WEEK 5 Flashcards

1
Q

association cortex

A

takes info from the primary and secondary sensory and motor cortexes, as well as the brain stem and thalamus. it sends info to the cerebellum, basal ganglia, and hippocampus, and info also flows between the association cortexes.

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2
Q

top down effect of perception

A

the association cortex integrates sensory and motor info to produce a meaningful perception of the world around, as well as allowing for abstract representation and flexible behavior.

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3
Q

3 subdivisions of the association cortex

A

1) posterior/parietal: important for attention and the convergence of sensory info

2) limbic/temporal: important for long term memories and emotional responses

3) anterior/frontal: important for planning, decision making, and working memory. particularly important for mental health, as the PFC is involved in many disorders.

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4
Q

executive functions

A

higher order cognitive processes that allow flexible behavior: generating, planning, monitoring, switching, inhibiting. these are important when faced with novel situations or challenges.

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5
Q

Wisconsin card sort test

A
  • tests cognitive reasoning and set-shifting
  • classify cards according to: color of its symbols, shape of its symbols, number of shapes on each card.
  • the only feedback you get is if you’re doing it correctly or not.
  • suddenly a rule will change. you are prone to making more mistakes. the task measures how well you adapt to the rule change.
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6
Q

tower of Hanoi test

A
  • tests cognitive ability and ability to plan
  • you have 3 pegs and a number of discs stacked on one of the pegs in order of size. your task is to transfer the whole tower onto a different peg, disc by disc in order of size, but you cannot place a bigger disc on a smaller one - so you have to plan ahead.
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7
Q

stroop task

A
  • tests inhibitory control
  • you are presented with a number of colored shapes and are asked to name the colors as fast as you can from left to right.
  • you are then given a similar list but this time you’re presented with colored words. however, the words read different colors than they actually are - which makes the task so much harder. it takes effort to suppress the meaning that reading generates.
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8
Q

n-back task

A
  • tests attention and working memory
  • you are asked to look at a sequence of objects. in the 2-back test, you are asked to respond when you see an object repeated after sequence of 2 images have been displayed. in the 3-back test, you have to wait until you see the same image after a sequence of 3 images has been displayed.
  • the test gets harder as you have to hold longer intervals in mind (working memory)
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9
Q

Hampshire et al. (2016): activation in frontal regions and practice

A

frontal regions are activated when learning novel tasks, but their activity decreases once a skill is developed.

FINDING: activation in frontal regions decreases across the blocks of an inhibition task as volunteers become more practiced at the test.

CONCLUSION: frontal regions are essential to respond flexibly to our environment.

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10
Q

disorder and executive function

A
  • ASD (especially poor performance in planning tasks like the tower of Hanoi and set-shifting tasks like the Wisconsin card task). preference for repetition reflects impairment of frontal functions necessary for adaptive response to change and novelty
  • schizophrenia
  • BD
  • MDD
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11
Q

Frith-happe triangles

A

fMRI in healthy controls show activation of medial PFC and temporal poles and sulcus while doing the task. in ASD, brain activity is completely different while doing the task, even when they can answer it correctly.

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12
Q

Loth et al. (2010): reduced top-down in ASD

A

people with ASD don’t show strong top-down effects, especially when looking at faces versus other objects.

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13
Q

basal ganglia nuclei

A

1) striatum: caudate + putamen + ventrical striatum + nucleus acumbens

2) globus pallidus (GP): internal and external domains, GPi and GPI

3) sub thalamic nucleus (STN)

4) substantia nigra pars reticulata (SNr)

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14
Q

BG: 3 reentry loops

A

1) sensorimotor

2) associative

3) ventral

different cortical areas and connections among the BG are involved

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15
Q

movement modulation

A

the output nuclei (GPi/SNr) maintain a high level of discharge (high ATP activity). because they have inhibitory connections to the thalamus, this high tonic activity suppresses it, keeping the thalamus quiet, meaning no excitatory activity on the cortex: no movement.

movement occurs through disinhibition of the thalamocortical target regions: you would need an impaired activity of the output nuclei, which in turn disinhibits the thalamus which will cause excitatory activity towards the cortex. the normal tonic activity of the output nuclei is interrupted, which means that during this gap, the normally inhibitory activity to the thalamus is interrupted. because the thalamus has excitatory activity to the cortex, you see cortical activity in the gap: movement occurs.

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16
Q

direct BG pathway

A

the direct connection from the striatum to the output nuclei (SNr/GPi). This is an inhibitory connection. the basal firing rates in the striatum are very low, and dependent on cortical excitation. if the striatum is not activated by excitation, there’s not much activity, hence its inhibitory connection to the output nuclei is low. under these conditions, stratal firing has little impact on the output nuclei, meaning they continue to inhibit the thalamus. phasic cortical excitation drives excitatory discharge in the striatum. this causes a transient inhibition of the output nuclei, so they are no longer inhibitory on the thalamus.

activation of the direct pathway, then, promotes action.

17
Q

indirect BG pathway

A

the striatum has an inhibitory connection to the GPe, which has an inhibitory connection to the STN, which has an excitatory connection to the output nuclei. because striatal neurons have a low firing rate, without stimulation, it does not impose inhibitory activity on the GPe. strong phasic cortical excitation causes a transient inhibition of the GPe, which disinhibits the STN, and excites the output nuclei, causing enhanced thalamus suppression - so the suppression of action.

activation of the indirect pathway, then, suppresses action.

18
Q

dopamine signaling in the two BG pathways

A

1) D2 signaling in the indirect pathway: suppresses firing in the indirect pathway neurons. this results from the reduction of inward depolarizing currents and the increase of hyperpolarising currents, therefore diminishing the spiking of the indirect pathway. as a consequence, it reduces its inhibitory effect, facilitating movement.

2) D1 signaling in the direct pathway: enhances calcium currents and reduces potassium currents, increasing the spiking of the neurons in the striatum. that causes an inhibition of the. output nuclei, facilitating movement in the presence of cortical drive.

19
Q

BG dysfunction and behavioral abnormalities

A
  • motor abnormalities
  • impaired memory formation
  • attention deficits
  • affective disorders
  • sleep disturbances
20
Q

Parkinson’s: mechanism

A

loss of DA input into the striatum. because of the loss of DA neurons in the SNc, you lose the nigrostriatal pathway - DA no longer has an impact on the striatum. the direct pathway becomes less active, and the indirect pathway becomes more active. this causes the symptoms of Parkinson’s: tremors, rigidity, sleep disturbances.

21
Q

Abulia/Athymhormia

A

caused by lesions of the GPe and its connection to the striatum (striatopallidal pathway - the indirect pathway). characterized by inertia: action is impaired in its initiation and maintenance, and progress - it tends to stop unless kept up by external stimulation.

22
Q

reward

A

pleasurable feelings following a reward provide positive reinforcement, ensuring the behavior is repeated.

it is appetitive, and has 2 categories:

1) natural rewards: food, water, sex, nurturing. this can be dysregulated in Eds, anhedonia, dysphoria, SUDs.

2) artificial rewards: money, for example.

23
Q

reward pathway in the brain + interacting circuits

A

1) ascending mesolimbic DA pathway, which connects the ventral tegmental area (VTA) - one of th principal DA producing regions - with the nucleus accumbens - strongly associated with motivation and reward.

2) mesocortical pathway travels from the VTA to the PFC. essential to execute well-planned, motivated behaviors.

activation of the pathway tells the individual to repeat what they did to obtain a reward, as DA is released following the obtaining of a reward.

  • other circuits work in tandem with the reward pathway to develop appropriate goal-directed actions which rely on the interplay of sensory input, emotional input, and memory of prior outcomes.
  • the amygdala (conditioned forms of learning) acts with the mesolimbic pathway to determine the rewarding or aversive value of an environmental stimulus, creating associations from past experiences.
  • the hippocampus (declarative memory) establishes memories of drug experiences which are important mediators of relapse.
24
Q

Olds & Milner (1954): discovery of the reward pathway

A

implanted electrodes in the brains of rats allowing them to self-stimulate by pressing a lever that delivered electric stimulation to the neurons.

FINDINGS: in certain parts of the brain, particularly the septal area close to the nucleus accumbens, electric stimulation would produce the strongest effect making rats self-stimulate repeatedly. it was later discovered that the most sensitive areas are situated along the length of the medial forebrain bundle (nerve fibers that travel between the VTA, lateral hypothalamus, and towards the nucleus accumbens). rats chose stimulation over food and sex. further, they could stop rats from pressing the lever by administering DA antagonists.

25
Q

reinforcing drugs

A

when some drugs are taken, they can release 2 to 10x the amount of DA that natural rewards do. this occurs almost immediately when smoked or injected. and the effect lasts a long longer than produced by natural rewards. moreover, the dysregulated DA release affects other circuits, alerting other brain regions of novel rewarding experience and recruiting all neurotransmitter systems. when the reward circuit is activated, the brain notes that something important is happening, it needs to be remembered, and that we have to do it again and again.
“drug abuse is something we learn to do very well”.

26
Q

stiatal DA transmission abnormalities: PET scans

A

individuals who are addicted or obese have reduced levels of DA D2Rs and D3Rs in their striatum. this reduction shows that neuroadaptations occur in the brain following over activation of the reward pathway, and that the brain reacts to overwhelming DA surges by producing less DA or reducing the number of DA receptors.

27
Q

DA reward mechanisms: the current view

A

DA does not cause hedonic reactions or pleasure, but rather, it increases the motivation components of reward - incentive, wanting without causing liking.
other theories posit that DA causes learning about rewards.

28
Q

monetary incentive delay (MID) task

A

measures behavioral mechanisms of reward via neuroimaging.

  • subjects lay under an MRi and play repeated trials in which they win or lose incentives depending on their reaction times. brain patterns are recorded when a reward is anticipated after the cue is given but before they hit their target, or when receiving the outcome.

FINDING: the NAc is activated (plus other reward regions) when rewards are anticipated.

29
Q

MID task experiment with ADHD + alcoholics

A

several clusters were associated with reward anticipation:

1) the reward cluster (caudate + putamen + NAc = striatum)

2) the attention cluster (occipital cortex)

3) the response preparation cluster (cortical, somatosensory, and motor areas)

FINDINGS:
- low activation in the reward cluster is associated with high ADHD-related hyperactivity in boys.

  • the attention and response preparation clusters showed significant negative associations with lifetime alcoholic consumption.

CONCLUSION: specific reward-related processes relate to distinct and clinically-relevant behaviors. functional collections related to reward anticipation are differentially associated with adolescent ADHD and alcohol consumption.