Psychology test 1
1. Neurotransmission
Inhibitory v Excitatory Neurotransmitters
Substances that affect Neurotransmitters/Neurotransmission: Agonist vs Antagonists
Neurotransmitter: Acetylcholine (ACh)
Effect of ACh on spatial memory as seen in the Martinez & Kesner (1991) study and Antonova et al. (2011) study
2. Techniques to Study the Brain
Invasive Techniques
Case Studies
Strengths and Limitations
MRI (Brain Scans for Structure)
Strengths and Limitations
fMRI (Brain Scans for Function/Activity)
Strengths and Limitations
3. Localization and Distribution of Function
Theory of Localization of Function
Theory of Distribution of Function
Connectomes/Neural Networks
The Case Study of HM and the evidence it provides for localization and distribution of long term memory
Note: When studying the research, it is important to review the procedure and findings of the studies carefully. You must always describe the research in your own words in responses to questions. It is also important to make sure that you explicitly state the connection between the topic of the question and the procedure.
NeurotransmissionThe process of communication between neurons.
Types of messages sent: electrical and chemical messages.
Neurotransmitters: The chemical messengers. When messages reach the end of the neuron chemical messengers called neurotransmitters are released into the synapse.
Synapse: The space between the neurons.
Excitatory Neurotransmitters: bind to receptors and increase the chances of the post-synaptic neuron firing. (accelerator)
Glutamate
Acetylcholine
Inhibitory Neurotransmitters: bind to a receptor site and reduce the chances of the post-synaptic neuron firing. (break)
GABA (Gamma-Aminobutyric Acid)
Glycine
Bind to receptor sites on another neuron to send a message
Get reuptaken or repackaged into vesicles by the neurons that released them
Get degraded by enzymes.
Agonists: are chemicals that amplify the effects of a neurotransmitter by binding to the receptor of that neurotransmitter and activating them.
Antagonists: are chemicals that block the effects of neurotransmitters by binding to and blocking the receptor sites of that neurotransmitter.
Both can be good or bad depending on the situation.
Example:
GABA(neurotransmitter) — Increase — Alcohol(chemical) increases GABA so it’s an Agonist.
Glutamate(neurotransmitter) — Decrease — Alcohol(chemical) decreases Glutamate so it’s an Antagonist.
Acetylcholine (ACh): A neurotransmitter that plays an important role in learning and short-term memory and is responsible for muscle contraction.
It’s between the junction between motor neurons and skeletal muscles.
Acetylcholinesterase (Cholinesterase): An enzyme that will degrade ACh into its A and Ch parts.
Aim of the study: To determine the role of the neuurotransmitter acetylcholine on spacial memory.
Procedure of the study: The researchers taught the rats how to go throuhg the maze by giving them food once they were able to get out. Once the rats were taugh they split them into 3 groups 2 of them where injected and one was not:
Group 1 | Group 2 | Group 3 |
They were injected with scopolamine. | They where injected with physotigmine. | This was the control group and they where not injected. |
It decreases ACh as they were slower at finding their way around the maze making scopolamine an antagonist. (artificially decreaased) | It increased ACh as they were able to go through the maze faster than any of the other two groups with fewer mistakes making physostigmine an agonist. (artificially increased) | It doesn’t increase or decrease normal levels of ACh. They have the normal levels of ACh. |
Findings:
Group 1 | Group 2 | Group 3 |
They made their way through the maze slower and took a lot of wrong turns, as the ACh receptoirs were blocked. This means that their memory of doing the maze before was basically erased, so they couldn’t remember how to navigate it. | They preformed better and were able to find their way through the maze with fewer mistakes than any of the other groups. This is because physostigmine activated the rececptors allowing them to have better recollection of their memories. | This group preformed neutral as they were the ones not injected with any subjstance. They preformed better than the ones injected with scopolamine but slightly worse than the ones injected with physostigmine. |
How does ACh affect memory?
Based on the results of the study it can be concluded that ACh plays a significant role in spacial memory formation. This can be seen when the ACh receptors were blocked and the rats memories and recolection of the maze was worse causing them to complete it slower and make more mistakes. However when they were injected with the physostigmine they preformed better as their memory and recollection of the maze was better allowing them to complete it faster with fewer mistakes.
Aim of the study:
To test the spacial memories in humans when the ACh was blocked by scopolamine or by a placebo(null).
Procedure of the study: They used 20 healthy male adults with a mean age of 28 years old. They were asked to play “Arena task” where their goal was to reach a pole in an “arena”.
Group 1 | Group 2 |
They were injected with scopolamine which blocked the ACh levels in their brains. This makes scopolamine an antagonist (artificially decreased) | They were injected with the placebo, which didnt block the ACh levels in their brains meaning they have netural levels of ACh. |
3-4 weeks after the participants were first tested: the pasticipants recieced the opposite injection they got in the first round of studies.
When did the participants preform best? | When did the participants preform less well? |
The participants preformed the best when they were injected with the placebo because it didnt bloack the ACh in their brain. | The participants preformed less well when they were injected with the scopolamine because it blocked the ACh in their brain. |
What did the researchers find with the fMRI scans?
The researchers found that the participants ability to create spatial memories was by the activation of their hippocampus.
What does this suggest about the role acetylcholine plays in memory formation?
It suggests that ACh plays an important role in the short-term memory and leaning abilities of an individual. It shows if ACh levels are lower they have less spacial memories compared to when they have netural ACh levels.
Invasive techniques: are invasive procedures of lesioning(scarring brain tissue) and ablation(removing brain tissue). Most of these invasive techniques were done on animals as researchers would damage the brain tissue of animals and then examine the effects of the damage on the animals behavior.
Raises ethical concerns about the treatment of non-human animals as these techniques remove or scar the brain tissue which is brain damage and all brain damage is irreversible.
Anytime someone is cutting into a live brain it causes brain damage which is why it is known as an invasive technique because they are directly working with the brain.
Case studies: were the most popular method to study the brain before the emergence of imaging technology.
These were medical studies.
Strengths of case studies:
They are naturally occurring brain damage (no unethical damage done to human brains to be used in a study.)
Has ecological validity, and no ethical violations.
All qualitative data has ecological validity
Longitudinal (long term, short term) examination of short-term and long-term effects of brain damage. (range of effects)
Examination of the range of effects of the damage rather than just focusing on a single behavior.
Triangulation of research methods for richer data and a more detailed picture of the case.
Interview with the family
Psychometric testing (IQ)
Experiments
Observations
Lots of different research methods to study one thing.
Limitations of case studies:
Cause and effect relationships cannot be determined, as there's no manipulation of an IV.
Findings cannot be generalized as each case is unique, and a single individual is studied. Lacks population validity as it's an extremely small sample size.
Replication is not possible because we cannot control the variables, and we can't harm other people to replicate a case study, as it would be unethical to cause harm to humans.
Accurate information can be difficult to obtain about what the patient was like before the damage took place.
MRI’s: are pictures of the structure of the brain produced by magnets and radio waves measuring the hydrogen nuclei in the body.
MRI scans can show
tumors
bleeding in the brain
nerve injury
damage such as that caused by strokes
changes in the size of particular brain structures
Strengths of MRI’s:
Can produce detailed 3D images that allow for diagnosis of tumors, bleeding in the brain, and damage caused by injury, infection, or stroke
It's a non-invasive, so it's safer than other techniques
It doesn't use radiation
The quality of images is continually improving
Limitations of MRI’s:
It can be very noisy
It's difficulty for people to stay still while they are being scanned, and movement affects the quality of the images
It cannot be used on people with metal inserts in their body as it uses very powerful large magnets
It's an expensive procedure
fMRI’s: measure brain processes through the flow of oxygenated blood through the brain. fMRI images can be turned into 3D,colored, moving image of the brain.
Strengths of fMRI’s:
The image is high quality, and it produces a film that demonstrates change in the brain over the period of the scan
It's non-invasive, so it's safer than other techniques
It doesn't use radiation
It can be combined with other techniques like EEG’s to get more detailed data.
Limitations of fMRI’s:
Its expensive
It records activity more slowly than an EEG
It cannot be used on people with metal inserts in their body as it uses very powerful large magnets
The fMRI is not a natural environment, which means research based on its use, may lack ecological validity
It's an environment that may make people feel anxious and that could affect the scan that is taking place
The use of colors may exaggerate the activity of the brain
Much of the brain activity is spontaneous and is not a reaction to stimuli
It's difficult to know exactly which areas of the brain are active in a behavior
The Theory of Localization of Function: is when a specific part of the brain is responsible for a specific function .
One specific part of the brain is responsible for a function.
Example: The brain stem (a specific part of the brain) is responsible for controlling our breathing and heart rate (specific functions).
The Theory of Distribution of Functtion: is when different parts of the brain are responsible for a function.
Two or more parts of the brain is responsible for a function.
Example: The frontal lobe and the cerebellum (parts of the brain) are both responsible for movement (function).
Connectome: A neutral network across which a certain function or behavior is distributed.
How is it related to both theories?
Areas of localization joined by neutral pathways that together make a connectome which is a neutral network across which a certain function of behavior is distributed.
What was the cause of HM’s brain damage?
The brain damage was caused by the surgery HM got by Dr. Scoville as he removed both of his hippocampi in 1953.
What structure in his brain was damaged?
The structure of his brain that was damaged was both sides of his medial temporal lobe, specifically both hippocampi.
What kind of memory did HM lose? What evidence exists for this in the reading/video?
HM lost his explicit long term memory as seen when he couldn’t remember memories from the past decade (episodic) before the surgery but could remember his child hood memories.
While he could work with information (semantic) he couldnt retain the information as seen when he would continuesly repete a number to himself and would be able to remeber it for about 20 min but then would forget about it.
He would also do something but would forget about it right after like when he would eat and forget he did so and eat again causing him to get sick.
What kind of memory did HM keep? What evidence exists for this in the reading/video?
He kept his implicite long term memory, specifically his procedural long term memory as he could still preform skills and learn them by muscle memory but could not remeber learning them.
Like when he was asked to do the mirror activity of tracing a star on a piece of paper while looking at the reflection in the mirror. He did the activity multiple times but couldnt remeber doing it. however every time he did it again he go better as he still has muscle memory.
He also kept his emotional conditioning long term memory as he could remeber JFK’s assasination in 1963 since it was very shocking even though he shouldnt have been able to as it was 10 years after his surgery.
How does HM’s case support the TLF?
HM’s case provides evidencce that a specific part of the brain is in charge of a specific funtion as seen when he lost both hippocampi and then lost his explicit LTM.
How does HM’s case support the TDF?
HM’s case provides evidence that specific funtions are distributed in different parts of the brain as with HM as he still has his implicite LTM which is controlled by the basal ganglia and the cerebellum (two different parts of the brain).
1. Neurotransmission
Inhibitory v Excitatory Neurotransmitters
Substances that affect Neurotransmitters/Neurotransmission: Agonist vs Antagonists
Neurotransmitter: Acetylcholine (ACh)
Effect of ACh on spatial memory as seen in the Martinez & Kesner (1991) study and Antonova et al. (2011) study
2. Techniques to Study the Brain
Invasive Techniques
Case Studies
Strengths and Limitations
MRI (Brain Scans for Structure)
Strengths and Limitations
fMRI (Brain Scans for Function/Activity)
Strengths and Limitations
3. Localization and Distribution of Function
Theory of Localization of Function
Theory of Distribution of Function
Connectomes/Neural Networks
The Case Study of HM and the evidence it provides for localization and distribution of long term memory
Note: When studying the research, it is important to review the procedure and findings of the studies carefully. You must always describe the research in your own words in responses to questions. It is also important to make sure that you explicitly state the connection between the topic of the question and the procedure.
NeurotransmissionThe process of communication between neurons.
Types of messages sent: electrical and chemical messages.
Neurotransmitters: The chemical messengers. When messages reach the end of the neuron chemical messengers called neurotransmitters are released into the synapse.
Synapse: The space between the neurons.
Excitatory Neurotransmitters: bind to receptors and increase the chances of the post-synaptic neuron firing. (accelerator)
Glutamate
Acetylcholine
Inhibitory Neurotransmitters: bind to a receptor site and reduce the chances of the post-synaptic neuron firing. (break)
GABA (Gamma-Aminobutyric Acid)
Glycine
Bind to receptor sites on another neuron to send a message
Get reuptaken or repackaged into vesicles by the neurons that released them
Get degraded by enzymes.
Agonists: are chemicals that amplify the effects of a neurotransmitter by binding to the receptor of that neurotransmitter and activating them.
Antagonists: are chemicals that block the effects of neurotransmitters by binding to and blocking the receptor sites of that neurotransmitter.
Both can be good or bad depending on the situation.
Example:
GABA(neurotransmitter) — Increase — Alcohol(chemical) increases GABA so it’s an Agonist.
Glutamate(neurotransmitter) — Decrease — Alcohol(chemical) decreases Glutamate so it’s an Antagonist.
Acetylcholine (ACh): A neurotransmitter that plays an important role in learning and short-term memory and is responsible for muscle contraction.
It’s between the junction between motor neurons and skeletal muscles.
Acetylcholinesterase (Cholinesterase): An enzyme that will degrade ACh into its A and Ch parts.
Aim of the study: To determine the role of the neuurotransmitter acetylcholine on spacial memory.
Procedure of the study: The researchers taught the rats how to go throuhg the maze by giving them food once they were able to get out. Once the rats were taugh they split them into 3 groups 2 of them where injected and one was not:
Group 1 | Group 2 | Group 3 |
They were injected with scopolamine. | They where injected with physotigmine. | This was the control group and they where not injected. |
It decreases ACh as they were slower at finding their way around the maze making scopolamine an antagonist. (artificially decreaased) | It increased ACh as they were able to go through the maze faster than any of the other two groups with fewer mistakes making physostigmine an agonist. (artificially increased) | It doesn’t increase or decrease normal levels of ACh. They have the normal levels of ACh. |
Findings:
Group 1 | Group 2 | Group 3 |
They made their way through the maze slower and took a lot of wrong turns, as the ACh receptoirs were blocked. This means that their memory of doing the maze before was basically erased, so they couldn’t remember how to navigate it. | They preformed better and were able to find their way through the maze with fewer mistakes than any of the other groups. This is because physostigmine activated the rececptors allowing them to have better recollection of their memories. | This group preformed neutral as they were the ones not injected with any subjstance. They preformed better than the ones injected with scopolamine but slightly worse than the ones injected with physostigmine. |
How does ACh affect memory?
Based on the results of the study it can be concluded that ACh plays a significant role in spacial memory formation. This can be seen when the ACh receptors were blocked and the rats memories and recolection of the maze was worse causing them to complete it slower and make more mistakes. However when they were injected with the physostigmine they preformed better as their memory and recollection of the maze was better allowing them to complete it faster with fewer mistakes.
Aim of the study:
To test the spacial memories in humans when the ACh was blocked by scopolamine or by a placebo(null).
Procedure of the study: They used 20 healthy male adults with a mean age of 28 years old. They were asked to play “Arena task” where their goal was to reach a pole in an “arena”.
Group 1 | Group 2 |
They were injected with scopolamine which blocked the ACh levels in their brains. This makes scopolamine an antagonist (artificially decreased) | They were injected with the placebo, which didnt block the ACh levels in their brains meaning they have netural levels of ACh. |
3-4 weeks after the participants were first tested: the pasticipants recieced the opposite injection they got in the first round of studies.
When did the participants preform best? | When did the participants preform less well? |
The participants preformed the best when they were injected with the placebo because it didnt bloack the ACh in their brain. | The participants preformed less well when they were injected with the scopolamine because it blocked the ACh in their brain. |
What did the researchers find with the fMRI scans?
The researchers found that the participants ability to create spatial memories was by the activation of their hippocampus.
What does this suggest about the role acetylcholine plays in memory formation?
It suggests that ACh plays an important role in the short-term memory and leaning abilities of an individual. It shows if ACh levels are lower they have less spacial memories compared to when they have netural ACh levels.
Invasive techniques: are invasive procedures of lesioning(scarring brain tissue) and ablation(removing brain tissue). Most of these invasive techniques were done on animals as researchers would damage the brain tissue of animals and then examine the effects of the damage on the animals behavior.
Raises ethical concerns about the treatment of non-human animals as these techniques remove or scar the brain tissue which is brain damage and all brain damage is irreversible.
Anytime someone is cutting into a live brain it causes brain damage which is why it is known as an invasive technique because they are directly working with the brain.
Case studies: were the most popular method to study the brain before the emergence of imaging technology.
These were medical studies.
Strengths of case studies:
They are naturally occurring brain damage (no unethical damage done to human brains to be used in a study.)
Has ecological validity, and no ethical violations.
All qualitative data has ecological validity
Longitudinal (long term, short term) examination of short-term and long-term effects of brain damage. (range of effects)
Examination of the range of effects of the damage rather than just focusing on a single behavior.
Triangulation of research methods for richer data and a more detailed picture of the case.
Interview with the family
Psychometric testing (IQ)
Experiments
Observations
Lots of different research methods to study one thing.
Limitations of case studies:
Cause and effect relationships cannot be determined, as there's no manipulation of an IV.
Findings cannot be generalized as each case is unique, and a single individual is studied. Lacks population validity as it's an extremely small sample size.
Replication is not possible because we cannot control the variables, and we can't harm other people to replicate a case study, as it would be unethical to cause harm to humans.
Accurate information can be difficult to obtain about what the patient was like before the damage took place.
MRI’s: are pictures of the structure of the brain produced by magnets and radio waves measuring the hydrogen nuclei in the body.
MRI scans can show
tumors
bleeding in the brain
nerve injury
damage such as that caused by strokes
changes in the size of particular brain structures
Strengths of MRI’s:
Can produce detailed 3D images that allow for diagnosis of tumors, bleeding in the brain, and damage caused by injury, infection, or stroke
It's a non-invasive, so it's safer than other techniques
It doesn't use radiation
The quality of images is continually improving
Limitations of MRI’s:
It can be very noisy
It's difficulty for people to stay still while they are being scanned, and movement affects the quality of the images
It cannot be used on people with metal inserts in their body as it uses very powerful large magnets
It's an expensive procedure
fMRI’s: measure brain processes through the flow of oxygenated blood through the brain. fMRI images can be turned into 3D,colored, moving image of the brain.
Strengths of fMRI’s:
The image is high quality, and it produces a film that demonstrates change in the brain over the period of the scan
It's non-invasive, so it's safer than other techniques
It doesn't use radiation
It can be combined with other techniques like EEG’s to get more detailed data.
Limitations of fMRI’s:
Its expensive
It records activity more slowly than an EEG
It cannot be used on people with metal inserts in their body as it uses very powerful large magnets
The fMRI is not a natural environment, which means research based on its use, may lack ecological validity
It's an environment that may make people feel anxious and that could affect the scan that is taking place
The use of colors may exaggerate the activity of the brain
Much of the brain activity is spontaneous and is not a reaction to stimuli
It's difficult to know exactly which areas of the brain are active in a behavior
The Theory of Localization of Function: is when a specific part of the brain is responsible for a specific function .
One specific part of the brain is responsible for a function.
Example: The brain stem (a specific part of the brain) is responsible for controlling our breathing and heart rate (specific functions).
The Theory of Distribution of Functtion: is when different parts of the brain are responsible for a function.
Two or more parts of the brain is responsible for a function.
Example: The frontal lobe and the cerebellum (parts of the brain) are both responsible for movement (function).
Connectome: A neutral network across which a certain function or behavior is distributed.
How is it related to both theories?
Areas of localization joined by neutral pathways that together make a connectome which is a neutral network across which a certain function of behavior is distributed.
What was the cause of HM’s brain damage?
The brain damage was caused by the surgery HM got by Dr. Scoville as he removed both of his hippocampi in 1953.
What structure in his brain was damaged?
The structure of his brain that was damaged was both sides of his medial temporal lobe, specifically both hippocampi.
What kind of memory did HM lose? What evidence exists for this in the reading/video?
HM lost his explicit long term memory as seen when he couldn’t remember memories from the past decade (episodic) before the surgery but could remember his child hood memories.
While he could work with information (semantic) he couldnt retain the information as seen when he would continuesly repete a number to himself and would be able to remeber it for about 20 min but then would forget about it.
He would also do something but would forget about it right after like when he would eat and forget he did so and eat again causing him to get sick.
What kind of memory did HM keep? What evidence exists for this in the reading/video?
He kept his implicite long term memory, specifically his procedural long term memory as he could still preform skills and learn them by muscle memory but could not remeber learning them.
Like when he was asked to do the mirror activity of tracing a star on a piece of paper while looking at the reflection in the mirror. He did the activity multiple times but couldnt remeber doing it. however every time he did it again he go better as he still has muscle memory.
He also kept his emotional conditioning long term memory as he could remeber JFK’s assasination in 1963 since it was very shocking even though he shouldnt have been able to as it was 10 years after his surgery.
How does HM’s case support the TLF?
HM’s case provides evidencce that a specific part of the brain is in charge of a specific funtion as seen when he lost both hippocampi and then lost his explicit LTM.
How does HM’s case support the TDF?
HM’s case provides evidence that specific funtions are distributed in different parts of the brain as with HM as he still has his implicite LTM which is controlled by the basal ganglia and the cerebellum (two different parts of the brain).