Final Exam Flashcards

Topics for final exam

1
Q

Describe HPA Axis

A

HPA AXIS: hormonal stress response system:
Hypothalamus, pituitary gland, adrenal gland
CRH (corticotropin releasing hormone) is released which binds to hypothalamus, hypothalamus releases ACTH (adrenocorticotropic hormone) which binds to adrenal gland, then adrenal gland releases cortisol
This isn’t a very fast system, takes about 15 minutes for the cells in the body to react to the cortisol

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2
Q

What down regulates the HPA Axis system?

A

Hippocampus

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3
Q

What are the types of glucocorticoid receptors?

A
○ Mineralocorticoid receptors (type 1) are used for everyday metabolic processes like blood pressure -- respond to low levels of cortisol
Glucocorticoid receptors (type 2) respond to a high level of cortisol because they have a low affinity
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4
Q

Who is Walter Cannon?

A

Walter Cannon came up with a lot of the things we’re studying in this class, came up with terms homeostasis and fight or flight response, all stressors cause the same response

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5
Q

Hans Selye stress theory

A

General adaptation syndrome: alarm phase, resistance phase, exhaustion phase
The exhaustion phase is incorrect, the pathology doesn’t have to do with “running out” of energy or neurotransmitters

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6
Q

Bruce McEwen Stress Theory

A

Allostasis

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7
Q

What makes things stressful?

A

Perceived lack of control and perceived lack of predictability

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8
Q

What is the allostatic stress model?

A

○ Prediction of future threats is incredibly important
○ Also about balancing various ranges
○ Homeostasis on steroids: finite amount of energy that you’re going to move around to deal with threats
○ The way that mammals especially have evolved to deal with the complexity of the world, is through a brain that can be predictive, which can mobilize responses before the threat is actually there

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9
Q

Describe sympathetic and parasympathetic nervous system

A

§ Sympathetic: innervation
□ Energetic, deployment of energy reserves, which is now going to be used up in responding to this threat
□ Acetylcholine released at the preganglionic fibers (very short), norepinephrine is released at the postganglionic fibers
□ Adrenergic receptors are present in something like a heart (some sort of organ), which will respond to norepinephrine
§ Parasympathetic: rest/digest is a quick way to describe it
□ Much less organized than the sympathetic, no chain ganglia, some ganglia come out of the brain stem while some come out of the pelvis
□ Preganglionic fibers are very long in this case, which also respond to acetylcholine
□ Postganglionic fibers are short in this case, also uses acetylcholine which binds to the muscle

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10
Q

How is the HPA Axis system down regulated?

A

Glucocorticoids released by the adrenal cortex build up, and turn down the response due to receptors in the hippocampus, which have the highest density of glucocorticoid receptors, which then shuts off the pathway

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11
Q

What is the master gland of stress?

A

The brain: we are capable of suppressing the physical response

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12
Q

Describe positivity offset

A

under no threat, organisms have to be curious. Under conditions of threat, if there’s any hint of them, there’s a negativity bias: the threat weighs very heavily on the brain

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13
Q

What is the inverted U?

A

• The Inverted U: this is an incredibly important concept
○ Stress is not inherently a bad thing: we need it, to respond to stuff and to be motivated
We know how to remove stress, but it isn’t the inherent problem: when it becomes a pathology, where you are constantly on the very right end of the U

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14
Q

Is stress adaptive or maladaptive?

A

• Is stress adaptive or maladaptive? It really depends
○ What task/situation is the individual in?
○ What is the particular context?
○ Individual variability in skill, preparation, experience
○ The time scale: short term or long term outcomes?
○ The criteria used to determine good or bad
§ Stress responses, self report, performance, coping strategies
○ Availability of alternative responses

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15
Q

Describe LTP and LTD

A

○ LTP: same input results in a higher output over time, partially done through changes in receptors (more), but also could be changes in the amount of synaptic vesicles/neurotransmitters that are released
LTD: same story but the reverse effect, where the same input results to a lower output

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16
Q

Discuss NMDA receptors

A

• Basic neurophysiology: NMDA receptors
○ Glutamate is the primary excitatory neurotransmitters
Glutamate system is one of the primary reasons that apoptosis/necrosis happens: too much glutamate causes excitotoxicity, which is overcharging a given neuron to the point where it can’t really do anything anymore

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17
Q

Describe the startle response and how it happens

A

○ There’s two pathways from the visual cortex: one has many layers and ends up in the amygdala, while another goes very quickly to the amygdala
○ You might not even necessarily be away of what you’re responding to (image of spider flashing on screen where you can barely see it)
○ It’s the fastest response we can get – the startle response
§ Pretty much the same across the board for mammals
○ The amygdala decides that basically everything is a threat – err on the side of caution

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18
Q

Is the amygdala all about fear?

A

○ The amygdala isn’t the fear center of the brain – it increases overall emotional activity
○ Think of it as a volume switch – either more reactive or less reactive
○ It’s a hub, not just one thing – the primary job is to react very fast to latent information
○ The prefrontal cortex “tunes” the amygdala through projections
○ Also, the more stressed you initially are, the more likely you are to have a strong reaction to a possible threat

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19
Q

Describe how/where chronic stress causes neural remodeling

A

○ Under conditions of chronic stress, amygdala neurons become larger and more interconnected
§ This is technically safer, it’s a defensive move
The hippocampal and prefrontal cortex neurons atrophy significantly

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20
Q

What’s happening when someone is in pain?

A

• What’s happening in the context of pain?
○ Damaged tissue, information is passed up through the spinal cord
○ However, first thing that happens is a reflex
○ There isn’t one part of the brain where everything comes together, it’s distributed to a bunch of different areas (memory, attention,
• Parallel processing: damage is conveyed through at least 4 different neurons -> large and small fibers
○ C fibers are partially responsible for pain information
○ Beta fibers are for mechanoreceptors, things like cutting
○ Delta fibers are associated with temperature, so pain from burning
Alpha fibers: proprioceptors of skeletal muscle

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21
Q

How does stress analgesia occur?

A

• Stress analgesia: you don’t notice that you’re in horrendous pain when you’re in a situation that you need to be functional
○ Periaqueductal grey and hypothalamus are involved, where specific things are released and the sensory component isn’t received

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22
Q

Describe attentional and emotional modulation

A
  • Attentional modulation: if you’re distracted from the pain, the intensity and unpleasantness of the pain (rated from 1-10) is slightly less than if you’re focusing on the region of pain
    • There’s also emotional modulation: if you’re in a good mood, the intensity was really just barely lower, but the unpleasantness of it is considerably better than if you’re in a bad mood
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23
Q

Is pain super dependent upon context?

A

○ Different descriptions of the situation: “you have to resist as long as you can” versus “the more you resist, the larger the benefit”
§ Same task, but different context going in -> 9/10 versus 5/6
§ What’s the goal? What’s the motivational context?
○ Different description of the situation: “moderate pain is worse than no pain”, versus “moderate pain is better than severe pain”
○ Remember, pain is an emotion

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24
Q

Describe the connection between motivation and pleasure

A

• Being hungry:
○ Initiating food procurement/foraging, appetitive phase, dominated by wanting
○ Engaging with consumption, consummatory phase, dominated by liking
○ Satiation, strong learning, satiety phase -> the pleasure drops off dramatically
Motivation is dictating the level of pleasure

25
Q

How bad is social stress really?

A

Really bad:
• Mice experiment with a constant state of social instability
○ Comparison with mice that were shocked
○ No matter what they did, the social instability with “bully” mice led to a much higher mortality rate, 90% versus 10%
And:
• Effects of chronic social isolation, versus pair housed animals
○ What happens when you do 7 minutes of cardiac arrest on these mice, before restarting their hearts?
○ In the hippocampus, there’s a ton more cell death in the animals that were isolated
§ Most sensitive part of the brain to ischemic damage
○ It doesn’t matter what sort of other stressors you do, you never see anything to this level
○ After this, the isolated animals basically had no hippocampus left

26
Q

Why do we live in social groups?

A

○ When the benefits of living together outweigh the costs of living alone, animals tend to form groups
○ Costs for social species across the board (automatic)
§ Increased competition for resources
§ Increased likelihood of disease transmission
§ More conspicuous to predators
§ Increased probability of losing offspring due to intra-species killing
○ Benefits to group living (not automatic)
§ Susceptibility to predation may be reduced
□ Aggressive group defense, using group as a cover, increased vigilance in large groups
§ Increased efficiency in food gathering
□ Cooperative effort results in lions being able to take down large prey
§ Extreme localization of non-food resources
□ Breeding sites, sleeping locations

27
Q

Why are our brains so complicated and big?

A

§ Recognizing subtle emotions is a vastly complex computational problem that the world’s best supercomputers can’t do
§ But our brains have evolved to be able to do this, so it’s automatic for us

28
Q

What is the motivating factor in social situations?

A

Loneliness

29
Q

Describe the vole study with the nucleus accumbens and oxytocin

A

• Two very similar vole species: montane vole is highly polygynous, and prairie vole which is socially monogamous
○ High density of oxytocin receptors in nucleus accumbens in the prairie vole: very rewarding to have a tight social connection with one animal
○ The montane vole has oxytocin receptors too, just in a different place
○ If you overexpress oxytocin receptors in the accumbens in the montane vole, it will start to act like the prairie vole

30
Q

Describe cytokines

A

broad and loose category of small proteins that are important in cell signaling
§ Think of them as neurotransmitters of the immune system
§ However, they’re not just limited to the immune system

31
Q

Describe interleukins

A

multifunctional cytokines that are produced by a variety of lymphoid and nonlymphoid cells and whose effects occur at least partly within the lymphopoietic system

32
Q

Describe toll-like receptors

A

class of proteins that function as a type of pattern recognition receptor, and recognize molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as a pathogen-associated molecular patterns (PAMPs)

33
Q

Describe antigens

A

substance that causes your immune system to produce antibodies against it

34
Q

Describe antibodies

A

protein produced by the immune system when it detects antigens

35
Q

Describe the body’s innate immune defense system

A

○ Surface barriers, with skin and mucous membranes
○ Internal defenses: phagocytes, fever, natural killer cells, antimicrobial proteins, inflammation
When we talk about getting sick, we’re talking about the innate response - standard inflammatory response

36
Q

Describe the adaptive immune response components

A

○ Humoral immunity (B cells, involved with blood, making antibodies, free-floating in the circulation), and cellular immunity (T cells, the fact that T cells need to come into contact)
○ High specificity and diversity, has a memory where subsequent exposure to the same agent induces an amplified response
○ It just takes time, about 14 days for the level of antibodies to build up in your system
○ Antibody-mediated immunity (AMI)
§ Involves B lymphocytes, plasma cells, and antibodies
○ Cell mediated immunity (CMI)
§ Involves T lymphocytes, antigen-presenting cells and MHC (major histocompatibility complex) molecules
§ Cellular immunity
§ Induction of apoptosis, complement proteins which poke holes in the infected tissue, does everything it can to kill the cell

37
Q

Describe how astrocytes work in immunity

A

○ Most common cells in the body, providing the scaffolding and support structure of the brain
○ They also play a huge role in immune function
○ Forms/maintains the blood brain barrier, basement membrane
○ Neurotransmitter sink: soaks up glutamate, protecting against excitotoxicity
○ Immune function:
§ Astrogliosis: creating a scar which acts as a second BBB, walling off the source of infection

38
Q

Describe how microglia function in immunity

A

○ Phagocytosis and scavenging - not particularly good at it though
○ Cytokine production
○ Immune receptors: Toll-like and cytokine
○ After interacting with cytokines, they completely change their structure, become reactive, and are able to move through the brain to the source of infection
○ Interaction with astrocytes: activation/modulation
Tight regulation of microglial response is necessary

39
Q

Describe the behavioral sickness response

A

○ Lethargy, nausea, anhedonia (things you generally like you have no interest in, you don’t want to do things that sound fun)
○ This is entirely brain mediated: the virus doesn’t want this
○ The reason it does this is to give the immune system more energy to do its thing
○ Motivation: immune system is conducting info that you’re infected, and a huge response is coming from the brain

40
Q

How does the brain communicate with the immune system?

A

The vagus nerve afferents, which has connection to every type of tissue of interest, extremely complicated

41
Q

How can one simulate a sickness response?

A

You can simulate a sickness response by injecting interleukin 1 beta into the brain, suggesting that that’s what’s mediating the sickness response

42
Q

What is an emotion?

A

§ Evolutionarily well conserved
§ Coordinated set of physiological and behavioral responses to something
§ The something differs as a function of species
§ Processed at many levels of CNS
Occur on the order of seconds to minutes

43
Q

What is biased information processing?

A

• Biased information processing: you’re seeing shifts in behavior because of emotions, emotions change based upon the needs of the animal (mouse diagram and avoidance behavior with the electrical grid and food)
Different emotions change the way an organism sees the world, perception isn’t a passive filtering of information, it affects what you see

44
Q

What does anxiety do?

A

Anxiety leads to increased threat attention and hyper-vigilance, leading to a colored perception of the world where more threat is perceived

45
Q

What’s the smoke alarm principle?

A

if you’re going to make a mistake, your brain usually makes a mistake in the direction of negative, it assumes the worst

46
Q

What is a mood?

A

○ Like an emotion, but:
§ Not necessarily tied to a specific stimulus
§ Much less differentiated
□ Positive or negative
§ Can occur over much longer time periods
§ Not as clearly associated with physiological states

47
Q

What are the characteristics of major depression?

A

§ Depressed or irritable mood
§ Decreased interest or ability to experience pleasure (anhedonia)
§ Significant weight gain or loss
§ Insomnia or hypersomnia
§ Psychomotor agitation or retardation
§ Fatigue or loss of energy
§ Feelings of worthlessness or excessive guilt
§ Diminished ability to think or concentrate
Recurrent thoughts of death or suicide

48
Q

What’s the inflammation theory of depression?

A

○ Very strong overlap with the sickness response, induced by the same cytokines within the brain (interleukin 1 beta)
○ The only way to distinguish sickness response and depression is by looking at timelines
○ If you give a mouse that’s suffering from sickness response, you can reduce sickness response by getting serotonin in the brain
○ Primary mechanism that’s modulating this is levels of serotonin
○ Patients that were suffering from cancer, some given interferon chemotherapy treatment (immune) and some were given a different kind of chemotherapy
The patients who had the immune chemotherapy had much worse off mood, more depression symptoms, elevated immune levels in the blood years later

49
Q

Why do we display emotions?

A

○ Serves an adaptive purpose: flexion reflex with pain
○ Serves to communicate to conspecifics: alarm call, crying, laughing
○ Serves to communicate to predators: pronking or stotting
○ Serves to change behavior in target: smiling
○ We often implicitly alter our behavior based upon who we’re around, whether they’re people we don’t like, or family, or close friends

50
Q

What is the difference between challenge and threat responses?

A

○ The challenge state is feeling like you have a “fighting chance”, while threat state is about feeling like you’re outmatched

51
Q

What are emotions typically associated with?

A

Emotions are typically associated with pronounced patterns of activity in the autonomic nervous system and HPA axis

52
Q

What is a genetic moderator of resilience?

A

serotonin transporter gene, which is responsible for taking serotonin out of synaptic cleft, individual polymorphisms make the transporter more or less effective

53
Q

What is stress inoculation?

A

○ Comes from the inverted U idea
○ It is the case that exposure to moderate stressors throughout your life makes you better at dealing with them
○ US Army on exercise - “progressively greater exposure to physical stressor is required”, mild to moderate stressors that are increasing over time
○ Familiar stress over time - you habituate to it
○ Also remember the placebo effect
○ Repeated stress, but the worst case scenario doesn’t actually happen, so your stress responses get less extreme and more manageable

54
Q

What is active coping?

A

gather information, acquire skills, confrontation, problem solving, seek social support, and cognitive reappraisal (challenge as opposed to a catastrophe, seeing the bigger picture)

55
Q

What is passive coping?

A

deny the problem, avoid or withdraw, substance use, negative venting, cognitive rigidity, blaming

56
Q

Controllable is blank focused, while uncontrollable is blank focused

A

Controllable is problem-focused, while uncontrollable is emotion-focused

57
Q

What are some good habits associated with resilience?

A

○ Acquire information about stressor
○ Learn skills necessary to deal with or adapt to stressor
○ Have a plan and a back-up plan
○ Practice plan and back-up plan
○ Discuss stressor with trusted colleagues when possible
○ Don’t be afraid to fail (if you fail correctly)
There are a lot of different ways to fail

58
Q

What are the psychosocial factors of resilience?

A
○ Find resilient role models
		○ Humor - making light of something
		○ Develop active coping strategies
		○ Practice regulating emotions
		○ Help others
		○ Take advantage of social support
		○ Cognitive flexibility (positive reappraisal)
		○ Physical and psychological training
		○ Allow time for physical and emotional recovery
Focus on purpose and meaning - refocus