Weeks 1-5 Flashcards
What did Aristotle believe the role of the brain was
Thought brain was cooling mechanism, heart gets hot with thoughts and sensation and would send blood through brain to be cooled
What were Galens definitions of the brain, heart and liver
He defined
Brain as the Rational Soul
Heart as the Passionate Soul
Liver as the Appetitive Soul
Where did Galen believe thinking occured
Galen attributed this thinking & rational thought processes to the ventricles (fluid filled areas in brain) - thought cerebral spinal fluid would connect to brain stem and transmit these signals
Who critiqued the ideas of Galen
Andreas Vesalius. He went against Galen and said it was not the ventricles through conducting illegal dissections on human brains
What was Andreas Vesalius’s understanding of the brain
places the brain as seat of all thought, feeling and action
What was Luigi Galvanis contribution to neuroscience
Following the discovering of electricity which occured during his lifetime, figured out the brain used electricity to function.
Describe Luigi Galvanis neurostimulation study and what it found.
He created electrical potential to make frogs leg twitch
Brings about the ideas that there are neurons in the brain which communicate electrically
Franz Galls ideas about the brain
Different brain areas have different functions (novel idea at this point) Believed that continuously using a function caused it to “grow” creating bumps on the skull
Where was Gall right (somewhat) and where was he wrong. What were his incorrect findings used to justify?
- Localisation (right in the idea that different areas have different functions) but wrong functions
- Brain function entirely unrelated to skull shape
Used to justify racism (across culutres, differences in shapes of skull, thought this would explain personality differences between races)
- Brain function entirely unrelated to skull shape
Phineas Gage as a real-life contribution to neuroscience
Working railway and survived a metal pole. Shows that you can take a chunk out of someone’s brain and still operate
Pierre Paul Broca
- Collected the deceased brains of numerous patients that lost ability to speak (that could still comprehend what was going on) and found repeated dead tissue/lesion in the same spot in each of these brains.
Named this area of the brain the “seat of language” and this region was later terms “brocas area”
How did broca change the way physicians/neuroscientists approached studying the brain
Contributed to cognitive neuropsychology as now they could look for patterns (how damage to specific regions can continuously lead to the same symptoms)
Dualism
Brain and mind/soul are separate things
Monoism
Brain and mind are two manifestations of the same thing. Mind IS what the brain DOES
Functionalism
The mind carries out functions, which are implemented by the brain
Wilhelm Wundt
First Psychology Lab - 1879
Conducted experiments trying to understand thought
Hermann Ebbinghaus
First studies of memory - 1885
William James
First psychology textbook - 1890
Turing machine & computer science contribution to understanding of the brain
- Turing machine Proposed idea that you could create what looks like thought through inputs and outputs
Metaphors of Mind/Brain Function
Our understanding of the brain is a reflection of the era we are in.
Industrial revolution = mind is a series of gears
Modern day = brain is a computer
How many neurons in the brain
86 Billion, and the vast majority (69 billion are in cerebellum)
How many connections does each neuron roughly make
20,000
What factors change our brain
Genetics, pre natal factors, pre pre natal factors, injury, psychedellics (and so so many other things)
Do genetics mutation cause disease
No, they only increase the risk. The only case in which a single mutation causes a condition is with narcolepsy.
Prenatal factors influencing the brain - Maternal infection
Risk of major depressive disorder in children from mothers who had virus/bacteria during pregnancy is significantly higher than those that did not
Pre-pre-natal factors influencing the brain - alcohol tolerance
Study done in rats showed that Children & Grandchildren of alcoholics are significantly less affected by alcohol
“The man with no brain”
44 yo man, mild leg weakness for 2 weeks. married with a child and only slightly below average IQ. Brain scan found he only has 1/10th of his brain, the rest being filled with CSF
“The woman with no cerebellum”
24 yo woman, dizziness, mild motor impairments was found to have no cerebellum
Psychedellics - the power of a single dose of psilocybin
- After one SINGLE dose individuals depressive symptoms can subside for up to 6 months. These drugs must fundamentally change something in the brain
Roger Sperry
Neurophysiologist who studied differences between left and right side of the brain. Made contributions to the practice of severing the corpus callosum to prevent epileptic storms
When does brain development start
2 weeks after conception
What is the first embryonic stage of brain development
Edges of the embryo fold over to create the neural tube. In the next few weeks, the neural tube will close completely and brain & heart bulges will form
Is the early stage of brain development universal
Yes, it is seen in almost every species and completely driven by genes
What genes drive early brain development
Homeobox genes, and they determine what limbs grow where. Removing/altering the homeobox genes in species can cause legs to grow where antenna should be.
How does the forebrain grow during brain development
In early stages, the forebrain, midbrain and hindbrain are roughly equal sizes. Over time, the forebrain becomes dominant and takes over as the largest part of the individual
How much does the brain weigh at birth
300g
How much does the brain weigh after 1 year
1000g (almost adult size which is 1300g/1400g)
Do sensory or integrative systems develop first
sensory
When does the motor system develop
Near to last. However, at the spinal cord level, spontaneous activity already drives muscle movement before the brain motor system develops
Stage 1 of Brain development
Neurogenesis
Neurogenesis
Formation of neurons that starts from week 3
What is stage 2 of brain development
Gliogenesis
What is stage 3 of brain development
Synaptogenesis
What is synaptogenesis
Forming of synaptic connections that happens mostly after birth
Stage 4 of brain development
Myelination
What is myelination
Insulation axons to increase the speed of synaptic transmission - happens last in the prefrontal cortex at around 20 years.
Stage 5 of brain development
Synaptic pruning
What is synaptic pruning and why does it occur
Synapses are formed indiscriminately, but this means a lot of extra “noise” and energy use in the brain. Synaptic pruning is the process of strengthening good synapses and disconnecting unnecessary ones to refine synaptic connection. This process is most active between the ages of 2 and 10, but finishes at around 20
Viral infection in pregnancy is associated with…
Higher chances of autism and major depressive disorder
Maternal infection in second trimester specifically is associated with
Higher chances of developing schizophrenia
Fingerprints & Schizophrenia
In the second trimester, our fingerprints are formed. When looking at the fingerprints of schizophrenic individuals, they are less organised and formed than healthy individuals. This is because maternal infection in the second trimester increases the likelihood of schizophrenia, and also decreases the proper formation of fingerprints.
The Serotonergic system
Uses serotonin as neurotransmitter
Why study the optic nerve connection in lizards
If you sever/disconnect Salamanders optic nerve, it will regrow. This is not the same for most other species.
Describe the study on lizards that aimed to figure out “how axons know where to go?”
Researched turned the eye of the lizard 180 degrees around so that what was front was back and what was up was down. By doing this, he could see whether the origin of the cells in the eye determines where they go, or if the terminal region in the brain tells the axons where to come from. He found that after flipping the eye, the axons regrow and attach to the same target neuron as before
Conclusion of lizard study on eye
Cells of origin determine where the axon needs to go
How do axons know where to go?
Chemical highways that are formed early on in life. Axons will follow that highway depending on their type (red cells = red highway, green cells = green highway)
Do chemical trails remain in the brain over the whole course of our life
No, they only exist during development. Even if embryonic cells capable of developing axons are implanted in adult brain, they have nowhere to go since the highway is gone. It was thought that cell implantation could be a means of restoring lost connections in parkinsons patients but since the axons have no where to go the implanted cells will simply die off.
Nerve Growth Factors
A protein released by the post synaptic cell (target) after it has been used enough times
What do Nerve growth factors do
Strengthen the axon. If the target does not release NGF, the axon will degenerate and the cell will die through apoptosis.
Cell body & terminal reigon role in the brain
Cell body - determines where the axon will go
Terminal region - determines whether to “keep or kill” through the release of NGF.
What increases and what decreases adult plasticity
Learning and memory = increase this by forming new synaptic connections
Chronic stress = decrease this
What is depression accompanied by
A decrease in dendritic spines
How do antidepressents work in terms of plasticity
They can grow synapses and dentritic connections to restore those lost as a result of depression
Brain Adaptation in blind individuals
Measured blind people doing braille while measuring their brain activity in fMRI. Found that activity of the occipital cortex is activated in blind people when they read braille. However when fully seeing people read braille their occipital cortex is not activated
What happens when you use TMS to deactivate the occipital cortex in blind people and what does this show
They have trouble reading braille, this shows us that touch takes over the function of sight in those who are blind
Post-mitotic
Neurons are post-mitotic so once they are formed they cannot divide
Embryonic stem cells
Can grow (NOT DIVIDE) into neurons, often in the hippocampus, olfactory bulb and striatum. These cells are often related to learning and memory NOT recovery of lost cells.
Stroke
Temporary distruption of blood flow to the brain
Ischemia
Stroke caused by loss of blood, leading to lack of oxygen and glucose
Hemorrhage
A kind of stroke that means there is too much blood, causing excess oxygen and Ca2+.
What does stroke do to the brain
Impair the Na/K pump, leading to excess Na+ inside the cell. This leads to enhanced glutamate release, which can ultimately kill cells.
How long can brain cells go without oxygen for
5-10 minutes
Ways in which the brain recovers from stroke
- Compensation through increased activity in surrounding areas
- Increasing activity in the brain regions that the damaged neurons project to
- Peripheral axons can grow back (CNS ones cannot)
- Collateral sprouting due to release of neurotrophic factors
- Denervation supersensitivity
Collateral sprouting
Axons form additional connections to compensate for the loss
Denervation supersensitivity
The number of receptors on the post synaptic cell increases. This means that less activity of a neuron is needed in order to activate the cell. This helps to compensate for those that have died
Recovery from stroke is all about…
COMPENSATION - from other brain areas, from receptors, from axons. All alter their activity to compensate for the loss.
What happens in the somatosensory cortex following amputation
Areas in the somatosensory cortex do not go “silent” after amputation, instead the areas of the remaining digits become larger
What causes phantom limb
Reorganisation of the somatosensory cortex. Eg. after amputation of the hand, the “hand area” of the cortex is taken over by the face and the shoulder. However, this area is still the “hand” area, so stimulating the face can feel like touching the hand. The solution to this is artificial limbs to reorganise the information.
Foundation of fMRI
Brain cells in action need MORE energy, therefore these areas that are being used (active) will have MORE blood flow
Two aspects of methodology
Manipulation and Imaging
Manipulation
- Using methodologies to alter brain states and see the consequences
Phineas Gage
Because of his accident where part of prefrontal cortex was cut off, his changes in behaviour were put down to his damage of PFC
Manipulation - Brain damage
Since we cant give individuals brain damage ethically, often multiple areas of the brain are damaged and its not localised. Use animal research to put small lesions in the brain as this cant be done on humans
Advantages of studying brain damage
Has helped us learn about the role of specific brain areas
Disadvantages of brain damage
In humans, lesions are often large, encompassing multiple brain regions. Moreover, it is difficult to find people with the same lesions
Animal studies on brain damage
Use electrolytic lesions
Rat study on lesion to different places in the hypothalamus findings
Lesion to the Lateral hypothalamus will result in a decrease in food intake for rates as hunger cues are affected
Lesion to the ventromedial hypothalamus will result in an increase in food intake for rats, causing their hunger cues to dissipate and them to eat uncontrollably.
Limitation of using electrolytic lesions in animals and a solution to this
Limitation: Electrical lesions kill cells within the area, but also fibres that go through the area (are not completely localised)
Solution: Chemical lesions
Parkinsons disease
- Nerve degenerative disorder when dopamine producing cells start to die
Characterised by tremmor, rigid muscles, masked face
Best way to treat Parkinsons
Deep brain stimulation
What is deep brain stimulation
Direct stimulation of the brain (electrical or magnetic) which almost fully alleviates parkinsons symptoms
Requires surgery so is often restricted to extreme cases when the drug isn’t working
what is Transcranial Magnetic Stimulation (TMS)
- Changes electrical activity in the brain
- Low level of stimulation, excite cells = more active
- High level = neuronal inhibition
- Mostly used for cortical studies (2-3cm deep)
Not applicable for subcortical reigons due to depth restrictio
Advantages of TMS
Reversible, so can be turned on an off.
TMS doesn’t require surgery
Limitations of TMS
- All cells are stimulated or inhibited
TMS is limited to cortical areas
different types of Imaging
EEG, fMRI, PET, Microscopy
Microscopic Imaging benefit and limitation
- We can measure almost anything at a very high spatial resolution
Limitation: Can only properly be done post-mortem
Electroencephalogram (EEG)
- Electrodes on the skull (though sometimes in the brain)
- Participants asked to do something, or observe basal activity
- Can be used to investigate sleep phases (on the basis of electrical activity in the brain)
Advantages of EEG
Very fast (high temporal resolution), as fast as cells fire, easy to measure from multiple brain regions simultaneously
What is Temporal resolution
how fast changes in signal occur
What is spatial resolution
how detailed can u differentiate between brain region
Magnetic Imaging (MRI)
- Based on measuring hydrogen
- Good resolution (mm) and contrast
Well suited for detecting structural changes
Functional MRI
- Mainly based on measuring BOLD (blood oxyegn level dependent)
- Higher brain activity higher oxygen levels
- Always compare two conditions
Red and blue in fMRI scan
- Blue = increase in activity before and after
Red = decrease in activity before and after
Tower of Hanoi
- Used on patients suffering from autism
- Found that interaction and connectivity is critically dependent for behaviour
Parietal cortex
sensory info, spatial awareness, and movement
Autism tower of hanoi study while in fMRI
PFC in harmony with partial cortex in healthy volunteers
In patients with autism, no synchrony between PFC and Parital cortex when solving
Limitations on magnetic imaging (fMRI and MRI)
Can only measure correlations between brain and behaviour, does not give information on neurotransmitters and temporal resolution is not that great, though improvements have been made (now around 4 to 5 seconds)
Advantages of magnetic imaging
Good spatial resolution (about 1.5 m3), can measure both structural and functional activity.
2 related techniques of magnetic imaging
Structural and functional Magnetic Resonance imaging (MRI).
James Watson and Francis Crick
- Explained the structure of DNA in a small, published paper
Changed the fields of biology, medicine, forensics etc
Pea Plant study
Gregor Mendel looked at characteristics of pea plants that could only occur in 2 forms, could take green plant & yellow plant and observe colour of offspring. Mendel was lucky because unlike most crosses of different species, the offspring of 2 different species of pea plants together can still produce fertile offspring
Mendels conclusion from his pea plants
Every organism inherits 2 elements of heredity, one from the father, one from the mother. In some cases, one element dominants the other recessive one
Homozygous
alleles are identical
Heterozygous
alleles differ
How many chromosomes do we have
- 23 pairs of chromosomes
What 6 elements does DNA consist of
- Sugar & Phosphate bound together. 4 bases, adenine, thymine, cytosine, guanine
Lock and key model in DNA
A can only ever bind with T, and C can only bind with G. If you split them and allow two new chains to be formed on each side, the new chains will always be the exact same copy
Is everyones DNA different
In most cases yes however identical twins have the same DNA. This is because when sperm & egg combine, THAT cluster of cell divides into 2 and two embryos develop.
Transcription
DNA –> RNA. U swaps T but sequence is exactly the same
Translation
- Amino acids are coded for by 3 bases ( a triplet). The transcribed chain is “read” by a ribosome in triplets, and a chain of amino acids is formed
Triplet
Three bases which determine the amino acid
COMT mutation (polymorphism)
COMT is an enzyme that is involved in the breakdown of dopamine
In position 158, you can have either Met of Val protein
Wisconsin Card sorting test
A card sorting game in which the psychologist testing the individual changes the rule halfway through the game. It involves cognitive switching.
COMT mutation and wisconsin card sorting test
_eople who have Val/val protein in COMT gene tend to keep making preservative errors in the game. This shows that just a single amino acid change can have direct consequences for behaviour
Epigentics
How tightly DNA is coiled and accessible to the machinery that reads genes
Why are brain cells different from kidney cells.
The reason is that while all cells contain the same DNA, every different type of cell makes its own RNA
For example, all cells in he body have the DNA for the voltage gated Na+ ion channels, but only in brain cells are these genes “turned on”
Histones
Special proteins that are positively charged to bind to the negatively charged DNA
Mutation
(Permanent change to the base code of DNA)
Epigenetic changes
lead to DNA being more open/more tightly coiled. More open = more RNA can be formed, and more protein can be made
Are mutations qualitative or quantitive changes?
qualitative changes as the actual protein produced is of different QUALITY (different amino acid in a chain)
Are epigenetic changes qualitative or quantitive?
Quantitative change as how tightly DNA is coiled affects how much RNA is formed and therefore the QUANTITY of proteins produced.
Why do neurons rely on electrical communication
Passively allowing the electricity to flow will never allow the signal to travel down the whole axon
Depolarisation
Increase in resting membrane potential
Hyperpolarisation
decrease in RMP
Ion Channels
Very specific. Will only allow one ion to go through, but none of the other types
Concentration of Na and K at resting state
High conc. of sodium on the outside. High conc of K+ on the inside
Depolarisation
The Na+ channels open, causing sodium to flood into the cell because of the chemical gradient (more sodium outside than inside, so sodium will flow in) and the electrical gradient (sodium is positively charged, inside is negative, therefore the negatively charged ions will flow into the more negatively charged cell)
Summation
The total of all incoming signals, eventually reaches a threshold that allows sodium channels to open (all or nothing)
What does all or nothing meaning
Once enough weak stimulation of dendrites reaches -60MV, the “flip is switched”, and all of the sodium channels will open, allowing sodium to flood into the cell (depolarisation) and the action potential has begun and will not stop
When to K+ channels open & what are the effects.
At around -60MV when sodium channels open. Initially, this does not do much (outside the cell is positive and so is K+, so the K+ cannot leave due to the electrical gradient). However, as sodium is flooding in, the inside becomes less negative (electrical current shifts) and therefore the concentration gradient will allow K+ to flood out
What happens at 30MV
The sodium ion channels will close, stopping the influx of sodium into the cell.
K+ channel closes later, allowing K+ to exit the cell and allowing the inside to become negative again
Na/K pump
A protein embedded in the cell membrane which restores chemical balance. This is an active process (therefore requires energy to occur) and is one of the reasons brain activity is so energy-consuming. The Na/K pump will actively move Na+ out of the cell and K+ into the cell
Propagation
“Domino effect” - As one Na channel opens up, the area of the cell near that ion channel becomes more positive, as Na+ floods in, and therefore this increase in electrical charge will cause the neighbouring Na Channel to open as well. This spreads like a domino effect down the axon
Refractory period
When Na+ channels close, they close in a refractory state (so tightly that even if it does reach 60MV it won’t open). This is a mechanism to stop the cell from firing, firing, and firing until it dies
Absolute refractory state
not responsive at all (about 1ms)
Relative refractory state
Only responsive to strong stimulus (about 2-4ms)
Cocaine & what causes its effect
Strong local anaesthetic (from blocking voltage-gated Na2+ ion channels)
Therefore pain signals do not get to the brain and local anaesthetics work
Unmyelinated neurons
In unmyelinated neurons, the action potential travels continuously along the axon. This is (relatively) slow (up to 10 m/s). - This is too slow
Myelinated Neurons
- In myelinated neurons, the action potential jumps from one Node of Ranvier to the next. This is much faster (up to 100 m/s).
This is referred to as “Saltatory Conduction”
Thomas Elliot
Found if you stimulate one branch of the autonomic nervous system, the heart rate will be affected (if you dribble adrenaline into the heart, it beats faster, too) Hypothesized that the sympathetic nervous system must produce adrenaline to increase HR. - If you stimulate parasympathetic nervous system, heart rate lowered. (collection of fluid around the heart, and dribble on another, and that heart will slow)
Neurotransmitters
Chemicals that are synthesized in the neuron and stored in vesicles
What happens when the action potential arrives at terminal region
Voltage gated Ca2+ channels open.Ca2+ enters the cell and activates many biochemical processes, including neurotransmitter vesicles fusing with the cell membrane, thereby releasing the neurotransmitter into the synaptic cleft.
What happens once the neurotransmitter is in the synapse
It will eventually attach itself to specific receptors (proteins) on the postsynaptic cell and this interaction induces a change in the postsynaptic potential (EPSP or IPSP)
What happens once the neurotransmitter is released from the receptor
It can diffuse away, be metabolized (broken down) or taken back up into the presynaptic terminal (recycling)
How do neurotransmitters find where to go
Neurotransmitters do not “know” where to go but is in high concentration in a small region of post-synaptic cleft, therefore bumps into receptors eventually
What do reuptake transporters do
return neurotransmitter back into the cell (efficient way of reusing neurotransmitters to conserve energy)
Why are neurotransmitters stored in vesicles?
- Every time neurotransmitter arrives, more or less the same amount will be released every time. Higher quantity = bigger chance of bumping into receptor
If its not packaged, neurotransmitters run the risk of being broken down by enzymes
Co-transmission
neuron the releases more than one neurotransmitter
Under what circumstances will a neuron release two different neurotransmitters
When a neuron has two neurotransmitters, there are usually two different vesicles WITHIN post synaptic cell and whether they fuse with membrane depends on how much calcium flows in (this can influence what vesicles fuse with membrane)
Neurotransmitter receptors
- Neurotransmitters interact with specific receptors
- There are almost ALWAYS more than 1 receptor per neurotransmitter
-Exception = oxytocin ( a hormone & neurotransmitter - the only neurotransmitter we know that only has one receptor)
Ionotropic receptors
Similar to voltage-gated ion channels. The neurotransmitter binds to the receptor, the receptor activates and an ion can flow into post synaptic cell.
- Positive ion (GLUTAMATE) = less negative = epsp = depolarisation = action potential = excited cell
- Negative ion (GABA) = more negative = ipsp = polarisation = inhibits cell
Glutamate
- Influx of Na+ ions
Excitatory - relevant for learning and memory
GABA
- Gamma amino butyric acid
- Influx of Cl- ions
Inhibitory - relevant for anxiety (reduced gaba)
Diazepam (anxiety meds) - how to they work
Prolongs the opening of the GABA receptor, which helps with anxiety. More inhibitory = decrease in anxiety
Metabotropic receptors
- Not a channel, it is a protein embedded right through the cell membrane
How to metabotropic receptors work
- Neurotransmitter binds
- Changes 3D structure of receptor
- Detected intracellularly and will release G-protein
- G-protein cause cascade of widespread effects
- Open ion channels, stimulate gene expression, lead to changes in cytoskeletal protein
This is a much BROADER influence than stimulating ionotropic receptors
In schizophrenia there is an excess of dopamine release causing psychosis. Antipsychotics therefore…
Block the dopamine receptor to counter that. This means dopamine is still released into synapse but has no receptors to stimulate an effect
Neurotransmitter Inactivation
After a neurotransmitter binds it rapidly detaches from the receptor.
This can be followed by:
- Renewed binding
- Diffusion away from the synapse (neuropeptides)
- Metabolic breakdown and inactivation
Reuptake in the presynaptic terminal Neurotransmitter
Monoamine oxidase inhibitors can help with depression by..
- Block breakdown of serotonin
More serotonin can survive & bind
Agonistic
stimulate neurotransmitter activity
Antagonistic
inhibit neurotransmitter activity
Does blocking mean that a drug is antagonistic
Not always. E.g., block serotonin reuptake transporter, more serotonin in synapse therefore more can bind to receptors and STIMULATES neurotransmitter communication
Is synaptic communication a static process.
No, for various reasons (synaptic plasticity) this can change.
More neurotransmitter released
- More bind to receptors
- Enhanced effect
Increase in number of receptors
- If same amount of neurotransmitter released
- More receptors = bigger chance of collision
Enhanced effect
Cellular basis of learning
Synaptic Plasticity
Dendritic spines
- Small intrusions that are studded on dendrites
- Excitatory, stimulatory connections mostly on dendritic spines
- Dendritic spines change their shape depending on the input they get
What happens if the post-synaptic size of dendritic size increases
More receptors in membrane = greater response
Long term potentiation
When a weak stimulus coincides with a strong stimulus, Long term potentiation occurs, making the impact of the weak stimulus stronger.
Dorsolateral Prefrontal-Cortex
- Mostly active during preparation for the stroop test = Attentional control
Phrase to remember how synaptic plasticity works
“Neurons that fire together, wire together”
Long term potentiation in glutamatergic neurons
These neurons have two receptors AMPA and NMDA, with the latter being blocked under normal circumstances. - Strong activation of the AMPA receptor removes the block and allowing the influx of Ca2= ions. This sets in motion a cascade of protein activations leading to more receptors and large synapse surfaces ultimately leading to a stronger synaptic communication.
When is the Anterior Cingulate Cortex activated
During incongruent phase of stroop test- error monitoring
What is the last part of the brain to develop
Prefrontal cortex
Caveat to monozygotic twin studies
While their genes are identical, their looks, upbringing and environment are usually quite similar which means similar trends in resulting behaviour cannot be placed 100% on genes.
Behavioural methods
use patterns of performance (RT, accuracy) to isolate cognitive processes and build models of cognition
Lesion methods:
Examining the effect of disruption to the brains activity on cognitive function (e.g., following brain damage -stroke/trauma in humans, or ablation in animals; or interfering with function artificially)
Recording methods
Using measures of brain activity as “markers” of different cognitive processes (e.g., single cell recordings, EEG/ERP, fMRI, PET, NIRS/DOI
4 assumptions of cognitive neuroscience
- A thought is MADE UP of a series of processes
- Thought takes time
- Thought happens in the brain
- Thoughts lead to behaviour
Donders Method of Subtraction (1868)
2 tasks, differ by each other by only one component, can isolate that thought/decision and then measure it
what were the two original task in Donders method of subtraction
Task 1 (simple RT)
- Press a button when you see a light
- Measure response time
Task 2 (Choice RT)
- Press one key if the light if on the left and another key if the light is on the right
Measure response time
Process Models in Donders method
Simple RT: Encode the stimulus –> Execute motor response
Choice RT: Encode the stimulus –> Decide location –> Execute motor response
(can measure the time it takes for extra step, in this case, around 200ms to make decision)
What things can Donders method investigate
How thought processes are affected by Individual differences (age, disorders), Interventions (drugs, training), and stimulus factors (complexity, number of options)
How does TMS work as a lesion method
- Temporarily and painlessly influence someone’s brain function for a few milliseconds while engaged in a cognitive task and see its effects
Dissociation
Damage affects some functions, but not others
Double dissociation
Two patients with opposite patterns of deficits and preserved abilities
What were H.M’s deficits and what was intact.
Deficits
- Could not create new memories
Intact
- Short-term memory
- Procedural memory (could learn new skills)
- Knowledge
- Language
- Personal identity
- Pre-surgical memories (but does not know who a photo of his current self is)
Retrograde amnesia
cannot remember events prior to brain damage
Anterograde amnesia
cannot later remember evets that occur after brain damage
Double dissociation in the case of H.M and K.F and what we learn from this
Phonological Loop (STM) was lost in K.F (but his LTM is fine as long as he relied on alternative methods of learning). With H.M, the opposite problem where STM was damaged but LTM preserved.
Tell us that the two systems are independent. You can damage one without damaging the other
Concerns about patient studies
- Rare - very small samples to generalise
- Atypical brains to begin with
- Rarely have pre-injury data
- Identifies only areas that are ESSENTIAL for the task (but there a likely many other areas involved in the task - entire network of structures)
- Brain reorganisation during recovery
- Lesions are not clean (tend to be big, messy, and have different boundaries)
Why are lesion studies in animals easier
A lot more control, can be entirely specific as to which region of the brain should be damaged
Single cell recordings
different neurons are sensitive to different stimuli. For example, placing a recording electrode into visual cortex while flashing bars of light. Allows you to record and see what neurons do when particular stimuli are exposed
Recording methods during brain surgery
Common for surgeons to place intercranial electrode into area they are going to remove - Encephalography
Record one or two neurons and see their effects
EEG - ELectroencephalogram
Record brain activity while participating in a task
Pick up small waves of electrical activity on the scalp while people are thing
ERPs - Event related potentials
- Measure activity when the event occurs
Compare to a control condition that is identical in all respects - except the event doesn’t occur (subtraction method!!)
Brain wave - semantic manipulation
What’s different when something makes sense vs not making sense
- Show the brain waves in response to things that don’t actually make sense
- Can use this to measure sense making. Found that 200ms after reading the confusing word (ie., throuse compared to throws) we consider sentence in grammatical sense and our brain activity is altered.
How does structural MRI work
Looks at the spin of water molecules in your brain since different brain tissue has different water densitry
What does diffusion Tensor Imaging show
The “fibre tracks” of the brain which are the super highways of neural communication.
How does
Diffusion Tensor Imaging map fibre tracks
Water wont pass myelin therefore can map the myelinated axons
How does fMRI work
- First, do a structural MRI
- Then measure oxygen levels in the blood that is in the brain
- Deoxygenated blood gives off different signal and correlates with higher blood flow THEREFORE brain activity
A problem in designing a functional neuroimaging study and how to combat this
PROBLEM: Even simple tasks activate multiple regions. SOLUTION: Donders situation in a tightly controlled experiment so your only left with the difference and can pinpoint it.
How does facial recognition differ for familiar and unfamiliar face
For unfamiliar faces:
Encode features → Combine into a face → Search memory → Decision → Response → Non-task processing.
For familiar faces:
All the same steps, but with one extra step (facial recognition), allowing the brain to identify familiar faces.
Two steps to designing a good neuroimaging study
- Choosing good control and experimental tasks/stimuli that differs in the crucial, face recognition requirement
- Subtract the two patterns of activation, so we’re left with the difference between familiar and unfamiliar faces
fusiform face area
tiny area on right side responsible for recognising faces (commonly damaged in stroke patients)
Psychophysics
The relationship between the physical world and the psychological world (via the neural world)
Olfactory epithelium
Skin of nose embedded with neurons which have receptors
Where do action potentials picked up by olfactory cells go?
straight to the olfactory bulb (which is right above nose)
Ethane is odourless to humans, what does this mean.
this doesn’t mean it doesn’t HAVE a smell, you just do not have a receptor for it
Why can dogs smell more than humans
Humans have 6,000,000 receptors in a typical nasal olfactory
In dogs, there are 100,000,000
They also have TWO smell organs; Olfactory epithelium, and Jacobson’s organ as well as long nasal passages which allows air to stay in for long time so they can experience smell for a while
Jakobsons organ
A smell organ of dogs which connects to a different part of brain which detects pheromones
Nociceptors
Pain
- Thin, unmyelinated - transmit to spinal cord and then to thalamus
Touch receptors
Fast, myelinated, straight to brain
Sound wave
- Air pressure wave
- Lots of molecules in air around us
When you speak, you disturb the air and create little waves (like a slinky)
- Lots of molecules in air around us
Reification
Treating something abstract or conceptual as a concrete, tangible thing or entity
Whats an example of top down knowledge ONLY
- Dreams
- Hallucinations
Synaesthesia
Form of neurodiversity in which peoples brains create experiences that don’t match sensory input
What does synaesthesia reveal
Perception is a subjective experience, - The experience in you mind is different to the information in the world being simply “translated” by a machine
Most common source of electromagnetic radiation
The Sun
why can we not see Gamma, X-Ray, UV-Ray
- Very short wavelengs
Pass through things
Why can we not see Infrared, Radar, FM, TV, AC circuits
Very long wavelengths
Go around things
Visible portion of EMR
- Perfectly sized wavelengths, (too big to go through, too small to go around) instead it bounces off objects as light bounces into our eye
- Our photoreceptors respond to light in this range
Optic nerve
A myelinated bundle of axons which sends visual signals to occipital cortex
Blind spot
- No photoreceptors where the nerve (cable) runs through from back of eye to brain
- Therefore, in each of eye we have spot that has no photoreceptors
IF we were to look at back of retina as flat spot
- Cones SPIKE when we close to fovea (fovea is almost all cones)
Rods high in periphery and DIP at the fovea
S - cones
- Most active around 420nm (blue)
Short wavelengths of light
M - cones
- Green cones
- Most sensitive to light at 525nm in the green range
Medium wavelength
- Most sensitive to light at 525nm in the green range
L - cones
- Red cones
- Most sensitive to light at 550nm
Long wavelength
- Most sensitive to light at 550nm
How does the brain create colour
Can determine which cones are being activated and then figure out what wavelength is coming into eye
Why are men more susceptible to colour blindness
Colour-blindness carried on X chromosomes
- Women need on both X
- Men only need on 1 X (more likely to be colourblind)
Adaptive advantage of colourblindness in the monkeys
- Since fruit is often red (dichromats blind to that) trichromats go and forage fruit (can do red/green discrimination)
- Dichromats- less blind/susceptible to camouflage so can spot hidden predator.
Why do cones not respond to weak light?
- Each signal will depolarise its own bipolar cell a little bit
Not enough to make cell fire (weak light)
Why are rods more sensitive in dim light
- Each signal depolarises the SAME bipolar cell
- These all combine and sum to reach the threshold to make the cell fire
- Therefore rods are MORE sensitive then cones
Why do cones have better acuity than rods
Because each cone activates one bipolar cell, the brain knows exactly where the light came from. Leads to sharp images. (different incoming signals to the brain)
Why do rods produce less sharp images
Because signals from several rods sum onto one bipolar cell, the brain doesn’t know exactly where the light came from. Leads to blurry images. (signals converge meaning only one signal to the brain)
Colour, sensitivity, acuity, and distribution of rods
- Colourblind
- More sensitive in dim light
- Blurry
- Periphery
Colour, sensitivity, acuity, and distribution of cones
- Can detect colour
- Less sensitive
- Good acuity
- Located in fovea
Where are ganglion cells located
The last stop in the retina before the signal gets to the brain (last layer of cells).
What do ganglion cells do
Takes all the incoming input, process it, and send the signals along the optic nerve to the brain
Lateral Inhibition
A way the brain can accentuate the strongest signal (and use this to inhibit the weak signals around it)
How does lateral inhibition work
Strong light in one set of photoreceptors inhibits the signal from surrounding cones.
Why is lateral inhibition useful
USEFUL for your brain to detect the edges of things (which helps us figure out what objects are)
- Making everything sharper
Less “fuzzy boundaries”
How does the Herman grid show lateral inhibition
- Edges of dark sqaures will win lateral inhibition contest
- This will DIM light from centre of white borders which will make it look grey
What are receptive fields
Areas of the visual field that produce activation in a given neuron
What happens to receptive fields as we progress up the visual system?
Receptive fields get bigger. While each photoreceptor corresponds to a miniscule spot in space, by the time signals get to the ganglion cells, they start to combine together (it is no longer just about points of light, but about whole edges falling in its range of vision
Thalamus
Sensory relay station where all senses converge, including vision
What is the Lateral Geniculate Nucleus (LGM)
- Region of the thalamus where visual information goes
- Like ganglion cells in which it responds to edges
Does the nasal hemi retina cross over or stay on the same side when travelling to the visual cortex
Visual system will cross each nasal hemi retina to the opposite sides
Does temporal hemi retina stay on the same side of visual cortex or cross
Stay on the same sde
What do simple visual cortical Cells (V1) do
They are the first stop after leaving LGM. Ganglion cell type input - respond to edges at particular orientation at particular place
Single cell recording
Record activity of single neuron while cat is looking at screen. Can see that neurons will respond to edges only at a particular orientation,
Complex Cells (V2)
These have a larger receptive field than V1 cells, and don’t care where stimulus/edge is, just the orientation of the shape.
What happens as visual info moves through from V1 - V8
As we move on to more complex areas of the brain, it combines more and more input (colour & motion, shape & texture, auditory input) which helps us make sense of what we see and where things are in space (neurons become more FLEXIBLE in what they respond to)
Why do we need visual input in developmental periods.
While we are born with myelinated pathways that go to LGM and from LGM to cortex, the actual networks that learn how to see are not developed until after birth and need visual input
Kitten study demonstrating the necessity of visual input
Kittens with one eye patched for first three months of life develop very poor visual response from the deprived eye, and very good response from the seeing eye. One eye will take over all the neurons that SHOULD HAVE responded to right eye
What is Amblyopia
Visual defects in the brain as a result of poor visual input during critical periods
What is Strabismus and the effects.
“lazy eye”, one eye does not move or track as well as another does, brain stops trusting it to rely visual input, relies on good eye, and we can have same effect as in the kittens as brain will not grow projections to be able to see from this eye.
What is an astigmatism
Eyeball is not perfectly spherical, has an odd angle that light may be coming in at one plane
If not corrected early in life, will be problematic forever (you cant correct brain)
Congenital Cataracts
Cloudy film in cornea which blocks light getting in. Need to correct as EARLY in development as possible so brain can organise itself appropriately
What is the outcome of damage to V1 area of brain
Blindsight
What does damage to the V1 area of the brain result in
“blind spots” in the visual field. For some people. They still have awareness of objects in this blind spot even they don’t consciously experience it.
What can people with blindsight sometimes detect
Motion, direction, emotion
Different pathways visual input can take
Information from LGN can bypass V1 and end up in the motion detection area (V5). This explains how blindside patients can pick up on objects, motion etc without conscious experience (bypasses V1-4)
Area V4 on occipital lobe
- Much more complex
- Things begin to approximate shapes of objects
What is Achromatopsia
The loss of the ability to see colour
What happens in the brain for achromatopsia to occur
V4 is not functioning therefore the brain does not know what to do with the information the cones send and perceive everything as greyscale
What is akinotopsia
Motion blindess
What causes akinotopsia
Damage to V5/MT
What are the two versions of akinotopsia
Either:
- See things as a series of snapshots or….
- things that are moving disappear completely, only when things are stationary do they have enough coherence to become visible
Two visual pathways from occipital lobe to frontal lobe
Dorsal stream and ventral stream
Dorsal stream
WHERE - vision for action that goes via parietal cortec
Ventral stream
WHAT - vision for perception which goes via inferior temporal cortex
How do we know about the dorsal and ventral streams
Study on monkeys
- Lesioned areas of inferior temporal cortex/parietal cortex
- Aimed to disrupt either WHAT or WHERE system and see effects of this
What happened to monkeys with a ventral lesion
Monkeys with damage to ventral system could not identify purple triangles from rectangle but were able to identify the correct rectangle based on its location
What happens to monkeys with dorsal lesions
Monkeys with damage to inferior temporal cortex could identify purple triangles from rectangles but NOT rectangles based on its location
What did the monkey study reveal about dorsal and ventral system
Double Dissociation
- Shows that “what” and “where” systems are unrelated
Patient DF
Carbon monoxide leak in shower wiped out inferior temporal lobes in both her brain making functionally blind.
What can patient DF see
Lights, edges, etc but cannot see anything beyond. This shows that she is only seeing with EARLY visual cortical areas
DF response to angle postcard test (what she can and cant do)
- If you asked her to take hand and line it up with the slot, she cannot do this
- If you asked her to post a letter into the slot she can move her hand, alter its trajectory, and it will go into slot (good at where, bad at WHAT)
How does a patient with dorsal stream damage respond to postcard angle test
They can accurately indicate the orientation of the slot, but cannot post a card into it. Good at what, but poor at where.
What is apperceptive agnosia
A problem of perception. Vision and input are intact, but there is impairment in assembling the input into meaningful objects.
What causes apperceptive agnosia
Damage to junction in pathway between occipital and temporal lobes
Can people with apperceptive agnosia copy model shapes, or draw objects from memory.
Cannot re-draw model shapes, however if asked to draw shapes from memory they can
Associative agnosia
Problem with associating perception with meaning. (loss of knowledge of what objects are)
Can people with associative agnosia copy model shapes, or draw objects from memory?
Can reproduce model drawings very well (however cannot tell you what they’ve drawn). However, if asked to draw an object from memory, it is not recognisable.
What is category-selectivity in ventral pathway
The ventral pathway contains some visual areas that are selective for a particular meaningful category
What four categories have specific areas in ventral pathway
words, faces, bodies, places
What is prosopagnosia
Inability to recognise faces
Is face blindness a spectrum, and who on it is face blind vs super recognisers
It is a spectrum, Bottom 2-3% are “face blind”
Top 1-2% are superrecognises
Pareidolia
Seeing faces everywhere
How do infant studies show that faces stimulate us before we can actually associate them with what faces are
Infants prefer facial to non-facial configurations within the first day of life
Measured through looking time
The thatcher illusion
When you flip a face, they loose its “faceness” and become just an object, We can process an upright face rapidly but not an inverted space
Holistic processing
Instead of face being eyes, ears, nose, mouth, it is one WHOLE object
Study which tested if there is a specific face area, or simply memory area for identifiable things (and we just have more experience w faces)
Greeble study which shows that greeble novices has no activation of fusiform face area, while greeble experts did
Method of Greeble study
2 groups, one which had studied greeble families for 9 hours and one which hadn’t. Found that when asked to view and categorise greebles, the novices has no activation of fusiform face area while the experts did
Greeble study conclusions
Over period of time people have recruited their face area to develop expertise in categorising non-familiar “species.” This suggests that fusiform face area is not some much about face recognition
But an area we recruit when needing an expert level of recognition/identification
Attention
- Narrows flow of information so only most relevant stuff goes into working memory
Metaphors of attention
- Spotlight
- Funnel
- Flexible pool of resources
The “glue” that holds our world together
Bottom up (stimulus driven) attention
- Salience
- Emotional stimuli
- Faces (more upright than inverted)
Visual Search Task
- A lot of things to look through and see how long it takes to find a particular thing
Visual search task snakes vs flowers finding (and what happens when there are more distractors)
Faster to find snakes among flower distractors than to find flowers among snake distractors
More distractors are a problem if you are looking for a flower, not so much if you are looking for a snake
Colour singleton test
- Move eyes to point that is a different colour
Colour singleton test results
Eyes often went to face rather than coloured spot, less so if it was inverted.
Top down processing
- Goal/task
- Emotion/physiological state (anxiety, threat, hunger)
- Motivation
Mindfulness
Biased competition model
Top down and bottom up will compete with each other for representation in visual cortex. Some things will be stronger and therefore out compete. This determines what goes in to memory system, and what we respond to (look at, reach out to, act toward)
Biased competition model house and faces
Face and house represented as different representations (which overlap), Hard to hold these both in brain at the same time, You can either attend house or face
How does biased attention model actually work
DAN - goal driven
VAN - stimulus driven Frontoparietal network - knows what the goal is, tells the DAN where to move attention to
Dorsal attention network
Fronto-parietal network directs the actions of DAN and VAN in line with goals
DAN (dorsal attention network)
goal driven
VAN (Ventral attention network)
stimulus driven effects, visual, emotion detecting, amygdala
Frontoparietal network
knows what the goal is, tells the DAN where to move attention to
How does VAN help your goals be overridden by salient and threatening things
- VAN can send signals to prefrontal cortex for salient and dangerous things
Hemi-spatial neglect is a disorder of ______ not _______.
Disorder of ATTENTION, not VISION
What would an individual with hemi-spatial neglect present with
Ignore sounds coming from left side of space, difficulty in moving towards/within the left side of space. No perception, vision or anything on one side of the world (etc, no awareness of “left” (but not due to blindness, its more about noticing and attention)
How does hemispatial neglect occur
Damage to the temporal and parietal area on one side of face (right hemisphere)
Temporal parietal junction
where DAN and VAN meet up
Why is hemi-spatial neglect most severe when damage is on the right side
DAN is bilateral system (this directs attention around and sometimes you need one hemisphere or the other)
VAN (bottom up) Is a right hemisphere system
Damage to left = only DAN is damaged
Damage to right = DAN and VAN are damaged
Where is VAN only in one hemisphere
It is the central controller of threat and fear, therefore more beneficial to have one place to control everything without having disconnect/having to communicate with other hemisphere
What do drawings of people with hemispatial neglect look like
Left half OF THE DRAWING they lose awareness of - often unfinished/blank
Can hemispatial neglect also affect mental imagery
Yes, our imaginative ability draws on our mental imagery which involves our VAN and DAN.
Can hemispatial neglect be overcome.
- Can sometimes be overcome with strong cues (bright lights, loud sounds, erotic scenes)
Engram
- Memory trace
- Like a spider web (connected to other things, connected to others etc)
A network (so how do you find the engram (core, central memory)
Karl Lashley rat study
- Trained rats to do all these things, mapped brains
- Tried to lesion rats brain to make them forget things
- The more he cut, the worse the rats were at doing what he trained them to do
Law of Equipotentiality
- All parts of cortex contribute equally to learning and memory (cannot pinpoint 1 area per memory etc)
Law of Mass Action
- Learning & Memory are distributed in the cortex as a whole; more cortex = better memory
“more brain better than less brain”
3 systems withing STM
- Phonological loop (store language and auditory related things “tape recorder”)
- Episodic buffer (keeping track of single events in current event, beginning, middle, end etc)
- Visuospatial sketchpad (visual version - memorising patters and configurations)
How do we prove memory systems are different (ie., different systems in place for LTM and STM)
Double dissociation
And 3 types of evidence
1. Behavioural performance
2. Lesion studes
3. Neuroimaging
Behavioural performance in terms of difference between LTM and STM
-STM = 4-7 things, LTM = seemingly unlimited
-STM = 18-20 seconds without rehearsal, LTM = years and years
- Lesion studies (animals, patients) proving that LTM and STM are different systems
-H.M - removal of hippocampus, LTM was damaged but STM was still intact (show STM & LTM must be different things)
4 brain structures important for memory
Hippocamus, striatum, cerebellum, prefrontal cortex
Korsakoff Syndrome
Amnesia (often anterograde) due to PFC not working. Caused by lack of vitamin B1 (common with patients with alcohol abuse history)
Confabulation
Seen in people with Karsakoff syndrome where they cant remember things to just them up
Alzheimer’s Disease
Widespread brain disorder, cause “tangles” in the brain. See a gradual breakdown of function with deficits in all sorts of memory. (episodic first, them semantic deficits)
What happens to brain as you age
- Working memory slows
- Lower memory capacity
- Reduction in processing speed
- Degradation in central excec
- Stored semantic memory and crystallised intelligence remain
Complex span task
4 sentences, need to remember last work while also answering questions about each of these. Shows fluid intelligence
How does depression effect working memory capacity
Results in deficits in working memory capacity which make it hard for them to think
Anterior Cingulate Cortex (ACC)
Attention controlled, monitors and directs attention
Where is the Visuo-spatial sketch pad active
Occipital lobe
Where is phonological loop active
broca and wernickes area
Where is episodic Buffer
- Activates broad area in parietal lobe (perceptual processing)
Consolidation
neural mechanisms, what changes in your brain as a result of experiences
Factors affecting consolidation
- Time
- Repetition (repeat experience)
- Elaboration (thinking about experience afterwards, reflection)
- Emotion (things that are strongly emotional tend to be encoded straight away)
- Sleep
What network is active when remembering and mindwandering
Default mode network
What occurs during remembering
Reactivation of perceptual systems active during original event
- Visual memorys, activity in occipital lobes
Active memory, motor activity
Anterior temporal lobe
Where we keep an index of semantic memory - temporal lobe is WHAT stream.
The Hub-and-spoke model of semantic memory
- Controls what we use at a given time
Hub binds all brain areas together
Semantic dementia
- Degeneration fo anterior temporal lobe (ATL)
- Loss of conceptual knoweldge
Is semantic agnosia similar to associative agnosia
No - visual agnosias dont know what a coffee cup is, but will know how to use it. People with semantic lose the UNDERLYING concept of coffee cups
Red nucleus
Executes motor response
Lateral intepositus nucleus
Learns association
Amnesiacs (hippocampal damage) response to eyeblink classical conditioning
Even though they want remember anything about conditioning, the next day you play the tone they will blink (this is because hippocampus in not involved in classical conditioning)
Patients with cerebellar lesions response to classical conditioning
- Impaired classical conditioning
You need the cerebellum to do classical conditioning learning
What kind of classical conditioning does hippocampus play a role in
Trace (where two stimulus occur seperately) as this involves holding memory of first stimulus
Procedural memory weather task
Where people guess whether its raining or sunny based on shapes. People start to recognise patterns and increase their ability although they cannot describe the rule
Procedural (implicit) learning
Slow learning of patterns, sequences and procedures
Striatum
Composed of basal ganglia and caudate nucleus
What kind of patients have damage to striatum
Parkinsons = degradation of basal ganglia (results in failure to learn implicit sequences - even though episodic memory is intact)
Double dissociation with patients with hippocampal vs striatum damage)
Lesions of median temporal lobe
- DEFICITS, episodic memory
- INTACT, procedural memory (H.M will be able to do weather task)
Lesions of striatum
- DEFICITS, procedural memory
INTACT, episodic memory
Semantics
The meaning of words (or parts of words)
Syntax
Rules dictate how sounds combine to make words, and how words combine to make sentences
Linguistic universals (which separate us from other species)
- semanticity, arbitrariness, displacement, productivity
Semanticity
Language is made up of symbolic units that combine to express meaning
Arbitrariness
Sounds, letters, pictographs, signs bear no direct relationship to meaning
Displacement
We can use language to talk about here and now, but also past/future and real/imagined
Productivity/Generativity
A fixed number of units can be combined in an infinite number of ways
Deficits in animals trying to learn language
- Complete syntax
- Displacement (talk about things in other places/times)
Cultural transmission (not used with offspring)
- Displacement (talk about things in other places/times)
- also lack vocal apparatus to speak
Capabilities of animas learning language
can acquire language ability of 2 1/2 year old child
- Learn symbols to represent meanings
- Good comprehension of conversational spoken language
- 2-3 symbol utterances
- Some unique words and phrases (productivity?)
