Limbic system and emotion Flashcards

1
Q

describe what makes up the hippocampal system

A

The hippocampal formation is composed of the subiculum , hippocampus (also called the hippocampus proper or horn of Ammon), and dentate gyrus (see Fig. 31-4 ), all of which constitute the allocortex of Brodmann. The subiculum is laterally continuous with the cortex of the parahippocampal gyrus and area of the periallocortex. Medially the edge of the hippocampal formation is formed by the dentate gyrus and the fimbria of the hippocampus.

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2
Q

what is the subiculum? (part of the hippocampal formation)

A

The subiculum of the hippocampal formation is the transitional area between the three-layered hippocampus (archicortex or allocortex) and the five-layered entorhinal cortex (paleocortex or periallocortex) of the parahippocampal gyrus
*This transitional zone, although small, can be divided into a prosubiculum, subiculum proper, presubiculum, and parasubiculum. These areas are essential for the flow of information into the hippocampal formation.

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3
Q

the dentate and hippocampus have how many cellular layers?

A

The dentate gyrus and the hippocampus are each composed of three layers (typical of that type of cortex - archicortex)

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4
Q

Describe the external and middle cellular layers of the dentate and hippocampus

A

The external layer is called the molecular layer and contains afferent axons and dendrites of cells intrinsic to each structure.

  • The middle layer, called the granule cell layer in the dentate gyrus and the pyramidal layer in the hippocampus, contains the efferent neurons of each structure
  • These layers are named according to the shape of the cell body of the principal type of neuron found therein.
  • The dendrites of granule and pyramidal cells radiate into the molecular layer.
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5
Q

What is declarative memory?

A
  • The ability to recollect events or facts that have a specific temporal and spatial context
    • “I was interviewed in this doctor’s office yesterday”
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6
Q

What is semantic knowledge?

A

• General knowledge about the world including new word meanings

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7
Q

HM, who lost his hippocampal formations bilaterally, did not also lose procedural memory. Why?

A
  • Procedural memory, or the ability to learn new motor skills, is not contingent on the hippocampal formation
    • He did not remember that he learned the task, but when pressed to do it he did it well without practice further
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8
Q

Where does fMRI evidence suggest long term declarative memories are stored?

A
  • Long term declarative memories are in the neocortex

* Different kinds of memories are stored in different areas of cortex

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9
Q

As far as number of layers in the cortex, what is the difference between the areas of the limbic system and the main cortex?

A

• Major argument for anatomic unification of the limbic structures is the nonisocortical character
○ Less than the 6 layers found in the isocortex/neocortex
• These structures included anatomically make up the limbic lobe

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10
Q

What brain areas are in the papez circuit?

A
  • Hypothalamus and mamillary bodies
    • Anterior thalamic nucleus
    • Cingulate gyrus
    • Hippocampus
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11
Q

What are the structures, not elucidated by Papez, that turned out to be highly engaged in the production of emotions?

A

• Ventral-medial frontal lobe
○ Orbitofrontal cortex
• Amygdala
• Ventral striatum
○ Nucleus accumbens
• Dopaminergic neurons of the ventral tegmental area
○ Just medial to substantia nigra pars compacta

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12
Q

What does emotion fundamentally involve in humans?

A
  • physiological arousal
    • Expressive behaviors
    • Conscious experience
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13
Q

Batson, Shaw and oleson described mood as what?

A
  • A tone and intensity and a structured set of predictions about future experience of reward or punishment
    • Unlike instant reactions that produce affect or emotion, and that change with expectations of future pleasure or pain, moods, being diffused and unfocused and thus harder to cope with, can last for days, weeks, months, or even years
    • Moods are hypothetical constructs depicting an individual’s emotional state
    • Researchers typically infer the existence of moods from a variety of behavioral referents
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14
Q

What does affect refer to?

A

• The experience of feeling or emotion
• Affect is a key part of the process of an organisms interaction with stimuli
• Affect display = facial, vocal, gestural behavior that servdes as an indicator of affect
• The external and dynamic manifestations of a person’s internal emotional state
○ Whereas mood might be a person’s predominant internal state at any one time

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15
Q

What does personality refer to?

A

• Characteristic patterns of thoughts, feelings and behaviors that a person exhibits fairly consistently throughout life
• Personality type refers to psychological classifications of different types of individuals
• Personality traits are more quantitative differences (introversion and extroversion are a continnuum with most people in the middle)
○ Type would make them fully separate, fundamentally different groups

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16
Q

What are the most important nervous system structures involved with the neurophysiology of emotion?

A
  • Amygdalae
    • Ventral tegmental area
    • Nucleus accumbens/ventral striatum
    • Ventromedial prefrontal cortex
    • They interconnect portions of the midbrain, diencephalon, striatum and cerebral cortex
    • Within each structure there are heterogeneous populations of cells, mixtures of excitatory and inhibitory types, varieties of neurochemical species, and a complex net of traversing axons passing between these and other structures
17
Q

Describe why the basolateral amygdalae are so important for emotion and memory formation

A

• Amygdalae perform primary roles in the formation and storage of memories associated with emotional events
• Much of our current understanding of the role the amygdale play is in fear conditioning
○ Neutral stimulus is matched with a painful one, and LTP will strengthen certain synaptic connections and mediate an emotional connection to a memory
• Memoreis of emotional experiences are imprinted in the strengths of synaptic connections in the lateral nuclei of the amygdale, collectively referred to as the basolateral amygdala (BLA)
• BLA neurons can elicit fear behavior through connections with eh central nucleus of the amygdalae (CEA) and the related bed nuclei of stria terminalis (BNST)
• The central nuclei are involved in the genesis of many fear responses, including immobility, tachycardia, increased respiration and stress-hormone release
• Damage to the amygdale impairs both the acquisition and expression of pavlovian fear conditioning

18
Q

What does damage to the amydalae do in experimental models?

A

• Damage to the amygdale impairs both the acquisition and expression of pavlovian fear conditioning

19
Q

What is meant by CEA?

A
  • BLA neurons can elicit fear behavior through connections with the central nucleus of the amygdalae (CEA) and the related bed nuclei of stria terminalis (BNST)
    • The central nuclei are involved in the genesis of many fear responses, including immobility, tachycardia, increased respiration and stress-hormone release
20
Q

What information flows into and out of the baslolateral amygdala

A

• Collectively, the lateral, basolateral and basomedial amygdalar nuclei
• Recieves sensory inputs from the cerebral cortex and thalamus
• Mainly glutamatergic cells project from the BLA to the central nucleus of the amygdala
• There are other cells in the BLA that project mainly to the nucleus accumbens
○ Also glutamate
• The CEA is the main output structure of the amygdala
○ Derived from the striatum and its output cells are GABA-ergic

21
Q

What does the CEA do?

A

• The central nucleus mediates expression of emotional responses
• Example - defensive response to a threatening stimulus consists of elevated heart rate (lateral hypothalamus) and a freeze state (central gray)
• Both of which receive input from the central nucleus of the amygdala
• Lesions to the lateral hypothalamus eliminate the effect on heart rate, but not the freeze state
○ Lesions to the central gray have opposite effect
• Both responses are evoked by amygdala stimulation

22
Q

How are the amygdalae involved in positive conditioning?

A
  • Appetite
    • Distinct neurons in the basolateral amydala respond to positive and negative stimuli but there is no clustering of these distinct neurons into clear anatomical nuclei
    • Those cells involved in appetitive, or reward-related conditioning appear to project to the nucleus accumbens in the ventral striatum
    • Those that are involved in fear or aversive conditioning project to CEA
23
Q

What does the BNST do?

A

• Bed nucleus of the stria terminalis
○ Derivative of the central nucleus of the amygdala
• Mediates the release of pituitary-adrenal stress hormone (CRH) in response to fear
• CRH causes the adrenal gland to release epinephrine and cortisol
• Chronic stress causes cortisol-induced release of epinephrine from the locus coeruleus to the amygdala, causing the vicious cycle to continue

24
Q

What is necessary for the formation of a stimulus-reward association?

A
  • Increases in glutamatergic synaptic strength of inputs to BLA neurons are necessary for the formation of a stimulus-reward association
    • That means for both fear and reward, it’s all about LTP and synaptic connections of neurons in the BLA
25
Q

How can the BLA neurons be responsible for both reward and fear using the same cellular mechanisms?

A
  • Projections
    • The BLA neurons project to many downstream regions, including the canonical circuits for reward and fear, and the neurons that project to different targets undergo distinct synaptic changes with positive or negative associative learning
    • BLA projects to the Nucleus accumbens that have been implicated in reward-related behaviors
    • BLA projections to the CeM have been linked to the expression of conditioned fear
    • Nac and CeM projectors are populations of BLA neurons that undergo opposing syaptic changes following fear or reward conditioning
26
Q

What is fear extinction?

A
  • An experimental paradigm in which a tone (conditioned stimulus) that predicts a shock (unconditioned stimulus) is repeatedly presented in the absence of the US (shock) causing conditioned fear responses to diminish
    • With sufficient extinction, subjects respond to the CS as if they had never been conditioned
    • Extinguished fear responses return with the passage of time, when the CS is presented in a different context, or following an aversive event
    • This is behavioral evidence that extinction does not erase fear memories, but instead generates an inhibitory memory capable of temporarily suppressing the expression of fear associations
27
Q

Use the rat experiements to describe the role that the prefrontal cortex plays in fear extinction

A

• Medial prefrontal cortex projects to BLA, CEA and the intercalated cell masses (ICMs)
• Stimulation of mPFC inhibits the CEA unit responses to afferent stimulation
• It’s not known exactly how this happens, but it’s thought to be either directly or indirectly
• (evidence for two different pathways)
○ ICMS are primarily GABAergic and receive projections from BLA and project to CEA, modulate CEA excitability and exhibit forms of synaptic plasticity including LTP and LTD

28
Q

What is the iowa gambling task?

A
  • Present subjects with 4 decks of cards
    • Each time they choose a card they win some money
    • Every so often, a card will indicate a monetary penaly
    • Some decks are bad or good.
    • Most healthy patients learn to stick to the good decks but
29
Q

People with damaged VMPFC handle the iowa gambling task in what way?

A

• VMPFC damage causes people to stick to choosing the bad decks, even though they know they are losing
• Healthy participants show stress responses with bad decks after only a few trials
○ It was this stressful emotion that preceded the explicit knowledge of the correct strategy
• VMPFC injured patients never develop this anticipatory physiologic reaction to an impending punishment
○ The had intact stress responses to the recipt of actual rewards and punishments, suggesting that the VMPFC is necessary for the prediction of consequences, but not for registering the weight of consequences

30
Q

If the periaqueductal grey matter is stimulated in rats, is that aversive or addictive?

A

• Aversive. They avoid that stimulus

31
Q

How is the VMPFC-nucleus accumbens circuit like the basal ganglia circuit?

A

• This corticostriatal loop is a network that can, through the presence or absence of dopamine, reinforce or reduce the activity in networks that generate predictions about the risks or rewards of a given behavior
• Excessive dopamine in this circuit will excessively reinforce the networks that were active during the behavior that produced the dopamine surge
• Cocaine - the active networks are those that predicted more reward and less risk with obtaining and using
○ Thus the hallmark of maladaptive use in addiction

32
Q

What region of the brain did rats LIKE to stimulate when they have the chance?

A

• Medial forebrain bundle
• The key neurons in this bundle are the dopaminergic neurons originating in the ventral tegmental area of the midbrain
○ Adjacent to the substantia nigra pars conpacta
• VTA neuronal pathways project to the nucleus accumbens in the ventral striatum
• Stimulation of the nucleus accumbens, like the medial forebrain bundle, is highly reinforcing
○ This is the area that receives input from, and projects output back to the VMPFC

33
Q

What is the reward prediction error hypothesis? Use monkey training experiments with a juice “reward” to illustrate

A
  • The reward prediction error hypothesis states that dopamine encodes the difference between the experienced and predicted reward of an event
    • During monkey training, there would be a set of stimuli that preceded the gift of the juice “reward”
    • Initially, the monkey didn’t think the reward was coming so DA was released to signal that something good happens with these stimuli
    • Eventually DA release is propogated up the series of stimuli to the first reliable stimulus
    • Eventually, however, the stimuli produced the EXPECTED result, so no more DA was released (DA is the correction of the expected and received error)
    • Thus, it is postulated that humans and animals use dopamine to update the value of different actions and stimuli
    • The value adds predictive value to the choosing of a given action
34
Q

In the reward error correction hypothesis for dopamine, what are the roles of the mesocortical and mesolimbic areas?

A

• In this model dopamine signaling serves to recalibrate the strengths of cortico-striatal synapses
• This reinforces certain networks that govern the organisms particular plans or behaviors.
• In addition to its projections to the striatum (mesostriatal DA system), the VTA has projections to the ventral striatum, amygdala and other limbic structures (mesolimbic DA system)
• VTA also has projections to the cortical areas important in the physiology of emotion such as the VMPFC
○ Mesocortical dopamine system

35
Q

Emotion and decision making go hand in hand. How does VMPFC injury illustrate this?

A

• People with VMPFC injuries often make decisions and engage in behaviors that are detrimental to their well-being
• The primary dysfunction, then, is postulated to be an inability to use emotions to aid in decision making, particularly in the personal, financial, and moral realms where there is typically significant uncertainty in the choices to be made
• This is also true of damage to amygdala, and patients with this also pick bad decks in the iowa gambling task
○ The difference here is they never showed conductance responses to actual receipt of rewards or punishment. They didn’t grasp the consequences

36
Q

What’s the takeaway on the amygdala and VMPFC’s roles?

A

• Amygdala triggers emotional bodily states in response to the rewards and punishments associated with specific behaviors or stimuli
• Through a learning process, these relations between inputs and outputs that the amygdala has constructed may be represented in the VMPFC as a set of predictions of the likely consequences of different actions
• Patients with damage to this latter gegion, but with intact amygdalae, may still feel aversive reactions to being caught committing a crime
○ But they will fail to anticipate that a criminal behavior would likely produce that negative result

37
Q

Follow the Papez circuit.

A

• Major point is that experience of emotion was determined mostly by the cingulate cortex with secondary help from other cortical areas
• Emotional expression (heart rate, sweating, vasomotor tone, etc) he though to be governed by the hypothalamus
• Pathway
○ Cingulate gyrus projects to hippocampus
○ Hippocampus projects to hypothalamus by way of the fornix
○ Hypothalamic impulses reach the cortex via relay in the anterior thalamic nuclei
• Thus, emotional experience in the cingulate becomes expression by indirect transmission to the hypothalamus
• Finally there is feedback back through the anterior nucleus of the thalamus