Lec 41 Limbic Behavior, Emotions, and Learning Flashcards

1
Q

What are the major functions of the limbic system?

A

amygala = emotions + drive
hippocampal formation = memory
hypothalamus = homeostasis
olfaction

the 4 Fs –> fear, food, fight, fornication

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2
Q

What is the function of amygdala?

A
  • assigns emotional valence to sensory input
  • adds emotional content to declarative memories
  • major output path to anterior hypothalamus [autonomic + endocrine]
  • fear conditioning
  • many connections
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3
Q

What are the 3 major areas of the prefrontal cortex?

A
  • orbitofrontal cortex
  • anterior cingulate cortex
  • dorsolateral prefrontal cortex
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4
Q

What is the function of the nucleus accumbens?

A
  • role in reward, pleasure, laughter, addiction, aggression, fear, placebo
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5
Q

What is the function of the hippocampus?

A
  • memory formation

- inhibitory control of HPA [hypothalamic-pituitary-adrenal] axis

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6
Q

What is the function of the dorsolateral prefrontal cortex?

A
  • cognitive control, solving complex tasks, working memory, decision making and planning
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7
Q

What is the function of the orbitofrontal cortex?

A
  • corrects and inhibits maladaptive emotional responses

- mediates socially appropriate behavior

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8
Q

What is the function of the anterior cingulate cortex?

A
  • mediates reward, anticipation, empathy, emotional response, motivation
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9
Q

What is the process of emotion perception?

A

stimulus present

  • -> appraised via amygdala + insula
  • affective state via amygdala, insula, anterior cingulate, orbitofrontal cortex, nuc accum
  • regulation by anterior cingulate, hippocampus and prefrontal cortex
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10
Q

What is the neurochemistry of schizophrenia?

A
  • hyperactivity of DA neruons in mesolimbic path mediates pos symptoms of psychosis
  • hypoactivity of DA neurons in mesocortical path mediates negative + cognitive symptoms
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11
Q

What do you see in fMRI of pt with schizophrenia?

A
  • decrease activity dorsolateral prefrontal cortex and dorsal anterior cingulate [ACC] during executive function/ memory
  • decreased hippocampal activity during memory
  • inability to engage amygdala, ACC, hippocampus in processing stimuli with high emotional valence
  • dysfunctional interconnectivity between frontal and temporal regions
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12
Q

What is the learning theory?

A
  • strengthen existing responses or formation of new responses to existing stimuli that occurs because of practice or repetition
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13
Q

What are the two types of non-associative learning?

A

habituation and sensitization

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14
Q

What is habituation?

A
  • decreased responding after repeated stimuli

ex. filter out continuous stimuli in our surrounding environment

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15
Q

What is sensitization?

A

increased responding after repeated stimulation

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16
Q

What are the two types of associative learning?

A

classical + operant conditioning

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17
Q

What is long-term potentiation?

A
  • example of sensitization

- mech underlying memory + learning

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18
Q

What is kindling?

A
  • type of sensitization
  • repeated stimulation hippocampal or amygdala neurons –> leads to seizures

after sensitized, little stimulation needed to produce seizures = model for epilepsy

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19
Q

What is central sensitization

A
  • type of sensitization
  • prolonged activity of dorsal horn neurons caused by repeated noxious stimulation causes increased neuronal responsiveness

–> cause hyperalgesia, allodyna = mech of chronic pain

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20
Q

What is drug sensitization?

A
  • type of sensitization
  • causes increased effect of drug with repeated doses
  • -> craving, drug adverse effects
  • -> neuroplastic changes in mesolimbic DA path
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21
Q

What is associative learning?

A

behavioral change caused by animal’s learning that particular temporal association occurs between two stimuli

ie associates presented stimulus with another stimulus or event such as reward or punishment

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22
Q

What is classical conditioning?

A

temporal association of neutral stimulus with a behaviorally vant unconditioned stimulus –> causes the neutral stimulus to bring about response similar to that normally associated with the unconditioned stimulus

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23
Q

What are the 4 key elements to classical conditioning?

A

unconditioned stimulus [US]: stimulus that without training produces a reflexive unlearned response [ex odor of food]

unconditioned response [UR]: response that occurs spontaneously to unconditioned stimulus [ex salivation]

conditioned stimulus [CS]: neutral stimulus that elicits conditioned response following learning [ex sound of a bell]

conditioned response [CR]: behavior learned by an association made between a conditioned stimulus and an unconditioned stimulus; = the response elicited by the conditioned stimulus [ex salivation in response to the sound of bell]

24
Q

What are the 4 characteristics of classical conditioning?

A

acquisition = period when conditioned response [CR] is acquired

extinction = reduced CR when CS is repeatedly presented in absence of US with which it had previously paired
CR = salivation at bell; CS = bell; US = smell of food

spontaneous recovery = increase in strength of extinguished CR after the passage of a period of time

stimulus generalization = elicitation of CR in response to new stimulus that resembles the original conditioned stimulus

25
Q

What is learned helplessness?

A
  • a type of classical conditioning
  • association between aversive stimulus and inability to escape
  • –> hopelessness, apathetic response during subsequent exposure to same or new aversive stimulus
26
Q

What is imprinting?

A
  • a type of classical conditioning
  • process by which learning occurs at particular age or life stage
  • rapid and independent of consequences of behavior
27
Q

What is fear conditioning?

A
  • type of classical conditioning
  • aversive stimulus associated with particular neutral context or stimulus
  • -> results in expression of fear response causing expression of fear response to the originally neutral stimulus
28
Q

What happens in fear conditioning?

A
  • components of implicit and explicit memory
  • amygdala may play important role –> neurons in amygdala undergo plastic changes [LTP-like]
  • hippocampus plays role in contextual fear conditioning
29
Q

What is the fear network?

A
  • sensory info comes into amygdala by 2 major paths
  • —- short loop = direct sensory input from sensory thalamus = rapid response to potentially threatening stimuli
  • —- long loop = from thalamus to cortex where processed/evaluated to amygdala to temper amygdala’s response
30
Q

What is theory of anxiety disorder associated with fear netowrk

A
  • anxiety disorder = deficit in higher cortical processing paths leading to failure to shut off amygdala
31
Q

What is operant conditioning?

A
  • trial and error learning
  • learning due to consequences of previous behavior
  • different from classical conditioning b/c deals with modification of voluntary behavior
32
Q

What is positive vs negative reinforcement?

A
positive = introduce stimulus results in increase in rate of behavior
negative = removal of aversive stimulus results in increase in rate of behavior
33
Q

What is punishment?

A

introduction of aversive stimulus aimed at reducing rate of unwanted behavior

34
Q

what is extinction?

A

gradual disappearance of learned behavior when reinforcement/reward is withheld

35
Q

Are behavior effects of punishment or reinforcement more likely to be long term?

A

punishment = more temporary

reinforcement = longer term

36
Q

What are the different types of fixed schedules of reinforcement?

A

continuous: reward given each time desired behavior occurs

fixed ratio: reward after designated # of responses

fixed interval: reward given after designated amount of time

37
Q

What are different types of variable schedules of reinforcement?

A

variable ratio: reward given after random + unpredictable # of responses

variable interval: reward given after random and unpredictable amount of time

38
Q

What is modeling?

A
  • 3rd type of learning
  • type of observational learning
  • individual observes others and imitates their behaviors
  • more efficient + faster than operant learning
39
Q

What is neurobiology of operant conditioning?

A
  • nucleus basalis ACh neurons activate after conditioned stimulus or primary reward
  • dopamine plays role in positive reinforcement and aversive learning
40
Q

What structures make up the reward pathway?

A
  • cortex receives and processes sensory stimulus indicating reward
  • sends signal to ventral tegmental area [VTA] of midbrain
  • VTA —> dopamine to nucleus accumbens, amygdala, and prefrontal cortex
  • amygdala acts on nucleus accumbens further
  • nuc accumbens activates motor function to go after stimulus via ventral pallidum and structures of extrapyramidal motor system
  • cortex allows integration of info, development learning and motivation
41
Q

What is the effect of drugs on reward paths?

A
  • activate brain regions normally control responses to natural rewards + important for survival
  • drugs of abuse activate mesolimbic dopamine system and increase dopamine levels in nucleus accumbens
42
Q

What type of reinforcement in drug use?

A
  • early/occassional use = positive reinforcement to motivate behavior
  • later/chronic/frequent use = negative reinforcement
43
Q

What is kluvery-bucy syndrome?

A
  • hypoactivity of limbic system [remove amygdala in monkey]

characterized by: hyperorality, hypersexuality, no fear, tameness

44
Q

What is urbach-wiethe disease?

A
  • rare autosomal recessive disease
  • have bilateral calcifications of anterior temporal lobes [esp. amygdala]
  • normal intelligence/ language/ memory for neutral stimuli
  • impaired long term memory for emotionally intense stimuli
  • cannot properly rate intensity of emotion or recognize a fearful expression
45
Q

What are the neural pathways for empathy?

A
  • insula = experience painful emotions, observe them in others
  • anterior cingulate cortex = tell when something is wrong
  • amgydala/orbitofrontal cortex/ventromedial prefrontal cortex = experience empathy and maintain socially acceptable behavior
46
Q

What are symptoms of sociopathy?

A
  • lack of respect for social norms
  • reckless, irritable, impulsive, aggressive
  • lack of remorse/guilt
  • lack of empathy, compassion, fear
  • repeated lying and conning other for personal benefit and pleasure
  • failure to plan ahead
  • symptoms generally onset before age 15
47
Q

What limbic dysfunction causes sociopathy?

A
  • amygdala and orbitofrontal cortex hypoactivity
  • ventromedial prefrontal cortex dysfunction
  • reduced activity insular and angterior cingulate cortex regions related to cooperative tasks, emotional recognition
48
Q

What is limbic encephalitis?

A
  • group of autoimmune disorders affecting limbic system

- usually caused by paraneoplastic autoimmune syndrome

49
Q

What is cardinal sign of limbic encephalitis? other symptoms?

A
  • subacute onset short term memory loss

other:
- behavioral, psych, confusion, seizures

50
Q

What is the neuropathology of limbic encephalitis? etiology?

A
  • mononuclear inflammatory cell infiltrates, loss of neurons, and proliferation of astrocytes/microglia in hippocampus and amygdala
    etiology: autoimmune –> anitbodies against intracellular antigens or neuronal surface antigens
51
Q

What are the 3 major groups of limbic encephalitis?

A
  • LE associated witih classic onconeural antibodies = majority associated with neoplasm
  • LE associated with antibodies agaisnt neuronal surface/synaptic antigens
  • LE associated with not known antibody = many associated with neoplasm
52
Q

What are clinical findings of limbic encephtalitis?

A

CSF –> may find anti-neuronal antibodies, high lymphocytes and protein

EEG –> seizure/epileptiform activity in temporal region or slow wave

MRI –> hyperintense signals, mild swelling medial temporal lobes

PET –> hypermetabolism in medial temporal lobes

53
Q

What kind of limbic encephalitis causes ovarian teratoma? other symptoms?

A
  • antibody to NMDA-R

other symptoms: psychiatric, dystonia, depressed consciousness, hypoventilation, seizures

54
Q

What is herpes simplex encephalitis?

A
  • usually caused by HSV1 infection of medial temporal lobe and inferior fronal lobe
  • due to direct transmission from periphery via CN 1, 5
  • causes inflammation, necrosis, hemorrhage

acute = confusion, seizures, impaired memory/consciousness
progressive in 7-14 days and often fatal if untreated

55
Q

What is temporal lobe epilepsy?

A
  • reccurent epileptic seizures from 1 or both temporal lobes [medial or lateral]
  • seizure symptoms: hallucinations, illusions, amnesia, mood changes, fear, anger
  • characteristic personality syndrome: hyperreligiosity, circumstantiality, hypermortality, altered sexuality
56
Q

What are signs of frontotemporal dementia?

A
  • personality change, inappropriate behavior, apathy, mood symptoms, language impairment
57
Q

What happens in alzheimers disease?

A
  • impaired memory and lanuga; paranoia and delusions

- due to hippocampal dysfunction