 3 were 60 percent remembered at age 7 but only 34 percent remembered at age 9 (Bauer et al., 2007). Two influences contribute to infantile amnesia: First, we index much of our explicit memory using words that nonspeaking children have not learned. Second, the hippocampus is one of the last brain structures to mature, and as it does, more gets retained (Akers et al., 2014).

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The Amygdala, Emotions, and Memory

25-4 How do emotions affect our memory processing?

Our emotions trigger stress hormones that influence memory formation. When we are excited or stressed, these hormones make more glucose energy available to fuel brain activity, signaling the brain that something important has happened. Moreover, stress hormones focus memory. Stress provokes the amygdala (two limbic system, emotion-processing clusters) to initiate a memory trace in the frontal lobes and basal ganglia and to boost activity in the brain’s memory-forming areas (Buchanan, 2007; Kensinger, 2007) (FIGURE 25.2). The result? Emotional arousal can sear certain events into the brain, while disrupting memory for neutral events (Birnbaum et al., 2004; Brewin et al., 2007).

Emotions often persist without our conscious awareness of what caused them. In one ingenious experiment, patients with hippocampal damage (which left them unable to form new explicit memories) watched a sad film and later a happy film. After the viewing, they did not consciously recall the films, but the sad or happy emotion persisted (Feinstein et al., 2010).

Significantly stressful events can form almost indelible memories. After traumatic experiences—a school shooting, a house fire, a rape—vivid recollections of the horrific event may intrude again and again. It is as if they were burned in: “Stronger emotional experiences make for stronger, more reliable memories,” noted James McGaugh (1994, 2003). This makes adaptive sense. Memory serves to predict the future and to alert us to potential dangers. Emotional events produce tunnel vision memory. They focus our attention and recall on high priority information, and reduce our recall of irrelevant details (Mather & Sutherland, 2012). Whatever rivets our attention gets well recalled, at the expense of the surrounding context.

Emotion-triggered hormonal changes help explain why we long remember exciting or shocking events, such as our first kiss or our whereabouts when learning of a loved one’s death. In a 2006 Pew survey, 95 percent of American adults said they could recall exactly where they were or what they were doing when they first heard the news of the 9/11 terrorist attacks. This perceived clarity of memories of surprising, significant events leads some psychologists to call them flashbulb memories. It’s as if the brain commands, “Capture this!”

The people who experienced a 1989 San Francisco earthquake did just that. A year and a half later, they had perfect recall of where they had been and what they were doing (verified by their recorded thoughts within a day or two of the quake). Others’ memories for the circumstances under which they merely heard about the quake were more prone to errors (Neisser et al., 1991; Palmer et al., 1991).

Our flashbulb memories are noteworthy for their vividness and our confidence in them. But as we relive, rehearse, and discuss them, these memories may come to err. With time, some errors crept into people’s 9/11 recollections (compared with their earlier reports taken right after 9/11). Mostly, however, people’s memories of 9/11 remained consistent over the next two to three years (Conway et al., 2009; Hirst et al., 2009; Kvavilashvili et al., 2009).

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Dramatic experiences remain bright and clear in our memory in part because we rehearse them. We think about them and describe them to others. Memories of our best experiences, which we enjoy recalling and recounting, also endure (Storm & Jobe, 2012; Talarico & Moore, 2012). One study invited 1563 Boston Red Sox and New York Yankees fans to recall the baseball championship games between their two teams in 2003 (Yankees won) and 2004 (Red Sox won). Fans recalled much better the game their team won (Breslin & Safer, 2011).

25-5 How do changes at the synapse level affect our memory processing?

As you read this module and think and learn about memory, your brain is changing. Given increased activity in particular pathways, neural interconnections are forming and strengthening.

The quest to understand the physical basis of memory—how information becomes embedded in brain matter—has sparked study of the synaptic meeting places where neurons communicate with one another via their neurotransmitter messengers. Eric Kandel and James Schwartz (1982) observed synaptic changes during learning in the neurons of the California sea slug, Aplysia, a simple animal with a mere 20,000 or so unusually large and accessible nerve cells. Other modules describe how the sea slug can be classically conditioned (with electric shock) to reflexively withdraw its gills when squirted with water, much as a battle-weary soldier jumps at the sound of a snapping twig. When learning occurs, Kandel and Schwartz discovered, the slug releases more of the neurotransmitter serotonin into certain neurons. These synapses then become more efficient at transmitting signals. Experience and learning can increase—even double—the number of synapses, even in slugs (Kandel, 2012).

In experiments with people, rapidly stimulating certain memory-circuit connections has increased their sensitivity for hours or even weeks to come. The sending neuron now needs less prompting to release its neurotransmitter, and more connections exist between neurons. This increased efficiency of potential neural firing, called long-term potentiation (LTP), provides a neural basis for learning and remembering associations (Lynch, 2002; Whitlock et al., 2006) (FIGURE 25.3). Several lines of evidence confirm that LTP is a physical basis for memory:

After long-term potentiation has occurred, passing an electric current through the brain won’t disrupt old memories. But the current will wipe out very recent memories. Such is the experience both of laboratory animals and of severely depressed people given electroconvulsive therapy (ECT). A blow to the head can do the same. Football players and boxers momentarily knocked unconscious typically have no memory of events just before the knockout (Yarnell & Lynch, 1970). Their working memory had no time to consolidate the information into long-term memory before the lights went out.

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Recently, I [DM] did a little test of memory consolidation. While on an operating table for a basketball-related tendon repair, I was given a face mask and soon could smell the anesthesia gas. “So how much longer will I be with you?” I asked the anesthesiologist. My last moment of memory was her answer: “About 10 seconds.” My brain spent that 10 seconds consolidating a memory for her words, but could not tuck any further memory away before I was out cold.

Some memory-biology explorers have helped found companies that are competing to develop memory-altering drugs. The target market for memory-boosting drugs includes millions of people with Alzheimer’s disease, millions more with mild cognitive impairment that often becomes Alzheimer’s, and countless millions who would love to turn back the clock on age-related memory decline. From expanding memories perhaps will come bulging profits.

One approach to improving memory focuses on drugs that boost the LTP-enhancing neurotransmitter glutamate (Lynch et al., 2011). Another approach involves developing drugs that boost production of CREB, a protein that also enhances the LTP process (Fields, 2005). Boosting CREB production might trigger increased production of other proteins that help reshape synapses and transfer short-term memories into long-term memories. Sea slugs, mice, and fruit flies with enhanced CREB production have displayed enhanced learning.

Other people wish for memory-blocking drugs. Among them are those who would welcome a drug that, when taken after a traumatic experience, might blunt intrusive memories (Adler, 2012; Kearns et al., 2012). In one experiment, victims of car accidents, rapes, and other traumas received, for 10 days following their horrific event, either one such drug, propranolol, or a placebo. When tested three months later, half the placebo group but none of the drug-treated group showed signs of stress disorder (Pitman et al., 2002, 2005).

In your lifetime, will you have access to safe and legal drugs that boost your fading memory without nasty side effects and without cluttering your mind with trivia best forgotten? That question has yet to be answered. But in the meantime, one effective, safe, and free memory enhancer is already available on your college campus: effective study techniques followed by adequate sleep!

FIGURE 25.4 summarizes the brain’s two-track memory processing and storage system for implicit (automatic) and explicit (effortful) memories. The bottom line: Learn something and you change your brain a little.

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