Below you'll find a review of the topics we've covered for Memory (corresponding to Chapters 8 and 9 in Purves - Introduction to Cognitive Neuroscience and the accompanying lectures in NE202/PS339).
We discussed experiments using several different techniques during this chapter:
Patient KC had severely impair episodic memory, but intact semantic memory. He had extensive damage to the medial temporal lobes, dorsolateral prefrontal cortex, occipital, and parietal cortices due to a motorcycle accident. His case teaches us that semantic memory (memory for facts) is separable from episodic memory (memory for specific experiences). KC's case can be compared to HM's in that HM could remember some early episodic memories, but it is debated whether or not he could acquire new semantic knowledge (see Granola- Jacuzzi experiment), whereas is was known that KC could acquire new semantic memories (slowly) but couldn't recall any episodic memories from his life. More info can be found here. There are several videos of him on youtube:
There are altogether 9 videos of KC, first demonstrating his relatively spared semantic memory, impaired short term memory for events, and impaired long term memory for events:
Youtube playlist of patient KCKorsakoff's syndrome is a disorder caused by thiamine deficiency usually due to prolonged ingestion of alcohol. Thiamine deficiency can cause damage to the mammillary bodies as well as some parts of the thalamus (and other diencephalon structures). Here's a video of Dr. House explaining Korsakoff's syndrome to some interns, after meeting a patient who is reporting many different causes of her injuries.
Dr. House would know, if he had read Wikipedia, that only 20% of cases of Korsakoff's syndrome are reversed with the administration of thiamine. The patient shows a classic sign of Korsakoff's, namely confabulation. By studying Korsakoff's syndrome, we learn that the mammillary bodies and other diencephalon structures play a role in memory.
This was an experiment done with Patient HM to see if he had acquired any new semantic knowledge since his loss of the ability to form new long term memories. From Sue Corkin's book (online access available to BU students), Permanent Present Tense:
We set out to assess Henry’s knowledge of new words that had been added to the Merriam-Webster Dictionary after 1954, words he probably encountered after the onset of his amnesia. The test stimuli were words like charisma, psychedelic, granola, Jacuzzi, and palimony. They were intermixed with old words (butcher, gesture, shepherd ) and pronounceable nonwords (phleague, thweige, phlawse). We wanted to know whether Henry considered the post-1954 words and the pronounceable nonwords to be legitimate words. Each trial began with the following question on the computer screen, “Is the following a real word?” Henry read the word and responded “yes” or “no.” He was right if he answered “yes” for the legitimate words and “no” for the nonwords. He correctly said “yes” to ninety-three percent of the pre-1950s words (which was normal compared to the controls’ ninety-two percent) and fifty percent of the post-1950s words (which was impaired relative to the controls’ seventy-seven percent). His ability to categorize nonwords as nonwords was borderline normal—eighty-eight percent versus the control group’s score of ninety-four percent. This relatively simple experiment strengthened the distinction between Henry’s preoperative semantic knowledge, which was intact, and his postoperative semantic knowledge, which was severely lacking.This confirmed that HM was not making new semantic memories after his operation. This experiment was repeated, but in a slightly different way. Sue Corkin and Brad Bostle wanted to see if these new words could be used as priming stimuli in a word-completion task. From the article, Corkin, S. (2002) "What's new with the amnesic patient H.M.?":
Knowing that H.M. showed normal word-stem completion priming with words that entered the dictionary before his operation, Bradley Postle and I were curious to know whether he would also show priming with words that entered the dictionary after 1965 (12 years after his operation and the onset of his anterograde amnesia). His task was to read words aloud as they were presented, one by one, on a computer screen. One minute later, he viewed three-letter stems, half corresponding to words in the study list and half corresponding to unstudied words, and was asked to complete each stem with the first word that came to mind. The measure of priming was the number of words completed to studied words minus the baseline score of stems completed to unstudied words. We predicted that he would be impaired on this test relative to age- and education-matched control subjects because he lacked representations in his lexicon of post-1965 words. As a result, there would be no traces to activate (or prime) during the study phase of the repetition priming test, and so he would complete word stems to words that he had acquired preoperatively. That is exactly what we found. Not only was H.M. impaired on the repetition priming task with postmorbid words, he also was impaired (as expected) on explicit measures of word knowledge; specifically, on cued recall of the words, generation of definitions and recognition of definitions. (As in previous studies, he primed normally with premorbid words, but could not recall or recognize them explicitly.)This also teaches us a bit about how priming works. Words (or memory traces) are "preactivated" by the prime, but if there are no memory traces, there is nothing to preactivate.
In class, we said that habituation and sensitization were two forms of non-associative learning. The terms habituation and sensitization are used in many contexts in psychology. The definition of habituation is:
the diminishing of a physiological or emotional response to a frequently repeated stimulus.The definition for sensitization is:
a non-associative learning process in which repeated administration of a stimulus results in the progressive amplification of a response.Repetition suppression and repetition enhancement usually refer specifically to neural responses, whether they are measured using electrophysiology or fMRI. Repetition suppression is essentially the same as habituation though; it is the diminishing of a neural signal after repeated presentations of the same stimulus. Sensitization is essentially the same as repetition enhancement; it is the amplification of a neural signal with repeated stimulus presentations. We talked about repetition suppression and enhancement when we looked at fMRI experiments of priming.
Sharpening theory is a theoretical model to explain repetition suppression in fMRI. It hypothesizes that the reason responses to familiar stimuli decrease with repetition is that when the stimulus is first seen, many neurons are activated, even ones that aren't involved directly in identifying the stimulus. After a few repetitions, those unnecessary neurons don't respond anymore; only the neurons crucial to recognizing the stimulus are activated.
From class:
Priming is a form of implicit memory (it occurs without conscious awareness).Priming experiments go something like this: you ask a person to read a list of words to themselves (these are the primes) and then, when they don't expect to be tested on those words, you give them some new task, (for example, word-stem completion). When there is a word-stem that could match a word they saw previously, they will be more likely to respond with that word (these are the targets). The first example in this video is semantic priming (the rest are kind of trivial, but are still examples of priming):
Priming can be direct or indirect. Direct priming means that the priming stimulus is the same as the target. You can use just the perceptual features in direct priming (this is supported by the sensory cortices) or the concept (prime the word "bear", then ask the subject to name the first animal they think of and they'll probably say "bear"). This conceptual priming is supported by the lateral temporal and inferior frontal lobes. Priming can also be indirect, meaning that the prime and target are different, but related. This is the case in semantic priming (supported by the more anterior temporal pole).
Mentalists often use priming and pass it off as magic. Derren Brown is a mentalist who explicitly says that he does not do magic, all of his tricks are just psychology. Here's a video of him doing a trick with two marketers:
Grid cells are neurons found in the entorhinal cortex that fire when an animal is in many different spatial locations. The different locations that the neuron is sensitive to form a hexagonal (six-sided) grid pattern. More info about the discovery of grid cells can be found here. Here's Part 1 of a video of Prof. Mike Hasselmo talking about what grid cells are and his own research on grid cells:
This is a short video of a grid cell being recorded from while a rat moves around a box. Every time you see a white dot left on the screen, that marks a place where the grid cell fired.
Place cells only fire in one particular location whereas grid cells fire in several locations. Here is a video of place cells firing as a rat walks through a track. Each different color represents a different place cell. Each dot records the location of an action potential.
Grid cells and place cells are certainly related. Many theories suggest that place cells become sensitive to a certain place because of the combined input from many grid cells. More info on that here.