Lecture 7- Memory and the Temporal Lobe

Question 1

What was Karl Lashley’s proposition for where memory was stored?

Answer 1

Came up with the principle of mass action where memories were stored/ distributed throughout the cortex. He didn’t think memories was located in a particular place.

Question 2

Which famous patient of psychology proved Lashley’s hypothesis for memory storage wrong?

Answer 2

H.M. :
Had a history of seizures suffering from age 10-16. He did not respond to medication so at age 27 he underwent temporal lobectomy removing the temporal lobe, hippocampus and surrounding cortex like the parahippocampal gyrus (as this is the part of the brain the seizures started at). The result was severe anterograde amnesia (unable to form new memories) and retrograde amnesia for 2 years prior to the surgery. His short term memory and remote memory was intact. This shows that in fact the temporal lobe is invovled in storing certain types of memory (it is localised in this way).

Question 3

For patient H.M. what was surprising about the acquisition of certain types of new information?

Answer 3

In mirror drawing task (i.e. procedural memory) H.M. improved with each consecutive day despite not having source memory/ episodic memory for having done the learning.

Question 4

What part of the brain does procedural memory (such as that displayed in the mirror drawing task) involve?

Answer 4

Striatum

Question 5

What part of the brain does priming memory involve?

Answer 5

Neocortex

Question 6

What are the different types of declarative or explicit memory, what area of the brain do they invovle and what was damaged for H.M.?

Answer 6

• Declarative (explicit) memory is spilt into facts (semantic) and events (episodic). Both of these are stored in the medial temporal lobe + diencephalon.
• Interestingly for H.M. only event/ episodic memory was damaged, semantic memory/ general logical sense of how the world worked stayed intact.

Question 7

What do H.M. deficits show?

Answer 7

• Dissociation of intelligence and memory (H.M.’s IQ score actually improved, you can still be intelligent and have poor memory).
• Dissociation of declarative memory from working and procedural memory
• The hippocampus is invovled in memory consolidation (this was removed bilaterally in patient H.M. leading to deficits).

Question 8

What happens when you disrupt the hippocampal circuit? What patient (not H.M.) shows this?

Answer 8

• Hippocampal circuit goes from the dentate gyrus to CA3 neurons to CA1 neurons
• For Patient R.B. an ischemic episode (problem with blood flow to the brain) after open heart surgery resulted in selective, marked anterograde amnesia and very minor retrograde amnesia
• Patient R.B. died shortly after and the brain was examined to show that the hippocampus had been compressed down a lot (loss of neurons). It’s the damage to the CA1 neurons in the hippocampal circuit particularly that leads to memory problems.

Question 9

What did damage to a small section of the hippocampus cause in the Rey-Osterreith figure test?

Answer 9

• Produced memory deficits
• The Rey-Osterreith figure test is where you show an image and the patient has to draw it first by copying and then from memory. Patient RB was fairly good at copying but way worse than controls when had to draw from memory.

Question 10

In Patient H.M. what other regions of the brain where damaged?

Answer 10

The cortical regions around the hippocampus, this is known as the rhinal cortex

Question 11

What was seen in the Rey-Osterreith figure test when the rhinal cortex was damaged as well as the hippocampus?

Answer 11

• Patients couldn’t remember anything! 1 drew nothing, 1 drew a horse
• When it was just hippocampal damage patients were not as good as those with hippocampus intact but generally got some of the elements or the outline of the shape correct.

Question 12

What did patient N.A. have?

Answer 12

• Diencephalic amnesia

- Damage to the mediodorsal thalamus and mammillary bodies

Question 13

What is Wernicke-Korsakoff Syndrome?

Answer 13

This syndrome, which occurs in heavy drinkers, produces similar
memory deficits to those that result from temporal lobe damage
Wernicke-Korsakoff syndrome is caused by lack of thiamine (vitamin
B1) which affects the brain and nervous system, rather than by
alcohol directly.

Lack of thiamine can occur because:
Many heavy drinkers have poor eating habits. Their nutrition is inadequate and will not contain essential vitamins.
Alcohol can inflame the stomach lining and impede the body’s ability to absorb the key vitamins it receives.

The syndrome is also known as ‘wet brain’ or ‘Beriberi’

Question 14

What regions of the brain are damaged in Wernicke-Korsakoff Syndrome? Therefore what type of amnesia is it an example of?

Answer 14

• Dorsomedial nucleus of the thalamus
• Mammillary bodies
• An example of diencephalic amnesia

Question 15

How were IQ scores and memory scores effected in patients with Wernicke-Korsakoff Syndrome?

Answer 15

• IQ scores were not overly effected

- Memory scores were however, a lot lower even compared to those with temporal lobe amnesia

Question 16

How did performance on a pair-associates memory task and story recall task compare across different groups of participants with memory conditions and to alcoholics?

Answer 16

• Low across all the memory conditions tested (lowest in KORS). Some groups didn’t remember anything (particularly in recall test)
• Alcoholics could still perform well although slightly less than the controls

Question 17

What is the hippocampal-diencephalon memory system?

Answer 17

• Spatial information goes to the parahippocampal gyrus, object information goes to the perirhinal cortex
• This information then integrates in the entorhinal cortex then via binding memories are stored in the hippocampus travelling up the fornix to the mamillary body and then into the thalamus
• From here memories are then linked to associations in the neocortex
• These associations can consolidation/ strengthen over time

Question 18

Why would it have initially been hard for researchers like Lashley to discover the hippocampal- dicephalic memory system?

Answer 18

Because the tasks they gave participants could be solved in many different ways

Question 19

What does the limbic system consist of?

Answer 19

• Cingulate gyrus
• Hippocampus
• Amygdala
• Fornix
• Parts of the thalamus

Question 20

True or false: new and recent memories are dependent on the hippocampal-diencephalic memory system?

Answer 20

True

Question 21

What does damage to the diencephalic-hippocampal memory system cause?

Answer 21

Both anterograde and retrograde amnesia

Question 22

What is a common test used to discover the relationship between the hippocampus and spatial information?

Answer 22

-The Morris water maze test (rats without a hippocampus struggle to remember where the platform is- don’t retain spatial information).

Question 23

What are the two ways we can represent our location in space?

Answer 23

Difference is in the reference frame:

Egocentric: the frame of reference is the individual
e.g. left/right, in front of me
Ego: Latin for “I” or “self“

Allocentric: the frame of reference is the external world
e.g. north, south, to the east of the tree.
between the tree and the house

Question 24

How do you manipulate the Morris water maze task to either be egocentric or allocentric? How did rats with hippocampal damage compare to controls in each of these two conditions?

Answer 24

• Constant start (egocentric): rats know they just have to perform a certain pattern of movement to reach the platform. Rats with lesion were nearly as good at this as controls (saw same rapid decrease in time to find the platform)
• Variable start (allocentric): means rats would have to use cues in room. Rats with lesions were far worse than controls (time remain consistently high indicating not much retention of the spatial information).

Question 25

What researcher extended the study of the Morris water maze to humans?

Answer 25

Eleanor Maguire:
Structural MRIs of the brains of humans with extensive navigation
experience, licensed London taxi drivers, were analyzed and
compared with those of control subjects who did not drive taxis.
Wanted to see if the four years of training/ learning the maps of London streets resulted in hippocampal changes.

Question 26

What was shown in the taxi driver study?

Answer 26

-Increased posterior hippocampal volume in taxi drivers compared to controls. The anterior part near the amygdala however actually got smaller. Not much change in the body.

Question 27

What is a concern for the taxi driver’s study validity and what study was done to address these concerns?

Answer 27

• Maybe its other factors: exhaust fumes, steering not the spatial mapping causing the hippocampal changes
• Study done in response was to compare taxi drivers to bus drivers. This way can control for a lot of the lifestyle factors/ driving but bus drivers don’t have to have the same degree of navigation maps because they just follow one route.
• The same differences in brain structure was found with the bus drivers. I.e. the taxi drivers had greater posterior hippocampus area and smaller anterior hippocampus area.
• Taxi drivers were better at both landmark recognition and proximity judgements they were however worse at delayed recall.

Question 28

Does time spent as a taxi driver correlate with hippocampal volume?

Answer 28

• Yes, the changes to the anterior and posterior hippocampus become more pronounced the longer drivers have been driving
• This was however a cross sectional study

Question 29

What is a better way than a cross-sectional study for showing that the changes to hippocampal structure correlate with time spent as a taxi driver?

Answer 29

• Problem with cross sectional as individuals are starting at different times/ may not have same experiences and this could be resulting in the differences not just the time as a taxi driver. I.e. they just took drivers who had been driving for not very long and drivers that have been driving for ages and compared but it might have actually been that the older drivers were trained differently or the way streets were set up forced them to do things differently etc. (there are two many possible contributing factors)
• Instead do longitudinal study: same group tested at different times. No difference in hippocampus size at start between the different groups (qualified trainees, unqualified trainees and controls). It’s the experience of navigating as a taxi driver that causes the change to the hippocampus qualified trainees saw big increase in hippocampal grey matter density).

Question 30

What type of cells are in the hippocampus and what do they have? How do they work collectively?

Answer 30

-Place cells with place fields (fire particular strongly in one place/ at one location)
-Each cell has a different field so can work together to represent a location/ environment
-Collectively hippocampal cells tile space
-For any location, a subset of hippocampal cells will be firing. This
pattern of activity could be incorporated into a memory
representation and so may underlie the ‘where’ of episodic memory.