Post Midterm Content Part 1 Flashcards
1
Q
What is cognition?
A
- Cognitive functions/mental functions/high-order functions
- the things in the world reach our sensory organs and we respond through motor interactions, cognition can be defined as anything that happens “in between”
- information and recombination and transformation - mostly in the cortex
- memory, learning, attention, executive functions
2
Q
What does cognition depend on?
A
depends on patterns of neural activity but information encoded at this level is more complex/multidimensional.
the higher up we go, the harder it is to make connectivity between the neural activity and the stimulus.
neurons in the periphery (closer to sensory organs) have a more direct correlation to the stimulus
3
Q
What is the cortex?
A
Wrinkled, two-dimensional sheet of layered neurons
4
Q
Sensory cortices
A
1ary and 2ary, auditory, visual, somatosensory, gustatory and olfactive
whatever gets processed in sensory organs will go up and have relays in the brain stem, the thalamus, and eventually arrive to primary sensory cortex.
For each sensory organ, we have one primary cortex (sensory cortex), part of cortex that processes sensory information.
5
Q
Motor cortices
A
1ary motor cortex, premotor and supplementary motor (2ary)
send signals to our muscles.
6
Q
3ary areas & association cortices
A
- the place where some of the cognitive functions are orchestrated
- regions of the cortex where injury causes cognitive deficits that cannot be explained by impairment of sensory or motor function alone.
- inputs: 1ary and 2ary sensory cortex, motor cortices, hippocampus, thalamus and brian stem.
- outputs: hippocampus, basal ganglia, cerebellum, thalamus & other cortical areas.
- have the parietal, temporal, frontal & limbic.
7
Q
In terms of input, how is primary sensory areas and higher-order sensory areas different?
A
Primary sensory areas:
- from thalamic sensory relay nuclei
Higher-order sensory areas (V3 and V4):
- from other thalamic nuclei and lower-order areas of sensory cortex (will receive input from V1)
8
Q
What is the difference between receptive fields in primary sensory areas and higher-order sensory areas?
A
- primary sensory areas have small receptive fields.
- higher-order sensory areas have large receptive fields.
9
Q
What is the difference in arrangement between primary sensory areas and higher-order sensory areas?
A
Primary:
- in a precise map of the sensory receptor surface
Higher order:
- Into more imprecise maps of the array of peripheral receptors (association areas are less precise, more vague- the map starts to get lost)
10
Q
What is the difference if there is an injury in the primary sensory areas, or in the higher-order sensory areas?
A
Primary:
- simple sensory loss
Higher-order:
- deficits of perception and cognition & intact detection of sensory stimuli
11
Q
What is the difference in connectivity in primary sensory areas and higher-order sensory areas?
A
Primary:
- limited connections to other cortical areas (only nearby, same modality regions) (V1 is connected to V2, V3, V4)
Higher-order:
- connected to nearby unmodal areas & distal areas in frontal and limbic lobes. (V3 and V4 start connecting to association areas - start sending information to areas of brain that integrate different stimuli)
12
Q
basic division of functional organization in the cortex
A
Information to primary sensory areas, then to secondary and third sensory areas, then association area, then motor areas, and then down.
Simplified: primary sensory areas, then higher order sensory areas, then association areas, then motor areas.
13
Q
Information flow in the Nervous System
A
Sensory organs relay in the thalamus, send information to sensory cortices, send information back to thalamus.
Basal ganglia/cerebellum connect to the thalamus, send information to motor cortex and to muscles.
Sensory cortices send information to association cortices, through connections that go from cortex to cortex. (temporal cortex to frontal cortex - and regulate behaviour)
Association cortices are modulated by brainstem modulatory inputs.
14
Q
Principles of: Information flow in the nervous system. important slide
A
1) Sensory information is processed serially.
2) Each area carries certain computations and conveys them to the next area, going higher in complexity and in abstraction of representation.
3) Higher-order areas project back to the lower-order areas from which they receive input. (serial - simple to complex, but the complexity will also project back)
4) Parallel pathways in each modality lead to dorsal (where) and ventral (what) association areas.
5) Goal directed motor behaviour is controlled in the frontal lobe.
15
Q
What is the difference in flow of information for the sensory stream and the motor stream?
A
The motor stream is descending, and the sensory stream is ascending. (these happen at the same time)
For every pathway that goes up, there is a pathway that goes down (bottom-up and top-down)
16
Q
How are functional areas in the cortex organized? What are the principles?
A
1) Structure.
2) Physiological response.
3) Connectivity.
Principles:
1) all areas fall into a few functional categories. (sensory, motor, association)
2) areas in a category occupy a discrete continuous portion of the cortical sheet. (one portion that we can identify that has common characteristic and perform specific function)
3) areas that are functionally related occupy neighbouring sites. (if two areas do the same thing, they have to be connected)
17
Q
Cortical structure (Lamination)
A
- we have different types of cortex!
- neocortex, paleocortex (piriform) and archicortex.
- cognition: we talk mostly about neocortex.
- areas around the hippocampus are the archicortex (and has 4 layers)
- piriform cortex (related to memory and olfaction - in many organisms beyond humans, has 3 layers)
- neocortex has 6 layers, some layers have neurons and some are dendrites.
- each level has different density of cell bodies, density of dendrites, discover by cutting and looking at a microscope.
18
Q
Cortical structure: Canonical circuit
A
1) Each layer has a primary source of inputs and a primary output target. (benefit to having 6 layers of neurons - organization of information)
2) Connections in the vertical axis (columnar or radial connections)
3) Connections in the horizontal axis (lateral or horizontal)
4) Cells with similar functions arranged in radially aligned groups.
5) Interneurons within layers give rise to axons that extend horizontally (linking functionally similar groups) (may be inhibitory - link neurons in different layers)
19
Q
Cortical organization: Regional variation
A
1) Korbinian Brodmann, cut the brain sliced it in every spot and made a map. He saw cytoarchitectural areas and draw that map. This was before there was fMRI. “regions of the brain with similar structures in. both cell type layering could produce a specific function” (gradient - cells start changing from one area to another)
2) Eventually…using histological staining techniques showed us cortical organization:
- cell density, cell size
- cortical thickness
-laminar size
—> the way we see the 6 layers of neocortex, is different from how we see it in visual cortex, motor cortex, etc.
-> the organization is not just related to structure but it is to function as well.
20
Q
What experiments confirmed brodmanns thinking of the cortical organization having regional variation?
A
1) Neurological case studies
- Broca & Wernicke - language of phinease Cage - PFC Brenda Milner - memory.
2) In-vivo electrophysiology in animals
- Decision making and reward - PFC.
3) Neurosurgical patients
- Wilder Penfield and the motor and sensory homunculi.
21
Q
What are modern neuroscience studies in humans?
A
1) Neurophysiological testing
2) Functional neuroimaging & Neuromodulation (temporarily activate or inhibit an area of the brain with pulses) combined with psychological tasks.
3) Lesion studies.
Ex. memorize this set of cards, record brain activity.
See the areas of brain that are active.
-> can map function to structure.
22
Q
What are unique features of association cortices?
A
1) Primary sensory cortices receive information from particular thalamic nuclei, lateral geniculate, medial geniculate.. association cortices will not receive most of their information/directly from the thalamus.
2) Some information that arrives from the thalamus has already been processed by sensory and motor areas.
3) Majority of input to association cortices come from corticocortical connections (other cortical areas communication)
-» Same hemisphere - U shaped fibres/long association fibres. (connect temporal to frontal example)
-»> Interhemisphere- long association through corpus callosum.
23
Q
What are association cortices modulated by?
A
- by subcortical nuclei (important source of innervation)
1) Cholinergic - brainstem and basal forebrain - memory, learning, attention (helps do cognitive activities)
2) Dopaminergic - midbrain - pleasure salience, motivation, reward-learning (linked to anticipation of pleasure/motivation)
3) Noradrenergic - brainstem - wakefulness, stress reaction (activator)
4) Serotoninergic - brainstem - mood, memory processing, sleep. (emotional states)
all association areas receive different neurotransmitters from the brain stem.
24
Q
Cholinergic
A
memory, learning, attention (helps do cognitive activities)
25
Dopaminergic
pleasure salience, motivation, reward-learning (linked to anticipation of pleasure/motivation)
26
Noradrenergic
wakefulness, stress reaction (activator)
27
Serotoninergic
mood, memory processing, sleep. (emotional states)
28
What does each association area have?
- a distinct set of subcortical connections
- has very own particular pattern of connections that go to different areas
- different within every human because we have all had different experiences
Ex. musicians have higher connectivity have higher association between motor coordination (hands) and auditory (music)
29
What is the functional specialization of the association area in the Parietal lobe?
- attention & perceptual awareness of body and stimuli around it
- integrates somatic, visual, acoustic and vestibular sensory information - spatial cognition and motor control of the eyes and extremities.
- the most anterior (more to front) part of the parietal cortex is the somatosensory cortex. So the first thing we encounter is the somatosensory cortex, then in the back, it stops where the visual cortex starts. It is also close to the auditory cortex (because that is in the superior part of the temporal lobe) = multisensory integration (integrates the 3 of them)
- linked to the where pathway (locates things in space)
30
What is the functional specialization of the association area in the Temporal lobe?
- categorization, object recognition, semantic memory (language comprehension)
- Lateral - auditory association cortices - including Wernicke's area (language comprehension are)
- Ventral - WHAT pathway - recognition of sensory stimuli - faces/words/objects - lesion: AGNOSIA (cannot recognize what we are presented with, but we can see it and we can describe it) - do not know what it is.
- if more apperceptive (more posterior) : cannot copy.
- if more associative (more anterior) : cannot associate objects (but can perfectly copy it)
- strong connection to the limbic system - emotion & memory (amygdala and hippocampus)
31
What is the functional specialization of the association area in the Frontal lobe?
- planning & regulation of behavior (decision making and behavioural inhibition)
- largest lobe/widespread connectivity/most complex functional anatomy
- integrates information from sensory & motor cortices, parietal & temporal association cortices.
- appreciation of self in relation to the world - allows selection, planning and execution of appropriate behaviour (social contexts)
- damage in the frontal lobe - change in "character" or "personality"
- short term memory functions and planning - more dorsolateraly
- value and decision making - more ventromedially
32
How did we discover that there was attention sensitive neurons?
- we have attention sensitive neurons in the parietal cortex.
1) have monkey that pays attention to different things, manipulate what it pays attention to with a reward and a stimulus appears, the monkey is very attentive to it, we record from parietal cortex and see that the neurons fire.
2) people listening to words, count the amount of times we hear the word STAR among random words. Waiting for the word star, paying attention to star. Record the activity starting each word. Saw that when it was STAR the parietal lobe showed WAY more activity.
33
Contalateral hemineglect syndrome
- Lesions in the right parietal lobe impair spatial awareness! -> leading to an inability to attend to stimuli on the left side.
- This suggests the right hemisphere's dominance in processing spatial information and integrating sensory inputs from both sides of the body.
- Lesions in the left parietal lobe do not produce the same attentional deficit, indicating that the right hemisphere plays a crucial role in attending to stimuli from both sides, while the left hemisphere predominantly attends to the right side.
- Role in Spatial Awareness (lateralized to the right)
- Important role in multimodal/sensorimotor integration
34
Case of Phineas Gage
- frontal association cortex
- functional deficits: cognitive disabilities, impaired restraint, disordered thought, perseveration and inability to plan appropriate action.
- Phineas gage became inconsiderate, intemperate etc.
- Joe A showed little restraint, lost initiative and creativity
- Frontal lobotomies
35
Limbic association cortex
- at the edge of the cortical surface, medial view of the hemispheres
- orbital and ventromedial cortex - connected to amygdala and hippocampus - emotional processes
36
The Circadian Cycle
The circadian rhythm, which governs physical, mental, and behavioral changes, follows a cycle influenced by external cues like light and daily routines. These changes include variations in alertness, mood, and activity levels.
External cues such as light, meal times, and social interactions help distinguish between day and night, regulating our cortical state of being awake or asleep. However, the duration of this cycle can vary from person to person. In an experiment, when external cues were removed, the circadian rhythm of a participant shifted by approximately 2 hours every day, indicating an intrinsic cycle length of 26 hours. When gave the person cues back, the cycle readjusted back to normal.
External cues regulate our cycle (how important light is and other routines)
37
What are visceral functions regulated by?
- they are regulated by the hypothalamus and the visceral nervous system
- hypothalamus is a structure that has a series of nuclei that will be important for regulating our hormonal states or visceral functions. Sends signals down different mechanisms to regulate.
38
Circadian rhythms
1) Internal or biological clock
- encoded in our genes
- homeostatic regulation
- temperature, levels of hormones (GH, cortisol)
- operates even in absense of external information
- hypothalamus (suprachiasmatic nucleus), adrenal glands
Regulation by environmental information:(associated with better physical and mental health)
1) Light (to fit day/night cycle)
-> sensors in the retina signal changes to the brain (hypothalamus - SCN - central or MASTER clock)
2) Physical activity
-> increased temperature and metabolism (muscle tissue and other organs - peripheral cloc)
39
Cortisol
1) Hormone associated to stress - Peaks happen in the morning (when you wake up) - 6am
2) opposite to melatonin
3) Periodic secretion is controlled by the circadian clock (central pacemaker 0SCN and adrenal gland clock)
4) plays a part in the synchronization of the cell-autonomous clocks
5) increased secretion with:
- immune system response, intense physical activity, physiological and emotional stress.
40
Melatonin
Hormone that peaks at 3 or 4am when you are in deep sleep
41
when does growth hormone peak?
Growth hormone peaks at night, we do important growing during our sleep.
42
Regulation of circadian rhythms by light
- sensors in the retina that will signal changes in light to our hypothalamus, and then this will regulate different hormones that we can release during the night or the day.
1) Intrinsically photosensitive ganglion cells - MELANOPSIN (sensitive to degree of light - when a lot of light, these cells are inhibited, when there is not, they are activated)
2) (hypothalamus) Suprachiasmatic nucleus "master clock" or pacemaker. (receives input from the retina)
3) Pineal gland - synthesizes MELATONIN.
43
Cyrcadian effects on learning and mood
- seasonal effective disorder "winter blues"
- less light in winter so the circadian rhythms are not regulated anymore.
- there is another pathway, that connects the photosensitive ganglion cells in the retina, directly to brain areas linked to emotion. (not only important to regulate circadian rhythms, it is also important to regulate mood)
44
What is the behaviour description of sleep?
- reversible state of perceptual disengagement from and unresponsiveness to the environment
- postural recumbence, behavioural quiescence, closed eyes
- "normal suspension of consciousness"
45
What are the sleep requirement's?
"a series of controlled physiological states governed by a group of brainstem nuclei" - restorative effect.
- requirements: 7-8 hours per day
- varies among individuals, varies with age. (at birth you need many more hours of sleep and this number goes down as you get older) (older people need less hours of sleep - requirements start getting smaller and smaller)
46
what happens if you have sleep deprivation?
- impaired judgement, reaction times
- mood swings and even hallucinations
47
what is the purpose of sleep?
1) Energy conservation:
- replenish brain glycogen levels
- decreased metabolism
2) We are highly dependent on visual information to find food and avoid predators to is is better to pause when its dark. (evolutionary safe)
3) Consolidation of memory:
- sleeping soon after increases recall
- sleep closes the gate between short-term and long-term memory stores (changes short term to long term during sleep)
4) Clearance of brain metabolic waste
- cerebrospinal fluid (while we are asleep, the flow of fluid reverses its direction which helps clean the debris from cells and neurons and blood vessels)
48
What are the stages of sleep? EEG basics?
N1 - STAGE I: Transition to sleep/drowsiness
- waves start showing lower frequency, higher amplitude
N2 - STAGE II:
- sleep spindles (periodic bursts of activity 10-12 Hz that last 1-2 seconds)
- even lower frequency/higher amplitude
N3- STAGE III & IV:
- slow wave sleep/delta wave sleep (the deepest sleep)
- number of spindles decreases delta waves (0.5-4 Hz)
R - REM sleep:
- EEG similar to awake stage
-Cycle of alternating NREM - REM sleep repeats several times in one night!
49
Describe the 4 stages of non-REM sleep
N1 (stage 1)
- transitional stage
- low arousal threshold
- slow, rolling eye movements
N2 (stage II)
- more intense stimuli required to produce arousal
- presence of sleep spindles
- presence of K complexes
N3 (Stage III & IV):
- parameters reach their lower values
- deepest sleep/higher arousal threshold
- occupy less time in the 2nd cycle
- might disappear from later cycles
- progressively fall into sleep, decrease in heart rate, temperature, blood pressure, metabolic rate.
- as it goes down, lower frequency and higher amplitude.
50
REM Sleep
- rapid ballistic eye movements
- physiological variables increase again
- pupillary constriction
- paralysis of large muscle groups
-> twitching of smaller muscles
-spontaneous penile erection
- greater prevalence of DREAMING
- REM sleep episodes usually become longer across the night.
- indistinguishable/similar to when the brain is awake.
51
When does dreaming occur? What is the difference between the two states of dreaming?
- dreams occur in both REM and non-REM sleep.
- Features of memory and hallucinations.
1) REM dreams: long, primarily visual, somewhat emotional, and usually not connected to the immediate events of everyday life.
-> sensory modalities:
Visual 100%, Auditory events 65%
Vestibular 8%, Temperature 4%
-> Emotional content of dreams
Anxiety (14%), surprise (9%)
Joy (7%), sadness (5%)
Shame (2%)
- men experience penile erections; women experience the physiological counterparts of sexual arousal.
2) Non-REM dreams: shorter, less visual, less emotional, more conceptual and usually related to the current life of a dreamer.
52
How can we tell if we are awake or dreaming?
1) Muscle paralysis
2) Do not respond to the environment
53
How does the type of sleep you have change throughout your life?
As you get older, you are awake more, and have less REM sleep and more NREM sleep.
54
What neural circuits govern sleep?
1) Electrical stimulation of the midbrain-pons junction -> Wakefulness and arousal.
2) Low frequency pulses to the thalamus -> Slow wave sleep.
55
Describe the neural circuits of sleep
patterned interaction between the brainstem (reticular activating system), the thalamus and the cortex.
regulated by neurotransmitters released by hypothalamus!
56
Thalamocortical interactions when awake
- Thalamus connects to the cortex (thalamic neuron projects to neuron in the cortex = thalamocortical)
- sensory information passes through thalamus and that gets sent to the thalamus. (very diverse and dynamic)
- when we record it while we are awake, this neuron is receiving a lot of information from the thalamus.
- see in EEG a lot of noise and rapid firing. Summation of activtity happening in cortical neuron.
- when we are awake, we say that the thalamocortical neuron is in TONICALLY ACTIVE state. receives information from senses and sends to cortex, encodes peripheral stimuli, thalamus is a gate and it is open.
57
thalamocortical interaction when sleeping
1) Intrinsic bursting state - OSCILLATORY STATE
- thalamocortical neurons are still firing, but they are not firing to encode the stimuli from outside world, they are firing in a rhythmic pattern.
- synchronized with the cortex
-rhythm that is encoded in its genes
(when asleep - the neurons are firing at the same time, the EEG is less all over the place)
58
What closes/open the gate of the thalamus for thalamocortical interactions?
- determined by the brainstem nuclei and the hypothalamus
- brainstem sends neurotransmitters that determines if the door is open or if it is closed
- nuclei in the brainstem that released noradrenaline, induces wakefulness, which opens the door/means they are in TONICALLY active state.
- cholinergic (up when we are doing cognitive activity - REM sleep we are doing this). So when we have this input, we have more activity in the brain during REM sleep/and wakefulness.
- Serotonin is linked to NREM sleep.
59
Thalamocortical feedback loop
1) Another kind of thalamic cells - GABAergic neuron in the reticular cells
-hyperpolarize thalamocortical cells
- receive ascending information from the brainstem
- receive descending information from cortical cells
- responsible for sleep spindles:
-burst of activity of neurons in reticular nucleus
-short bursts of action potentials in talamocortical neurons
During sleep, neurons in the reticular nucleus are a "mediator" of the activity of thalamocortical cells, and can hyperpolarize them further, causing a rebound burst of activity that is seen in the EEG as a sleep spindle.
60
Histamine
Activated by lateral hypothalamus, orexin.
It positively modulates noradrenergic and serotoniergic neurons by tuberomamilliary nucleus of the hypothalamus.
61
What is the affect of anti-histamine medication?
You get drowsy. Because you don't have the input to noradrenergic neurons, don't have adrenaline, then you go to sleep.
62
Orexin
Activates histamine
Linked to hunger
High quantities of it because you are hungry, increase histamine and increase noradenaline - which activates adrenaline and makes you awake.
63
what are the three neurotransmistters that induce wakefulness?
1) Histamine
2) Orexin
3) Noradrenaline
- Antidepressant increases the noradrenaline in the system and activates you, same as cocaine.
64
What neurons make you go to sleep ?
- series of neurons in the hypothalamus
called GABAergic neurons of the Ventrolateral preoptic (VPLO) nucleus of the hypothalamus**** makes you go to sleep
- uses GABA neurotransmitter (always inhibitory)
- inhibits the other nuclei that induce wakefullness through noradrenaline
65
Valium
medication that makes you go to sleep
stimulates GABA
ventrolateral preopotic nucleus inhibits the other nucleus that make you awake, closes the gate of the thalamus
66
what is the important neurotransmitter for REM sleep ?
- REM-on cholinergic neurons
- REM-off serotoninergic neurons
67
Where is activity increased and decreased when you are in REM sleep>
1) Increased: amygdala, para hippocampus, pontine tegmentum, anterior cingulate cortex (lymbic system - high emotion)
2) Decreased: dorsolateral prefrontal and posterior cingulate cortex (inappropriate social content) (less activity in activities related to decision making and impulse inhibition - less activity in prefrontal cortex - why dreams are inappropriate)
68
Three phenomena that happens in REM sleep:
1) REM Saccades: rapid eye movements happen cause mechanism in brain stem that sends input to our eye muscles. and inhibit own movement.
2) Hyper-polarization of spinal cord motor neurons
(all coordinated in the brainstem)
69
Reticular activation system
- group of brain stem nuclei that operate with 3 distinct neurotransmitters to promote wakefullness
(serotonin (NREM) , neradrenaline (awake) , acetycholine (REM))
70
Sleep Spindles
- sleep spindles occur during the depolarized phase of the slow oscillation and are generated in thalamic circuits as a consequence of cortical firing.
- linked structure - reticular nucleus (thalamus )
- during sleep, neurons in the reticular nucleus are a "mediator" of the activity of thalamocortical cells, and can hyperpolarize them further. causing a rebound burst of activity that is seen in the EEG as a sleep spindle.
71
Parasomnias
- sleep walking
-sleep talking
- confusional arousals
- night terrors
- NOT during rem sleep
->>> REM behavior disorder - Descending inhibition of motor neurons is impaired.
- Happen during stages 3 and 4 of sleep - delta wave of deep sleep. when short epoisodes, the EEG does not change. When they are longer, the EEG pattern changes to an "active" (awake or REM) pattern.
72
Alertness
- related to neuroadrenaline
- related to being awake
- related to being responsive to the environment
73
Attention
- attention is a cognitive function that focuses on some external or internal stimulus, at the expense of fully processing other information.
- we can't process everything at once.
- filter, selective mechanism that we choose where are neural recourses should go to.
"cocktail party effect" ( a lot of people talking and music and you have to chose what you listen to)
74
Attention as selective processing
- presenting different dialogues to each ear at the same time.
- subjects would accurately report the content of the attended channel, but only rudimentary information about the unattended.
- in the unattended channel, only 'salient' information would be processed.
75
What is the link between consciousness & attention?
- only attended information reaches threshold to enter consciousness.
- consciousness processing depends on "focusing neural resources according to the contingencies of the moment"
- influence of perceptual load - stimulus complexity/ presentation brevity
->>> the more complex the stimulis is, the harder it is to attend to different elements.
76
What is endogenous attention?
- spatial
- voluntary tasks: consciously direct attention to a particular aspect of the environment
- also called top-down attention: "based on prior knowledge, willful plans, and current goals"
- a particular location, feature, or object relevant to current behavioural goals is selected internally and forced upon or examined.
- facilitates processing: 300 ms to a few seconds.
77
Exogenous attention
- triggered by random environmental stimuli that attract attention automatically
- also called bottom up attention
- neurons are activated to a greater extent when salient stimuli - stimuli that stand out from their background appear in their receptive fields.
- improved processing: 75 ms to a few hundred ms.
- after 400 ms, inhibition of return.
78
How is spatial endogenous attention studied in neuroscience?
screen where red dot appears in centre and square that appears in right or left. before it appears you see arrow that will point to the side where the square will appear and then you click button when the square appears. so then you pay more attention to that side waiting for it. (reaction time decreased, you are faster to detect target!)
if they trick you and it points to the wrong location, you slower to click because what appears in attended location is processed in a more efficient way. (take even longer to respond)
neural cue where arrows points to both sides so you attend to the centre. (take longer to respond)
79
How is non-spatial endogenous attention studied in neuroscience?
- pay attention to a word, or listen to a song paying attention to an instrument vs another instrument.
-> Stroop task: you see words that are the same colour of what is written in word, ex. purple in purple. you have to say outside what is written in the word. eventually the word that appears does not match the colour, a certain moment that you are confused. But the information is conflicting so you consciously focus on the word and ignore the colour. this takes time to make this switch.
80
What experiment was done for exogenous attention in neuroscience?
- there is no instruction.
- they just say look at the screan and there are three squares, there is a flash but it can happen on either side. and then you see the actual target. you are faster to respond if there is another square that happens in the same location, your attention is already where the flash is.
- if nothing happens you attention is decreases, and this is called inhibition of return.... if nothing happens after a few seconds then you ignore it and then something that happens there is processed less efficiently.
81
Overt Attenion
- orienting head and eyes to a stimulus, aligning visual and auditory information and improving perception.
81
Covert attention
-even fixating gaze on a particular point on the visual field, information in the attended location is better reported.
82
Eye-tracking technology
- allowed to study mostly overt attention.
- starting with putting small mirrors glued to the eyes of the subjects that redirected light to phototracing paper.
(classical study)
-> looking at painting with different things going on, let subject freely look at picture. then you ask them to estimate the material circumstances of the family (focus on the room), then the ages of people on the images (focus on face and body)- allows us to know what we pay attention to more naturally, how long we pay attention to a specific area.
- measures saccades (REM) and fixations.
83
Supramodal Attention
- attention across sensory modalities
- stimuli in one modality concurrently stimulates another modality "spread of attention"
- sound cue - stimulates visual perception.
84
What brain systems control attention?
- strong overlap in the circuits that control attention and those govern movements of the head and eyes:
- communication between parietal and frontal areas
1) Intraparietal area
2) Frontal eye-field
3) SUperior colliculi
85
Inferior Pariteal Lobe (lesion)
1) Hemispatial neglect syndrom
- lesion on the right parietal lobe and you neglect the left.
- if you have a stroke and damage right parietal lobe, you may get this syndrome and ignore everything that happens on the left side.
- patients reported to be able to see some stimuli an the left field if they were very salient/very prominent - actives exogenous attention.
- dominance of the right hemisphere - non-existant in non-human primates.
- "extinction" phenomenon (clinical assessment)
- happens in parietal association cortex
86
Frontal Eye fields (lesions)
- lesions here will disrupt the ability to:
a) initiate eye movements to targets in contralateral visual field
b) to direct attention to that side
c) task switching/ignoring irrelevant information
- FEF normal functions generate saccadic eye movements to locations in visual space that warrant attention.
- FEF stimulation increases neuronal activity at the visual cortex.
87
Superior Colliculi (lesion)
- in brainstem regions can affect attentional control
1) Sprague effect - a lesion to the left superior colliculus can compensate the hemispatial neglect causes by the lesion of the right parietal cortex.
2) Parietal lesion-induced neglect arises from an imbalance of activity.
- two structures that help you pay attention to right, and one for left, if you lose the one that pays attention to left, you just have over attention to right.
- if you lesion the colliculus, you pay less attention to the right and can pay more attention to what is happening on the left.
3) The pulvinar nucleus of the thalamus connects SC to the parietal cortex.
- left colliculus goes to left parietal and processes what is happening on the right.
- the right colliculus goes to right parietal and helps process what is happening on the right and the left.
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Attentional control network
- frontal parietal!!!
- tasks involving attention activate a set of brain regions in the dorsal parietal and dorsolateral prefrontal cortices.
- slightly different structures for exogenous/endogenous.
- superior colliculus.
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What is the effect of attention on perception?
1) When participants direct sustained attention to a particular visual-field location, increased activity is elicited in extrastriate cortex as well.
2) Microstimulation of FEF improves performance in attentional tasks and increases activity in V4 - "pre-motor theory attention"
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Different cortical states during wakefulness
- to main networks in the brain that are anti-correlated!!!
1) When you have to do a task, you activate a series of structures that are related to attention, this is the central executive network.
-> cognitive tasks
- frontospatial attention regions, intrapariteal sulcus, ventrolateral prefrontal cortex
2) Awake, awake but without engaging in a particular task - default mode network.
- posterior cingulate cortex
- medial prefrontal cortex
- tempoparietal junction
- balance between these two networks is very important.
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Salience
- something that drives your attention even if you don't want to look at it
- flashing, perceptually intense, very loud, different from what your seeing.
- individual factors that may make something more salient, something that is novel (you have never seen it before). Something less extravagant then light but new will then become salient.
- algorithms on social media manipulate our attention, whatever is motivational or our interest.
- everything that is emotional is also salient.
- saliency changes from person to person.
- saliency is moving constantly, and your cortex is computing what is more salient, vs less salient.
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Are there ways to train our attention?
1) Mindfulness/attention/the wheel of awareness
Ex. paying attention to our breathe and not whats happening around us. that helps train our attention - helps us connect with what life brings (mental health)
"wheel of awareness" - many things going on, outside, bodily stuff, mental activities, and interconnection with other people, looks at attention as a wheel that will allow us to pay attention to different things.
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What is the definition of memory?
- ability to store information from past experience and retrieve it.
- you can see then retrieval through conscious recollection, or changes in behaviour.
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How is memory a neuro-chemical process?
1) Learning - processes through which new information is acquired by the CNS - plasticity.
2) Habituation - learning to ignore a novel stimulus (harmless).
3) Sensitization - heightened response when paired with a harmful stimulus.
- discovered in snail: Aplysia
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Cellular and molecular mechanisms of learning
- long term sensitization
- long term habituation
Imply:
- changes in:
-> structure in the presynaptic terminals
-> Functional effectiveness of the pre-existing synapses
"synapses change with experience"
- activity dependent plasticity at the circuit level also (Donad. O. Hebb "Neurons that fire together, wire together"
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Synaptic Pruning
- born with more connections than we need - in the first period of prenatal life you lose a lot of connections. (by the activity dependent plasticity at the circuit level)
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What are the qualitative categories of memory classification?
1) Declarative/ Explicit
- semantic (not an event, it is a name)
- episodic (event)
(can verbalize and recall the memory)
2) Deconclarative/Implicit (things that we cannot verbalize)
- Priming
- Associate learning (conditioning)
- Procedural
(would be in motor circuits)
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What are temporal categories of memory?
1) Immediate (for a second or so)
- sensory memory
2) Short-term memory (seconds to minutes) - working memory
3) Long-term memory (days to years)
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Working memory (short-term)
- information relevant to achieve a goal is stored for seconds to minutes
- delayed response task (monkeys)
- closely related to attention - pertinent to language reasoning and problem solving.
- works for declarative and non-declarative information.
- limited in duration and capacity.
- part of pre-frontal area.
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How do we go from short-term memory to long-term memory?
Consolidation!
- progressive stabilization of memories that follows the initial encoding of memory "traces" through conscious or unconscious rehearsal or practice.
- "Engram" - physical embodiment of any memory in neural machinery = changes in efficacy of synaptic connections, growth or reordering of such connections. (physical manifestation of a memory)
- Changes in protein synthesis and other mechanisms of synaptic plasticity - persistence of memories at the cellular level.
- when we are sleeping, cortical neurons are synchronizing in a slow way which is helping consolidate memories.
- hippocample traces part of STM, hippocampus transfers those traces to the cortex, physical changes happen, and then you consolidate LTM.
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Priming
"change in the processing of a new stimulus due to a previous encounter with the same or related stimulus"
- resistant to dementia, brain injury and aging.
-> semantic priming:
"I take my coffee with cream and..."
- Effect in reaction times and neurophsyological correlates - priming shows the importance of association
- works that are primed come faster/can also prime for something that sounds similar.
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What enhances memory span?
- associating! Mnemonist could remember up to 37,000 digits of pi.
- giving meaningful context to meaningless items (chess players, music aficionados)
- motivation (pictures vs. food when you are hungry)
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Associative (conditioned) learning
1) Classical condition
- Pavlov's dog
- Pairing normal trigger with unrelated stimulus through repeated association, the unrelated stimulus elicits the response.
- passive.
(ring bell and give cat food)
2) Operant conditioning.
- Thorndike & skinner.
- Increasing behavioural response by associating a response with a reward.
- more active leaning
- click on level cause association action with reward/punishment.
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Forgetting
- we forget things that have no particular importance, unused or unrehearsed memories over time.
- had a prodigious memory. it was hard to read for him for he could not get rid of irrelevant association/images. "S"- when he was reading he could not focus because associations were constantly popping up.
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Amnesia
- the pathological process of forgetting is called amnesia.
1) Retrograde amnesia (can't remember what happened before an accident)
2) Anterograde amnesia
(getting really drunk and can't remember what happens after)
- the study of amnesia has given us important keys on the brain systems underlying memory.
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What brain systems underlying memory?
1) diencephalic and medial temporal lobe structures - role in establishing new declarative memories.
2) Hippocampus, Amygdala - subcortical connections to thalamus and mammillary bodies (hypothalamus)
3) Limbic System: Parahippocampal gyrus, entorhinal, and perirhinal cortex.
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The case of H.M
- dissociation of memory brain systems
- H.M was a patient with epilepsy
- he underwent neurosurgery for his unremitting seizures
- his epilepsy was cured, but he was left with anterograde amnesia.
- recollection of early memories - preserved.
- capacity to encode and facts - lost.
- procedural memory (ability to learn new skills) - preserved!
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What structures encode declarative memories?
- medial temporal structures
- conclusions from HM: different brain systems underlie different aspects of memory.
- medial temporal structures: encoding and consolidate declarative memories.
- procedural and long term memory - independent from these structures.
- confirmed in other clinical cases as well as in studies of animals with lesions.
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What is the function of the hippocampus?
fMRI studies: activation of the hippocampus and adjacent cortex predicts memory performance.
robustness of encoding depend on structural and functional changes of neural connections as a result of experience. (London taxi driver)
posterior hippocampus -particular relevant for remembering
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Grid cells & place cells
- place cells: hippocampus - neurons that fire when animals traverse a specific locus. (fire in a specific location)
- grid cells - entorhinal cortex - neurons that fire when the rat was in different parts of the areana that formed an hexagon -> brain's GPS.
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What does procedural learning depend on?
- motor systems
- cerebellum
- basal ganglia
- affected in Parkinson's and Huntington's diseases
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What brain systems count for long-term memory?
1) Long-term memory is not stored in the diencephalic/medial temporal lobe structures.
2) The cerebral cortex is the major long-term repository for many aspects of declarative memory.
-> Karl Lashley's experiments
-> Damage to associative cortices
-> ECT treatments in psychiatry
-> Consequences of Alz-heimer's disease
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