1
Q
Attention
A
- Selective focus on one aspect of sensory input, while filtering out other stimuli
- Bottom-up and top-down attentional processes compete
2
Q
Bottom-Up Attention
A
- A stimulus demands attention
- Ex: sudden movement in visual field, smell of gas, hearing the phone right
- Sensation–> Perception–>Interpretation–> Evaluation–> Expectation–> Prediction
3
Q
Top-Down Attention
A
- You purposefully direct your focus to a stimulus or task
- Ex: Attend to your textbook instead of roommates talking, search for a specific shape of a puzzle piece
- Prediction–> expectation–> evaluation–> interpretation–> perception–> sensation
4
Q
How does attention increase task performance?
A
Accelerates..
- Sensory Processing
- Decision making
5
Q
How is attention detected neurally?
A
-fMRI can compare brain activity (BOLD response) in specific regions in response to specific attentional tasks
-Compared to “resting state”
–Not absense of activity, just default mode network
Brain region depends on: task, sensory modality, specific stimuli, employment of top down
6
Q
Default Mode Network
A
- Brain regions active at rest are consistent across individuals
- These active regions decrease activity when task is being performed
- Medial prefrontal cortex and posterior cingulate cortex show coordinated activity at rest
- Other regions: posterior parietal cortex, hippocampus, lateral temporal cortex, amygdala
7
Q
What does the default mode network do?
A
- Does not process sensory input
1. Sentinel hypothesis: - Constantly on the lookout for stimuli
- Depends on peripheral vision, not focus
2. Internal mentation hypothesis: - medial prefrontal cortex, posterior cingulate cortex activated when remembering past event or thinking of future event
8
Q
Common Attention Tasks
A
- Directed shifts in attention to different stimuli
- -Response may be monitored to confirm attention/motivation
- Complete a task while being presented w/ distractors
- -Responses may be monitored to see effects on accurate performance
9
Q
Brain and Multitasking
A
- Brain can easily and quickly shift btwn tasks, but cannot multitask
- -Especially when tasks rely on diff sensory modalities
- Errors increase when multitasking
- Time to complete tasks doubles
- Reduced recollection
10
Q
Salience Map
A
- Top-down input refines feature combos of stimuli
- Attention directed to most salient stimuli (what image to focus on)
11
Q
Fronto-Parietal Attention Network
A
- Attentional Pathway
- —Bottom-up attention
- ——-stimulus directs attention to eye movement
- —Top-down attention
- ——-Eye movement used to shift attention
12
Q
Bottom-Up Processing for Multisensory Input and attention
A
- Pairing sensory stimuli demands greater attention
- –Ex: hearing a crash and seeing a moving vehicle come to a stop
13
Q
Top-Down processing of multisensory input and attention
A
-Attention of several modalities simultaneously (limited)
14
Q
Conciousness
A
- The awareness of specific stimuli
- Concepts associated:
- –Self-conciousness, self-awareness, awareness, concious of stimuli, attention, concious states wakefulness
- Awareness of specific stimuli= attention
- No waking versus sleeping, instead diff states of conciousness
15
Q
Reductionism
A
- Method to study conciousness
- In search of the neural correlates of consciousness
- Individual parts summing up the whole
16
Q
Holism
A
-Something about entire being leads to conciousness
17
Q
Emergence
A
-Synergisitic effects add up to phenomenon of conciousness
18
Q
Dualism
A
-Something totally separate from body that explains conciousness
19
Q
Binocular Rivalry Experiments
A
- The brain can only “see” one percept at a time
- -Takes advantage of this
- Mokey trained to pull left lever w/ starburst, right for face
- Measure single neuron activity in inferotemporal cortex (Object ID)
- Showed impages to diff eyes
- Neuronal activity level corresponding w/ stimuli observed w/ associated lever pull
20
Q
3D Glasses experiment
A
- Glasses determine which eye sees which image (house or face)
- If see house then face, increased activity in PPA, folowed by increased in FFA
- If see face then house, increased activity in FFA, folowed by increase in PPA
21
Q
Neurpsychiatric Disorders
A
- Genes and environment both play role in neurodevelopment
- Common risk factors manifest differently in different individuals
- Difficult to treat disorders bcuz poor understanding of risk factors and how to intervene
- High contribution to disease burden
22
Q
How are disorders studied?
A
- DSM-5 has signs and symptoms
- Neuropsych. assessments
- Neuroimaging
- Biomarkers
- In order to diagnos, must exclude other disorders
- -Informs treatment options
23
Q
How is etiology studied?
A
- Environment
- Pathology
- Genetics
24
Q
Multipule Hit Hypothesis
A
- Genes have lifelong developmental effects
- Environmental insults (infection, toxins) and exposure to trauma (stress, isolation) have developmental effects later in life
- Lead to neurotransmitter dysfunction/imbalance, neurocircuitry dysregulation, structural abnormalities
- Spectra of symptoms/severity
- *Treatment focuses on symptoms
25
Schizophrenia and Genes
- 80% heritable= portion of trait within pop. attributed to genetics
- Difficult to identify specific genes w/ strong associations to disorder, although genetic component is proven
- Complex behavioral traits are controlled by many genes, each with small effects
- Biomarkers not always reliable
- -Enlarged ventricles w/ schizophrena
26
Construct Validity
- The etiology/cause is similar
| - Ex: transgenic mouse with mutation that is associated with the human condition
27
Face Validity
- The model ‘looks like’ the disorder (similar symptoms)
| - Ex: mouse model of autism spectrum disorder shows lower social approach
28
Predictive Validity
- The model is responsive to treatments that effectively treat the disorder
- Ex: rats given anti-depressant drugs decrease time spent immobile in forced swim test
29
Schizophrenia Windows of Vulnerability
- Pre/perinatal
- Adolescence
- -When neural development active
30
Positive Symptons of Schizophrenia
* Add onto experience
- Delusions
- Hallucinations
- Disorganized speech
- Grossly disorganized or catatonic behavior
31
Negative Symptoms of Schizophrenia
* Take away from normal experience
- Reduced expression of emotion
- Poverty of speech
- Difficulty initiating goal-directed behavior
- Anhedonia-> Loss of pleasure
- Social behavior deficits
32
Cognitive symptoms in Schizophrenia
- Learning and memory impairment
| - Presented early
33
Dopamine Hypothesis of Schizophrenia
- Psychosis triggered by activation of dopamine receptors
- Ex: high dosage of stimulants leads to this
- Conventional antipsychotics, act as antagonists at D2 receptors
- --Reduce the positive symptoms of schizophrenia
- Side effects= parkinsons symptoms
34
Glutamate Hypothesis of Schizophrenia
- PCP and ketamine lead to behavior affect synapses that use glutamate as a neurotransmitter
- --Inhibit NMDA receptors
-Diminshed activation of NMDA receptors in the brain
===Increade in mesolimbic DA and decrease in PFC
---Increased DA in NAc related to positive symptoms
---Decreased DA in cortex related to negative symptoms
35
Current Treatments of Schizophrenia
Antipsychotics:
--Block D2 receptors= improving positive symptoms
--Antagonists at 5-HT2 receptors= improve neg symptoms
--Target the acetylcholine system= improve cognitive symptoms
Drug therapy combined with psychosocial support
36
Declarative Memory
- Explicit/ "Knowing that"
- Episodic memory, semantic memory
- Brain Regions: medial temporal lobe, diencephalon, neocortex)
- Know facts, events, spacial info, relationships
- Ex: What is an NMDA receptor
37
Nondeclarative Memory
- Implicit/ "Knowing how"/unconcious
- Brain Regions: Medial temporal lon, diencephalon, neocortex
- Classical conditioning (amygdala, cerebellum)
- skeletal musculature (cerebellum)
- procedural memory/ skills and habits (basal ganglia)
- emotional responses (amygdala)
- habituation, sensitization (sensory/reflex pathways)
- perceptual learning/priming, recognition memory (neocortex)
- Ex: Playing the piano
38
Retrograde Amnesia
-Cannot recall old memories from before trauma
39
Anterograde Amnesia
-Cannot recall memories after trauma
40
Patient HM
- Anterograde amnesia
- Couldn't recognize doctor of 50 yrs
- No effect on intelligence, perception, personality
- Impaired memory for experience, but spared memories of skills and simple associations
41
Bottom-Up Attention Recruits...
- begins w/ stimuli input, recruits:
- -LIP--priority map constructed from bottom-up and top-down input
- -FEF--directs eye movement
42
Top-Down Attention Recruits...
- Begins in Prefrontal cortex (executive control of top down) and recruits
- -FEF
- -LIP
43
Sensory Memory
- Vivid, lasts seconds
- Sensory Cortex
- "Hearing but not listening"=repeating things said to you a few seconds ago when not listening
44
Short term memory
- Lasts minutes to days
- Limited in capacity
- Tends to be abstract
- Sensory cortex, hippocampus
45
Working Memory
- Mental sketch pad
- Dorsal prefrontal cortex
- Tested by N-back test
46
Consolidation
- Bringing info from short-term and working memory into long term memory
- Depends on sleep, time, protein synthesis
- Early LTP--> consolidation--> Late LTP
47
Long term memory
- Virtually limitless
- Most stable
- Two types: nondeclarative and declarative
48
Hebbs Rule
- Stimulus--> activation of cell assembly (group of neurons that work towards certain memory)
- ---Cells activated at same time to learn memory, connectivity increases w/ increased firing
- Neurons that fire together, wire together= Long Term Potentiation
- Neurons that fire appart, wire appart= long term depression
* *Changes in synaptic strength correspond to changes in EPSP and IPSP magnitude
49
Learning and Memory of Idea
- Learning and memory of idea occurs at synapses
- Ideas related to idea are strengthend w/ repetion
- Weakened if not releated to idea/not repeated
50
Neural Network Model
- Memories are constellations of neurons
- Advantage= memories can survive damage to individual neurons
- Graceful degradation of memories w/ gradual neuron loss
* Location for diff types of memory differ
51
Where are cell assemblies found?
- Found in hippocampus (part of the limbic system)
- ---In rat: caudal telencephalon
- ---In humans: temporal lobe
- ---Dentate gyrus nesseled in between hippocampus
52
Sensory info pathway
Sensory info--> cortical association areas--> parahippocampal and rhinal cortical areas--> hipocampus--fornix--> thalamus, hypothalamus
53
Long Term Potentiation in Rats
- Rat restricted to light side of box
- Dark side opened and rat explored--> shock
- Rat learns not to go to dark side of box
- LTP to avoiding dark side
54
Long Term Potentiation
- Strengthening of a cell assembly
- Strong depolarization of postsynaptic neuron
- Input 1 and Ca1 neurons fire together
55
Long Term Depression
- Weakening of cell assemly
- When post synaptic cell is weakly depolarized by other inputs, active synapses undergo LTD
- -Input 1 and Ca1 neurons fire appart
56
Glutamate receptors and LTP
- NMDA and AMPA= ionotripic receptors
| - Found on dendritic spines of excitatory projection neurons
57
Step 1 of glutamate receptors in LTP
- Glu released; Binds to AMPA and NMDA receptors
| - -NMDA receptor blocked by Mg2+; AMPA conducts Na+
58
Step 2 of glutamate receptors in LTP
- AMPA receptors depolarize membrane
| - -NMDA receptors conduct Ca2+ (Mg2+ released from pore)
59
Step 3 of glutamate receptors in LTP
- Ca2+ causes activation of CaMII, Protein Kinase A and C
| - --activates proteins necessary to establish LTP
60
What is a kinase?
-An enzyme that adds a phosphate group to other receptors to activate them
61
How Hebbs Relates to LTP and LTD
- When NDMA receptors are opened:
- --Glutamate--> firing of Ca3
- --Depolarization--> Ca1 fires
62
Step 4 of glutamate receptors and LTP
- Kinases catalyze synaptic plasticity
- --Exocytosis of more AMPA receptors to synaptic membrane
- --Increased conductance of AMPA receptors (greater depolarizations/EPSPs)
63
Step 5 of Glutamate receptors and LTP
- Consolidation (Late LTP)
- Kinases activate (phosphorylate) transcription factors and epigenetic markers
* IF THIS STEP DID NOT HAPPEN MEMORIES WOULD BE ERASED*
Exploring Neuroscience
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