Final Exam (Classes 9-12)

What is learning? What is memory?

• learning is the process of acquiring new information

  • the outcome of learning is memory

• memory refers to the processes by which our learning and experience shapes us, thus changing our brains and our behaviour

What are the different types of memory and what are the durations of each?

• sensory memory is held for milliseconds to seconds

• short-term memory and working memory persist for seconds to minutes

• long term memories can last between minutes to decades

  • declarative memory consists of our conscious memory for facts (semantic memory) and events we have experienced (episodic memory)

  • non-declarative memory consists of unconscious memories we cannot verbally report on

What are the three major processing stages of memory?

1. encoding: memories are acquired and created as incoming information is experienced — traditionally thought to be mediated by alterations in the synaptic strength and number of neuronal connections

   • the first step is acquisition in which sensory information is taken in and during the sensory buffer, the stimuli can be processed and some are sustained and acquired by short-term memory

   • the second step is consolidation, in which changes in the brain stabilize a memory over time, resulting in a long-term memory

2. storage: memories are stored, and often strengthened, over time

   • storage is the result of acquisition and consolidation

3. retrieval: memories are accessed

   • this can be conscious or unconscious

What is amnesia? What are the two forms?

• amnesia refers to memory deficits or loss as a result of brain damage from surgery, disease, and/or trauma — it’s a form of memory impairment that affects all of the senses

  • involves impaired episodic memory, but semantic memories are intact

• anterograde amnesia is the loss of memory for events that occur after the event — inability to learn new things

• retrograde amnesia is the loss of memory for events that occurred before the event

  • characterized by Ribot’s law in which there is a temporal gradient such that more recent memories are more greatly impacted than distant ones

What kind of damage results in amnesia?

• damage to bilateral regions of the medial temporal lobe results in amnesia

  • damage to the hippocampus, parahippocampal cortex, and amygdala

• the extent of the deficit depends on how much of the medial temporal lobe is removed or damaged — the more posterior along the lobe, the more severe the amnesia

Who was H.M.? What memory impairments did he display?

• H.M. had epilepsy and had bilateral surgery to remove portions of his medial temporal lobe — his perirhinal cortex and parahippocampal cortex were intact, the rest was removed

• he had intense anterograde amnesia and couldn’t consolidate and store new information in long-term memory

  • he also had retrograde amnesia for two years prior to his surgery

• his working memory was intact and had a normal working memory span

• his procedural memory was not impaired, however he couldn’t remember practicing the tasks he was doing better at

What is Korsakoff Syndrome? What areas are damaged? How is memory impacted?

• Korsakoff Syndrome is a chronic memory disorder commonly caused by severe alcohol abuse

• it’s caused by damage to the midline diencephalic region (mammillary nuclei and dorsomedial thalamic nuclei)

• patients exhibit anterograde and temporally-graded retrograde amnesia

• many patients engage in confabulation to fill their memory gaps, which may reflect frontal cortical damage

What is dementia? What are the common types and how are they caused?

• dementia is an umbrella term for the loss of cognitive function in different domains beyond what is expected in normal aging

• the most common cause is neurodegenerative disease, in which proteins misfold and aggregate in the brain (ie. Alzheimer’s with beta-amyloid proteins and neurofibrillary tangles)

• vascular dementia is caused by decreased oxygenation of neural tissue and cell death, which can result from many issues

• frontotemporal lobar dementias involve the accumulations of proteins in the frontal and temporal lobes and result in language and behavioural changes

What is medial temporal lobe epilepsy? How does it differ on the left and right sides of the brain? What are the common manifestations/symptoms?

• medial temporal lobe epilepsy involves seizures that start in or near the hippocampus or amygdala

  • the seizures occur from brain injury or abnormal scarring of the temporal lobe

• right temporal lobe epilepsy impacts non-verbal memory and learning whereas left temporal lobe epilepsy impacts verbal memory and language

• symptoms vary depending on etiology and pathology, but common manifestations include

  • anterograde amnesia

  • sense of familiarity or fear/anxiety

  • some experience visual or auditory hallucinations or even a “sensed presence”

What are the theories as to why patients with medial temporal lobe epilepsy sense a presence?

• one theory is that there are heightened connections between the sensory systems and the hippocampus and amygdala, which allows for senses to be paired with strong emotions

  • patients with TLE experience elevated physiological responses to emotional stimuli with heightened automatic responses when compared to controls

• another theory is that spiritual experiences are an artifact of temporal lobe functioning

  • if so, we should be able to induce similar experiences in healthy controls — “God helmet” stimulating temporal lobes had dubious effects

What is sensory memory? What are mismatch negativity and mismatch fields? What are the durations of echoic and iconic memory?

• sensory memory refers to our transient retention of sensory information

• mismatch negativity (electrical) and mismatch field (magnetic) are potentials that tell us about the duration of sensory memory

  • responses are generated by the presentation of a rare, deviant stimulus that is presented within a sequence of identical, common stimuli

• mismatch fields are elicited by deviant tones at intervals of 9-10 seconds, but after this point the amplitude was too small to distinguish — duration of echoic memory is 9-10 seconds

• neural traces for iconic memory lasts only 300-500 milliseconds

What is short-term memory? What is the modal model? Does it stand today and why?

• short-term memory persists for seconds to minutes, but it has a limited capacity

• the modal model suggests that information is initially stored in sensory memory before attentional processes move it to short-term memory and from there, it can be moved to long-term memory if it is rehearsed — strong serial structure of this model

  • at each stage, information can be lost by decay, interference, or a combination of the two

• patient studies have revealed a double dissociation for short and long term memory

  • this suggests that short-term memory isn’t the gateway to long-term memory as laid out in the modal model — maybe sensory memory can be encoded right into long-term memory

What is working memory? What is the central executive model? What are the components? What regions of the brain are the components localized to?

• working memory represents our limited capacity store for retaining information in the short term and for performing mental operations on the contents of this store — contents could originate from sensory inputs or be retrieved from long-term memory

• Baddeley and Hitch proposed the central executive mechanism in which long term memory interacts with two subordinate short-term memory stores

  • the phonological loop acoustically codes information — left-hemisphere network involving the lateral frontal and inferior parietal lobes

  • the visuospatial sketchpad permits storage in visual or visuospatial codes — right parieto-occipital regions

What is long term memory? What is declarative memory? What are the types?

• long-term memory refers to information retained for a significant time (up to decades)

• declarative memory refers to memories that we have conscious access to and can verbally report — also called explicit memory

  • episodic memory refers to memories of events that you have experienced (what happened, where, when, with whom)

  • semantic memory is objective knowledge that doesn’t include the context in which it was learned

What is long term memory? What is non-declarative memory? What are the types? What brain areas are associated with each?

• long-term memory refers to information retained for a significant time (up to decades)

• non-declarative memory is not expressed verbally, but through performance — also called implicit memory

• procedural memory is required for tasks that include learning motor and cognitive skills — often tested with serial reaction time tasks

  • subcortical structures, including the basal ganglia, have been implicated in this form of memory

• priming refers to changes in the response to a stimulus following prior exposure to it — it acts within the perceptual representation system

  • associated with lateral temporal and prefrontal regions

• classical conditioning (associative learning) involves the pairing of a conditioned stimulus with an unconditioned stimulus such that they elicit the same response

  • often associated with the hippocampus

• nonassociative learning doesn’t involve the association of two stimuli to elicit a behavioural change

  • habituation: the response to an unchanging stimulus decreases over time

  • sensitization: a response increases with repeated presentation of the stimulus

  • involves primary sensory and sensorimotor/reflex pathways

What is recall? What is recognition? Where do these forms of memory originate from?

• recall refers to when you can specifically remember something

  • shows larger positive peaks in posterior parietal regions

  • hippocampus and posterior parahippocampal regions

• recognition refers to a sense of familiarity surrounding something

  • shows larger negative peaks in frontal regions

  • perirhinal cortex

• the hippocampus is activated for retrieval of episodic memories, but not of memories based on familiarity

What does the medial temporal lobe memory system consist of? What are the steps of information encoding in this system?

1. information stems from different parts of the brain

   • spatial information comes from the retrosplenial cortex and parahippocampal gyrus

   • object information comes from the perirhinal cortex

2. this information converges at the entorhinal cortex

3. it gets transmitted to the hippocampus and travels through this structure and leaves one of two ways

   • back to the entorhinal cortex

   • to other brain regions via the fornix

What is transient global amnesia?

• transient global amnesia refers to retrograde and anterograde amnesia that resolve themselves in time

  • often caused by ischemic events that damage the CA1 subfield of the hippocampus

  • don’t know if it causes implicit memory deficits because the impairment doesn’t last long enough

• symptoms are similar to those of people with permanent medial temporal lobe damage

What are the roles of the parahippocampal and rhinal cortices in memory?

• input from all sensory cortices are transmitted to the parahippocampal and perirhinal cortices before flowing to the entorhinal cortex

• these areas are critical for encoding and recognition

  • the more familiar an item is, the less activation seen in the parahippocampal and rhinal cortices

What are the roles of the hippocampus in memory?

• it’s critical for encoding and consolidating memory

• it’s important for episodic memory

  • the anterior hippocampus is involved in encoding

  • the posterior hippocampus is involved in retrieval

• it also supports relational learning as it’s active during tasks where performance depends on acquiring memory for relationships

What specialized cells in the hippocampus help it support relational processing?

• the hippocampus helps in relational processing due to specialized cells that support cognitive maps

  • place cells in the hippocampus are cells that fire to specific locations within an environment

  • grid cells in the entorhinal cortex fire at certain locations in an environment that is outlined by a grid in the brain’s representation of the space

  • time cells in the hippocampus fire to the same relative location in time rather than space

What roles do the mammillary nuclei play in memory? What roles do the anterior thalamic nuclei play in memory? How are these regions connected to the hippocampus?

• the mammillary nuclei aid in memory consolidation and have been implicated in spatial memory

• the anterior thalamic nuclei support episodic memory and are involved in recency judgements

• both regions are connected to the hippocampus by the fornix

What roles does the amygdala play in memory?

• it’s important for encoding the affective qualities of an experience

• it modulates consolidation of memories associated with emotional experiences

  • it results in emotional events being more accurately and deeply encoded and it facilitates fear conditioning

What roles does the anterior temporal lobe play in memory?

• it’s important for the integration of sensory input

• it gathers information from modality-specific regions to create an amodal representation of information

  • it helps retain semantic information that isn’t linked to a specific modality

What roles does the prefrontal cortex play in memory? What does each region of this cortex do?

• the prefrontal cortex is activated during memory retrieval

  • the left PFC helps retrieve verbal information whereas the right PFC helps retrieve non-verbal information

• the posterior PFC is related to attempts of memory retrieval rather than the success of retrieval

• the ventrolateral PFC selects relevant information for encoding

• the dorsolateral PFC reorders/rearranges information for encoding

How are long-term memories encoded and retrieved?

• during encoding, neocortical areas associated with the relevant senses provide input to the hippocampus about the sensory information

• during retrieval, these sensory areas are reactivated

  • they’re higher levels of sensory processing that are associated with understanding (ie. encoding identity rather than just features)

What kinds of activation do the retrieval of true and false memories elicit? Why?

• true memories are associated with greater activation in the medial temporal lobe and sensory areas

  • these memories were actually experienced, so we see activation in the sensory areas and memory regions

• false memories are associated with greater activation in frontal and parietal regions of the retrieval network

  • these didn’t actually happen, so we don’t see bottom-up (sensory driven) activation, we see activation in regions associated with top-down cognitive control

What is the attention-to-memory model?

• the attention-to-memory model argues that the dorsal superior parietal lobe contributes to the top-down search of episodic memory for specific content

  • the ventral regions of the inferior parietal lobe are essential for capturing attention once the salient content is identified

What is consolidation? How does it influence Ribot’s law of temporal gradients for amnesia?

• consolidation is the process that stabilizes a memory over time after it is first acquired — this occurs at a cellular and systematic level

• Ribot’s law that retrograde amnesia is greatest for recent events is influenced by consolidation — recent items are lost because they’ve only undergone an initial consolidation and haven’t completed a permanent consolidation process

What is the standard consolidation theory? What doesn’t it explain? What is the multiple trace theory?

• the standard consolidation theory states that the neocortex is essential for storage of consolidated memories and the hippocampus plays a temporary role — when a memory is formed, representations are distributed through the cortex and the hippocampus binds them but as the memory is reactivated, connections within the cortex are formed such that the hippocampus is no longer needed

  • proposes the same process is involved for episodic and semantic memories

  • doesn’t explain why some people with amnesia from hippocampal damage have good LTM and others don’t

• the multiple trace theory suggests that long-term stores for semantic information solely rely on the neocortex whereas episodic memories, consolidated or not, rely on the hippocampus for retrieval

  • as an event is retrieved more, more traces are set down and are more resistant to hippocampal damage

  • proposes that slowly these traces are extracted into the “gist” of information and get stored as semantic memories in the cortex

What is the relationship between sleep and memory consolidation? How is this different to awake consolidation?

• during sleep, the hippocampus helps consolidate memories by replaying the firing of the spatial and temporal patterns that were activated during the initial learning

  • replay activity has also bee seen in the prefrontal cortex and ventral striatum

• when awake, replay can still take place in the hippocampus but the sequence or temporal order of the original experience is reversed

What is the relationship between stress and memory consolidation?

• during acute stress, adrenaline and cortisol can enhance initial encoding and consolidation of information

• high stress has a detrimental effect on memory

• the CA1 region of the hippocampus helps connect the hippocampus to the cortex, which aids in memory consolidation

  • the function of this circuit can be impaired by high levels of cortisol

What is Hebb’s law? What is Hebbian learning?

• Hebb’s law: cells that fire together wire together

  • synaptic connections between co-activated cells change in a manner dependent on their activity

• Hebbian learning: the mechanism underlying learning is the strengthening of synaptic connections that results when a weak input and a strong input act on a cell at the same time

What are the three major excitatory pathways of the hippocampus that extend from the subiculum to the CA1 cells?

1. the perforant pathway: allows neurons from the entorhinal cortex to synapse with granule cells of the dentate gyrus

2. mossy fibers: these unmyelinated axons of granule cells connect the dentate gyrys to the hippocampal CA3 pyramidal cells

3. Schaffer collaterals: these axon collaterals connect CA3 pyramidal cells to CA1 pyramidal cells

What is long term potentiation when it comes to the hippocampal excitatory pathways?

• stimulation of perforant pathway axons leads to greater synaptic strength so that when axons were stimulated again later, postsynaptic responses in the granule cells of the dentate gyrus were larger — LTP has also been found in the other excitatory pathways

  • long term potentiation refers to the strengthening of connections

  • note: if stimulation had low-frequency pulses, it had the opposite effect of long term depression

What are the three key properties of LTP in the CA1 synapses with regards to Hebbian learning?

1. cooperativity: more than one input must be active at the same time

2. associativity: weak inputs are potentiated when co-occurring with stronger inputs

3. specificity: only the stimulated synapse shows potentiation

note: inputs need to be excitatory and postsynaptic cells must be depolarized for LTP to occur — inhibitory inputs or hyperpolarized postsynaptic cells prevent LTP

Describe the molecular mechanism mediating long term potentiation. What is glutamate? What are AMPA and NMDA receptors? What roles do they play?

• LTP depends on glutamate, the main excitatory neurotransmitter in the hippocampus

• normal synaptic transmissions use AMPA receptors whereas LTP is mediated by NMDA receptors

  • NMDA receptors are central to producing LTP, but maintenance depends on AMPA receptors

• NMDA receptors are open in the postsynaptic cell when two conditions are met:

  • glutamate binds to the receptor

  • the membrane is depolarized

• when open, NMDA allows CA2+ to enter the postsynaptic cell and change enzyme activity to influence synaptic strength

What happens when LTP is blocked in the hippocampus?

• LTP can be blocked by inhibiting NMDA receptors (ie. with Mg2+) or by genetically knocking out the responsible genes

• without NMDA functioning, ability in place learning is impaired so LTP plays a critical role in spatial memory

Is play universal in animals? Why do animals engage in play?

• play isn’t universal, only five phyla engage in play

• it’s theorized that for species with a long juvenile development and dense social structures, play can simulate a loss of control, be unpredictable, and be safe and rewarding

  • play shocks and surprises them with no risk

  • these characteristics benefit executive functioning

What is executive functioning? What kinds of behaviours are involved?

• executive functioning refers to the set of psychological processes that enable us to use our perceptions, knowledge, and goals to bias the selection of action and thoughts from a multitude of possibilities → allows us to vary adaptively from moment-to-moment

• it allows us to achieve our extended, more complex goals, which involves

  • planning and organizing: set goals/subgoals, anticipate consequences, etc.

  • constrain behaviour based on the environment and past experiences

How are intelligence and executive functioning different? What kind of thinking do they use?

• intelligence and executive functioning are unrelated as they require different forms of thinking

• most standardized tests of intelligence examine convergent thinking, which involves finding a concrete solution to a problem

• executive functioning requires divergent thinking, in which one must find a creative solution to a problem

Why is the prefrontal cortex implicated in executive functioning?

• humans have a disproportionally large prefrontal cortex than other primate species → the expansion comes from more white matter, so our unique cognitive abilities may stem from new connections and not new neurons

• the prefrontal cortex matures late, which corresponds to the appearance of cognitive control late in development

What do the different regions in the prefrontal cortex do?

• the lateral prefrontal cortex has roles in working memory, inhibition, goal setting, action planning, and selective attention

• the frontal pole is involved in cognitive branching, hierarchical representations, and unconscious encoding of decisions

  • note: right behind sinus cavity, so the air makes it difficult to image activity here

• the orbitofrontal cortex is involved in sensory integration, emotional appraisal, reward encoding, and cognitive flexibility

  • also difficult to monitor due to sinus cavity

• the medial frontal cortex (anterior cingulate cortex) is involved in error detection, reward anticipation, conflict resolution, social appraisal, and consciousness

How do we know that working memory is different from long term memory?

• monkeys were trained on two delayed response tasks

  • working memory: learn the relationship between the location and the reward/snack

  • associative (long term) memory: learn the relationship between the cue/card and the reward

• lesions to the lateral prefrontal cortex impairs working memory, but not long-term memory

How does damage to the lateral prefrontal cortex influence performance on the Tower of London task?

• the Tower of London task evaluates executive functioning by looking at task sequencing to attain goals

• damage to the lateral prefrontal cortex impairs performance on the task

  • the left LPC is involved in creating subgoals whereas the right LPC is involving in considering the relationship between subgoals → the interhemispheric white matter tracts help predict task performance (the two sides need to be active and communicating to succeed)

How is executive functioning completed in the brain based on task complexity/level of abstraction?

• as tasks increase in complexity, activity shift to more anterior brain regions

• posterior regions handle less complex problems → the premotor cortex helps plan very simple responses

• anterior regions are responsible for complex or difficult problems → the frontal pole helps in very complex problems

What kind of behaviours come with prefrontal lobe damage?

• perseveration: persisting in a response even though they’ve been told it’s incorrect

• utilization behaviour: extreme dependency on prototypical responses for guiding behaviour → see a hammer, use it without inhibition of flexibility to environment/context

• inability to plan, make decisions, lack of inhibition

• difficulty prioritizing ideas and putting them into a plan

• behaviour becomes more stimulus-driven than goal-oriented

• unilateral damage produces mild deficits but bilateral damage makes dramatic change

What is environmental dependency syndrome? What are the symptoms?

• environmental dependency syndrome is a neuropsychological condition resulting from prefrontal cortex damage

  • extensively studied by François Lhermitte

• patients feel compelled to rely on environmental cues to complete goals or tasks, regardless of if it’s appropriate

  • engage in imitative behaviours and utilization behaviours (see an object, use it right away)

• note: behaviours were purposeful and meaningful to the patients, they were guided by their own background

  • the utilization behaviour of a non-smoker is to offer a pack of cigs to someone else, but a smoker would just start smoking

What are the two theories on the cause of environmental dependency syndrome?

1. the symptoms result from the supervisory attentional system of the PFC being damaged but the contention scheduling one being left intact

   • contention scheduling: learned routine system that enables automatic processing

   • supervisory attentional system: effortful flexible system that directs action through decisions

2. mirror neurons could explain the imitative behaviours involved in environmental dependency syndrome

What is chronic traumatic encephalopathy? What are the two main mechanisms of injury?

• chronic traumatic encephalopathy is a brain disorder caused by head injuries that result in the death of nerve cells → often damages the frontal cortex

• there are two main mechanisms of injury

1. direct damage: the brain can be damaged on the same side (coup injury) or opposite side (contre-coup injury) of impact

2. diffuse axonal shearing: the velocity of impact can cause axons to tear → orbitofrontal cortex is especially vulnerable

What occurs in each stage of chronic traumatic encephalopathy?

• stage I:

  • damage to neurons in the visual cortex

  • damage to neurons in the cerebellum → confusion, dizziness, headaches

• stage II:

  • atrophy of the prefrontal cortex

  • damage to nerve cells and alterations to tau protein structure → memory loss, impulsivity, emotional instability

• stages III and IV:

  • enlargement of the lateral and third ventricles

  • marked atrophy of the hippocampus, entorhinal cortex, and amygdala → memory loss, motor impairments, speech difficulties, aggression, depression

What are the three axes that prefrontal cortex functions can be organized along?

1. ventral-dorsal gradient for maintenance and manipulations: ventral pathways for “what” and dorsal pathways for “how”

2. anterior-posterior gradient for abstraction: more abstract/complex representations engage more anterior regions and posterior regions are active for more simple tasks

3. lateral-medial gradient for type of information influencing working memory: lateral for information about the environment and medial for information about personal history and emotional states

What are normative decision theories? What are descriptive decision theories? What do evolutionary psychologists think?

• normative decision theories define how people ought to make decisions that yield the optimal choice → these theories don’t predict what people actually choose to do

• descriptive decision theories describe what people actually do, not what they should do

• from an evolutionary standpoint, we see that our brain has been shaped by evolution to optimize reproduction and survival in a world that differs from that we currently live in → our decisions today seem irrational, but they match the environment that actually shaped us

What are the main ways we can categorize decisions?

• goal-oriented decisions are based on our assessment of expected rewards whereas habits aren’t under the control of rewards anymore

  • action-outcome decisions involve evaluation of outcomes whereas stimulus-response decisions are more habitual

• model-based decisions involve an internal representation of something that helps with the evaluation of different actions

  • model-free decisions only have input-output mapping, similar to stimulus-response decisions

• social decisions are those that involve other people

What are primary and secondary reinforcers? What are factors that contribute to our representation of value?

• primary reinforcers have a direct benefit for survival fitness and their value is somewhat hardwired in our genetics

• secondary reinforcers have no intrinsic value themselves (ie. money and status) but become rewarding with their association with other forms of reinforcement

• factors contributing to our representation of value

  • payoff: what reward is being offered and how big is it?

  • probability: how likely it is to obtain the reward?

  • effort or cost: is there a time or effort commitment? is it worth it?

  • context: how much would you benefit from the reward right now?

  • preference

What roles do the regions of the prefrontal cortex play in value representation?

• most cells in the medial frontal cortex (anterior cingulate cortex) respond to cost, probability, and payoff → play an overall role in value

• cells in the lateral prefrontal cortex mostly encode probability → reflects the role in working memory as probability judgements require the integration of consequences of actions over time

• cells in the orbitofrontal cortex encode payoff

  • this region is involved in temporal discounting as well

What is the marginal value theorem? What brain region is involved in this sort of decision?

• marginal value theorem: exploiting a foraging patch until the intake rate falls below the average rate of the whole environment, then you explore new patches

• activity in the anterior cingulate cortex (medial frontal cortex) positively correlates with search value (explore) and negatively correlates with the encounter value (exploit) → ACC signals exert a type of control that promotes behaviours

What role does dopamine play in reward-related decisions? What is reward prediction error?

• research has shown that activation of dopaminergic neurons is linked to the expectancy of reward → activity is higher when reward is unexpected rather than when it’s expected

• dopaminergic neuron activity should be viewed as a reward prediction error that represents the difference between the obtained and expected rewards

  • positive RPE: obtained reward > expected reward

    • increases the value

  • negative RPE: obtained reward < expected reward

    • decreases the value

What are the three components essential for developing and executing a plan?

• three components

  • the goal must be identified and the subgoals developed

  • in choosing among goals/subgoals, consequences must be anticipated → need to view action plans as hierarchical so that you can see how failure to achieve a goal can result from many things

  • requirements for achieving the subgoals must be determined

How is the prefrontal cortex a dynamic filtering mechanism? How does it do this? How is this linked to deficits in action planning?

• connections between the PFC and the posterior cortex allow for goals (in the PFC) to maintain task-relevant information from long-term memory (in the posterior cortex)

  • filtering allows for the PFC to access different memories to help figure out ways to achieve the goal

• damage to the prefrontal cortex results in a loss of dynamic filtering, so patients have difficulty maintaining focus on a goal

What are the costs and advantages to the delay in prefrontal cortex development?

• costs: kids have a hard time with delayed gratification, maintaining focused, and inhibition

• advantages: prefrontal cortex immaturity may make you more open-minded as you don’t have strong responses or representations yet → good for learning

How does the prefrontal cortex’s dynamic filtering contribute to attention?

• this filtering can allow us to accentuate attended information or selectively attend to something by excluding other information

  • note: enhancement and suppression involve different neural mechanisms and suppression is more sensitive to aging effects (so older people attend by enhancing signals)

  • inferior frontal cortex plays a role in inhibiting task-irrelevant information and dorsal frontal cortex enhances task-relevant information

• the frontal lobes modulate the salience of perceptual signals, and thus help us guide attention, by inhibiting unattended information

  • with prefrontal cortex damage, you can’t attenuate unattended signals so you have a harder time focusing on things and tasks (can’t block out distractions)

What brain activity do we see during the stop-signal or go/no-go task? What does this tell us about inhibition?

• in both successful and failed stop trials, there is activity in the right inferior frontal gyrus → this area is silent in ‘go’ trials

  • this suggests that an inhibitory process is recruited in both stop trials

• in go and failed stop trials, we see pre-stimulus/cue activity in the motor cortex → this suggests that even though a stop command is given by the prefrontal cortex, the initial activation in the motor area leads to a response that is too fast to stop

• the subthalamic nucleus of the basal ganglia is active during successful and failed stop trials → the basal ganglia is involved in response initiation but the STN helps maintain inhibition

What system allows us to ensure that our goal-oriented behaviours succeed? What brain region is involved? How does it do its job?

• we have a monitoring system that allows us to look at how progress changes → the medial frontal cortex/anterior cingulate cortex is a key part of this system

• the ACC is associated with arousal and it has been extended to be associated with tasks in which we need to monitor demands

• the medial frontal cortex has extensive connectivity with the brain, so it is able to influence decision making, goal-oriented behaviour, and motor control

What are the three main theories on how the medial frontal cortex acts as a monitor of behaviour? What are the drawbacks of each?

1. attentional hierarchy hypothesis: the medial frontal cortex is high in the attentional hierarchy, so it’s most active during novel conditions or during difficult tasks

   • it’s a descriptive theory, not mechanistic, so it doesn’t say how the MFC is recruited or the kinds of representations the area supports

2. error detection hypothesis: the medial frontal cortex provides signals (error-related negativity and feedback-related negativity) correlated with the occurrence of error and this helps increase cognitive control

   • the MFC is also active in error-free tasks and it’s active without mistakes so the signals could be a marker for unexpected outcomes instead

3. response conflict hypothesis: the medial frontal cortex evaluates response conflict, so we see it active during difficult or new situations → when conflict is high, it allocates more attentional resources via other brain regions

What are the two visual streams? Where do they start and project to? What does each pathway do? Are there similar pathways in the auditory system?

• the dorsal (occipitoparietal) stream: the superior longitudinal fasciculus goes from the striate and other visual cortices to the parietal lobe → this pathway is the “where” pathway, so it’s involved in spatial perception

• the ventral (occipitotemporal) stream: the inferior longitudinal fasciculus goes from the occipital striate cortex into the temporal lobe → this pathway is the “what” pathway, so it’s involved in object perception and recognition

• in the auditory system:

  • anterior parts of the auditory cortex are part of the ventral pathway and help with auditory processing

  • posterior regions identify the location of sounds and are part of the dorsal pathway

How do the receptive fields of neurons differ in the “what” and “where” pathways?

• 60% of neurons in the parietal cortex (part of the “where” pathway) have receptive fields that exclude the foveal region → this allows for detecting the presence and location of a stimulus, especially one that just entered the field of view

• the receptive fields of neurons in the temporal lobe (part of the “what” pathway) always encompass the fovea → this allows for full processing and object recognition

What parts of the brain have been associated with facial processing?

• the fusiform face area in the temporal lobe shows activity towards faces and face-like configurations in general, regardless of expression

  • greeble study showed that this area may not be specific to faces, but to things we’re experts in → this area is active when categorizing things we’re experts in, but the activation is more broad when it isn’t face-specific

• the occipital face area in the inferior occipital gyrus responds preferentially to facial features, regardless of configuration

  • it gives featural information to the FFA to make a holistic face percept

• the superior temporal sulcus is active when observing emotive faces (eye gaze, expression, lip movement)

How are different areas of the inferior temporal cortex specialized for facial perception?

• the lateral inferior temporal cortex is specialized for variation in face shape → activity varies as a function of shape

• the anterior inferior temporal cortex is specialized for variation in appearance → activity varies as a function of appearance

What is prosopagnosia? What is congenital and acquired prosopagnosia? What are the types of acquired prosopagnosia and what causes them?

• prosopagnosia is a disorder categorized by an inability to recognize familiar faces in the absence of other visual or intellectual deficits

  • usually due to damage to the occipital regions and fusiform face area

• congenital prosopagnosia is present since birth and has no brain damage associated with it → due to genetic mutations that disrupt aspects of development in the ventral visual pathway and fusiform gyrus

• acquired prosopagnosia occurs as a result of brain damage

  • apperceptive prosopagnosia is a perceptual deficit, so you can’t make same-different judgements when looking at two pictures of the same person → rely on other cues like voice or clothing to discern identity

    • caused by damage to the fusiform face area

  • associative prosopagnosia is a deficit in linking perceptual features to information about a person → can’t tie perception to memory

    • caused by damage to the anterior temporal lobe or connections between it and the fusiform face area

What is capgras delusion? What causes it?

• capgras delusion is a disorder in which a person believes that someone has been replaced by an imposter → recognize that this person close to them looks the same as before their injury, but believe that it isn’t truly them

• it’s caused by damage to connections between the superior temporal sulcus and the amygdala → your emotional response to the person changes, so you now perceive them as an imposter (ie. wouldn’t recognize your mom if you suddenly felt entirely different emotions toward her)

How does object processing differ from facial processing?

• object perception relies on feature processing → it uses individual features to understand a whole object

• facial perception relies on holistic processing → looking at something as a whole and seeing the configuration of features helps us process faces

How is the frontal cortex related to social behaviour?

• the prefrontal cortex develops throughout childhood and adolescence → this development is accompanied by changes in social behaviour

• people with orbitofrontal cortex damage have impairments in emotional processing, which is part of social cognition

• many neurodevelopmental disorders, such as ASD, APD, and schizophrenia, are associated with deficits in social behaviour

What is social cognition? What role does the default mode network play?

• social cognition involves processing and interpreting information about other people and social situations

  • understanding social norms

  • understanding what others know

  • understanding emotional states

  • sharing of emotional states

  • distinguishing self from others

• the default mode network has increased activity at rest before mental state tasks → the default mode network prepares us for social cognition

What is self-referential processing? What area of the brain is associated with this?

• self referential processing refers to when we distinguish ourselves from others in order to engage in social interactions

  • we process things that reference ourselves more, which is adaptive → study showed that we remember adjectives from self-referential conditions better than those in the other-referential condition

• the medial prefrontal cortex is most active in self-referential conditions and the activity positively predicts memory performance

What is theory of mind? How do we test it? What brain areas are involved in this?

• theory of mind refers to our understanding that others have minds separate from our own → allows us to make inferences about what others are thinking and feeling

  • the Sally-Anne (false-belief) task where an object is moved without one person knowing is used to test ToM

• many areas from the default mode network, including the medial prefrontal cortex, are involved in theory of mind

  • we need to distinguish ourself from others to infer another person’s perspective

What is empathy? What is empathetic accuracy? What brain areas are involved?

• empathy refers to the perception of another’s emotion and the consequential triggering of somatic and autonomic responses such that we share the emotional state

  • empathetic accuracy is one’s ability to correctly infer a target person’s thoughts and feelings

• in studies on empathy, activity in the anterior cingulate cortex (medial frontal cortex) and right insula is active when you’re being shocked and when your partner is shocked

  • empathy shares neural correlates with experiencing those emotions ourselves

What are the two theories about how we accomplish empathy? What brain regions are involved?

• mental state attribution theory (also called theory theory): our theories about what we know about another’s past, current situations, family, gaze direction, body language, etc. allow us to infer their mental state → doesn’t account for the fact that our understanding of others is immediate

  • the medial prefrontal cortex helps us understand others as it helps us represent information about them

  • the right temporoparietal junction helps us reason about another’s mental state

  • the superior temporal sulcus helps us infer mental state from eye gaze direction

• experience sharing theory (also called stimulation theory): we observe another’s behaviour, simulate it, and use our own mental state produced by the stimulation to infer their mental state

• we likely do a bit of both theories