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Biological Basis (Test 2) > Lecture 7 > Flashcards

Lecture 7 Flashcards

1
Q

Are facial expressions common across cultures?

A
  • yes, they are common across cultures
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2
Q

What occurs in facial expressions of blind children?

A
  • children born blind are similar to children who can see. They can express facially just like children who can see.
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3
Q

The recognition of facial expression is what?

A
  • automatic, rapid, and generally accurate?

- we are good at recognizing emotions and do not need a lot of detail in order to recognize these emotions

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4
Q

What is the function of the right hemisphere in recognizing emotions?

A
  • plays a more fundamental role than the left.

- It utilizes emotional cues directly

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5
Q

What is the role of the left hemisphere in recognizing emotions?

A
  • tends to rely on the meaning of words.
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6
Q

What is prosody?

A
  • when we speak, there is a flow that we have.

- the RH is very sensitive to that

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7
Q

What occurs with an aphasia?

A
  • damage to the left hemisphere

- issues with recognizing words, but can recognize emotions

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8
Q

What occurs with right hemisphere damage?

A
  • damage impairs recognition of emotions from facial expression and voice tone
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9
Q

What is bilateral prefrontal activation?

A
  • when identifying emotion from word meaning
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10
Q

What is right prefrontal activation?

A
  • when identifying emotion from tone of voice

- if we have damage in the right ear, then we would have a hard time recognizing emotion

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11
Q

What is Affective blindsight?

A
  • people with unilateral visual cortex lesions are shown faces in their visual field, but do not recognize the face or emotion. However, the person with the lesion will still make a facial expression
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12
Q

What explains why affective blindsight occurs?

A
  • explained by the amygdala’s reliance on the magnocellular system, which provides rapid input bypassing the visual cortex
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13
Q

What is an implication for normal emotional recognition?

A
  • we rely on a “gut reaction” for understanding facial expression before actually seeing the face.
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14
Q

What area of the brain is critically involved in the recognition of facial expressions?

A
  • right somatosensory cortex
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15
Q

What is the simulationist hypothesis?

A
  • we understand emotional expressions by imitating them; the resulting somatosensory perception allows identification, understanding, and empathy
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16
Q

True or False: Recognition is accomplished to a great extent by the mirror neuron system

A

True

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17
Q

What is an implication for normal emotional recognition?

A
  • we rely on a “gut reaction” for understanding facial expression before actually seeing the face.
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18
Q

What area of the brain is critically involved in the recognition of facial expressions?

A
  • right somatosensory cortex
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19
Q

What is the simulationist hypothesis?

A
  • we understand emotional expressions by imitating them; the resulting somatosensory perception allows identification, understanding, and empathy
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20
Q

True or False: Recognition is accomplished to a great extent by the mirror neuron system

A

True

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21
Q

Where are mirror neurons located?

A
  • ventral premotor cortex

- posterior parietal cortex (reciprocally connected)

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22
Q

What is Volitional facial paralysis?

A
  • damage to the face region of the primary motor cortex
  • people cannot control the left half of their face
  • Can involuntarily respond, but cannot voluntarily respond to emotion
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23
Q

What is Moebius syndrome?

A
  • caused by the defective development of the 6th and 7th cranial nerves
  • results in facial paralysis and inability to make lateral eye movements
  • people who have this syndrome cannot make facial expressions & have difficulty recognizing facial expressions of others
24
Q

True or False: Facial expressions are automatic and involuntary

A

True

25
Q

What is emotional facial paresis?

A
  • damage to the insular region of the prefrontal cortex. white matter of the frontal lobe or parts of the thalamus
  • partial facial paralysis
  • cannot express emotions involuntarily, but can do so voluntarily
26
Q

What do emotional facial paresis and volational facial paresis tell us about the brain mechanisms underlying facial expression of emotion?

A
  • ## It tells us that the frontal lobe is a localized are for facial expressions
27
Q

What are Kimeric faces?

A
  • composites of the face are on the same side
  • basically determines that the left side is more expressive
  • Right hemisphere is in charge of expression on the left side of the face
28
Q

What is the James-Lange theory of emotion?

A
  • emotional stimuli evoke physiological reactions including muscle contraction
  • sensory feedback from reactions perceived by the brain to generate feelings
29
Q

True or False: High spinal cord transections produced smaller reductions in emotional intensity

A

FALSE: greater reductions

30
Q

What is the case of H.M.?

A
  • hippocampus was removed

medial temporal bisected due to epilepsy

31
Q

What is learning?

A
  • process by which experiences change our nervous system

- acquisition of knowledge

32
Q

What is the neural model of classical conditioning?

A
  • Unconditioned stimulus (US) is paired with a conditioned stimulus (CS)
  • neuron in somatosensroy (US) and in the auditory system (CS) are activated
  • Synapse P - strong (US) and Synapse T - weak (CS) connect to create the action
  • (blink) occurs with the unconditioned response (UR) and the conditioned response (CR)
  • the key is that the stimulus is repeatedly paired together in order to create the response
33
Q

What are the different types of learning?

A
  • perceptual, stimulus-response, classical conditioning, instrumental conditioning, motor, relational
34
Q

What occurs in the perceptual , stimulus response, and motor learning?

A
  • Stimulus occurs
  • Next is perceptual learning (Changes in neural circuit that detects a particular stimulus)
  • Stimulus response learning occurs
  • Then motor learning (changes in neural circuit that controls particular behavior)
  • Response is created
35
Q

How does instrumental conditioning work?

A
  • we see something, and then detect a stimulus
  • This is another name for operant conditioning
  • Relationship between stimulus and response that was not there before.
36
Q

What i the Hebb Rule?

A
  • synapse that is repeatedly active at about the same the time the postsynaptic neuron fires will be come stronger
37
Q

What does the Hebb rule imply?

A
  • implies that repeated neural activity will produce physical changes in the neurons system
38
Q

Synaptic plasticity?

A
  • LTP: Long-term (lasting) increase excitability of neuron to particular synaptic input caused by repeated high-
    frequency activity of that input
  • Hippocampal Formation: Forebrain structure of temporal lobe, constituting important part of limbic system; includes hippocampus proper, dedrate gyrus, and subiculum
  • Population EPSP: Evoked potential that represents EPSPs of population neurons
39
Q

What is the stimulation and recording of LTP?

A
  • input arrives at the interinal cortex
  • From there it goes to the dendrate gyrus
  • if we want to produce LTP, then we can apply a strong electrical current to the neuron and then measure it
40
Q

What are the components of the hippocampal formation?

A
  • Entorhinal cortex, dendrate gyrus, CA1 field
41
Q

What is the entorhinal cortex?

A
  • provides major source of input to the hippocampal formation through the preforant path
42
Q

What is the dentatate gyrus?

A
  • receives input from the entorhinal cortex and projects to the CA3 field
43
Q

What is the CA1 field?

A
  • receives input form the CA3 field, and projects outward toward the subiculum
44
Q

What is the relationship between associative long-term potentiation and the induction of LTP?

A
  • LTP in which concurrent stimulation of weak and strong synapses to a given neuron STRENGTHENS WEAK ONES
  • induction occurs through repetition
45
Q

What is the relationship between induction of LTP and non-associative LTP requires an addictive effect?

A
  • Series of pulses delivered at high rate all in one burst will produce LTP, but same number of pulses given at slow rate will not
46
Q

The role of summation in LTP?

A
  • Low rate of stimulation does not deporlarize membrane membrane sufficiently
  • Threshold for establishment of LTP
  • EPSPS produced by a high rate of stimulation summate and reach the threshold
47
Q

Continuation of induction of LTP

A
  • Rapid rate of stimulation causes excitatory postsynaptic potentials to summate, because each successive EPSP occurs before previous one has dissipated
  • Rapid stimulation depolarizes postsynaptic membrane much more than slow stimulation does
48
Q

Process of LTP?

A
  • strengthening of a synapse occurs when it is stimulated while he postsynaptic neuron is depolarized
  • LTP requires both activation of a synapse and depolarization of postsynaptic neuron
49
Q

What is the function of the NMDA function?

A
  • NDMA receptors in the hippocampal formation, particularly in CA1
  • CA++ channel controlled by NDMA receptor is NT and voltage-dependent
50
Q

Process of the NMDA receptor?

A
  • Magnesium is always there
  • Ca++ cannot rush in because magnesium is still sitting there
  • Depolarization needs to occur so the channel is opened and the calcium can enter
  • Neurotransmitters need to bind to the receptor of glutamate AND depolarization needs to occur at the same time!!!
51
Q

True or False: action potential can occur in dendrites as well

A

True

52
Q

How are dendritic spikes triggered?

A
  • They are triggered when an action potential occurs along the axon.
  • There is a backwash of depolarization across the cell body and up the dendritic trunk that causes the spike
  • the spike evicts the magnesium ion in the NMDA receptors
53
Q
  • What occurs with weak synapses with LTP?
A
  • If a weak synapses activates simultaneously with dendritic spike, Mg in the NDMA receptor is dislodged and calcium can rush in
54
Q

What strengthens the synapse?

A
  • insertion of additional AMPA receptors
  • Calcium floods into the receptor after depolarization occurs
  • The more AMPA receptors, the more influx Na+, the stronger the EPSP
  • The calcium enters and ectivates the enzyme CaM-KII and stimulates the AMPA
  • When that happens the stronger there is more influx of sodium and the stronger of the EPSP
55
Q

True or False: Does the dendritic spine change shape during

LTP?

A

True

56
Q

What is the role of PKM-zeta in long-term potentiation?

A
  • protein will generate constantly and get into the postsynaptic membrane via mRNA
  • Does not get produced because of the enzyme Pin1, but CAM-KII supresses the Pin 1
  • Without early LTP, Pin1 blocks mRNA PKM-zeta transcription; with early LTP Pin1 is deactivated by CAM-KII and PKM-zeta is produced
  • Once the PKM-zeta is activated , then it will always suprsses Pin1
  • The final is the PKM synthesis, and this becomes self-sustaining. Late LTP requires an additional step of the PKM-zeta being produced and self-sustaining and also keeping the AMPA produced.

Biological Basis (Test 2) (3 decks)

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