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Biopsychology > exam 4 > Flashcards

exam 4 Flashcards

1
Q

• Contribution of Broca and Wernicke to the biological basis of language

A

Broca: Determines that language is lateralized to the left cerebral cortex.
Wernicke: Suggests that comprehension and speech are regulated by different areas of the left cerebral cortex

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2
Q

• Brain regions involved in speech recognition, comprehension, and production *

A

Auditory cortex: Detects sounds

Wernicke’s area: Detects words

Posterior language area: Detects meaning and may house phonemes (parts of words)

Broca’s area: Finds and sequences words

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3
Q

• Functional and structural changes related to speaking a second language

A
  • As you get better at speaking the language, your brain becomes more efficient and you use less of it
  • Second language processed by same brain regions as first one, but involves a wider area of brain activation
  • Bilinguals have a slightly larger left auditory cortex
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4
Q

• Comparison between language and algebraic comparisons

A

Language Grammar is not math grammar.
-Brain processes linguistic arguments differently than algebraic arguments.
(Language mainly left hemisphere, Math mainly left and right parietal.)

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5
Q

• What is aphasia and what are the symptoms of Broca’s and Wernicke’s aphasia?*

A

Aphasia: a primary disturbance in comprehension or production of speech
Wernicke’s aphasia: problems with understanding speech
Can not recognize spoken words
Can not comprehend the meaning of words

Broca’s aphasia: problems with producing speech
difficulty finding words
difficulty in using grammar
Difficulty with articulation and sound sequence

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6
Q

• Neuroanatomy of reading – phonetics vs. whole word reading*

A

[Reading a word activates pathway between visual and temporal cortex]
Phonological reading activates the phonological, meaning, and articulation part of the brain (Wernicke’s area, posterior language area, and Broca’s area, respectively.)
Sight (or “whole-word”) reading also activates an object recognition area of the brain. (Fusiform cortex)

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7
Q

• Brain regions and genes involved in dyslexia

A

Individuals with dyslexia may have problems:
word recognition (posterior inferior temporal cortex)
whole word reading (fusiform gyrus).
If one identical twin has dyslexia, about 90% of the time the other twin has dyslexia.
Mutation in FoxP2 gene associated with language deficits

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8
Q

• Describe the three theories of where emotions come from: James-Lange theory, Cannon-Bard theory, and Schachter-Singer theory*

A

James-Lange Theory: States that emotions are a consequence of bodily changes
Perception (e.g., concert)>Autonomic
arousal (e.g., increased heart rate)>Feedback to brain: Subjective Emotion (e.g., happy)
Cannon-Bard Theory: States that the subjective feeling of emotion occurs independent of autonomic arousal.
Perception>Processing in
brain (thalamus)>Feedback to brain: subjective emotion, and Autonomic arousal
Schachter-Singer theory: States that subjective feeling of emotion depends on autonomic arousal AND the current context one is experiencing
Perception>Cognition/Context (e.g. happy people around you), and Autonomic Arousal>Feedback to brain: Subjective Emotion

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9
Q

• Evidence of amygdala involvement in fear and the neurotransmitter that may reduce amygdala activity *

A

Kluver-Bucy syndrome: monkeys lose fear after temporal lobe damage.(Amygdala included in removal)
Perception of fearful faces or aversive stimuli activates the amygdala.
GABA neurotransmission in the amygdala reduces fear.

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10
Q

• Role of amygdala in emotional memory, and implicit prejudice *

A

-Better memory for emotional words associated with greater amygdala activation during learning.
-Even if one is not racist, they may demonstrate unconscious biases in favor of their race on a reaction time task.
(Bias on this task is positively correlated with greater amygdala activity.)

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11
Q
  • Mesolimbic dopamine system in pleasure *
  • Evidence from animal studies
  • Evidence from human studies
A
  • Damage to the MDS blocks the self-administration of euphoria-producing drugs by rats.
  • All reinforcing stimuli (food, water, sex, drugs) increase dopamine levels in the MDS. (in rats?)
  • Activity in the NAcc increases when humans are shown a product that is so good, they will pay money for it. (MDS connects VTA to NAcc)
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12
Q

What part of the brain is responsible for feelings of disgust

A

Insula or insular cortex activated by aversive stimuli such as disgust or empathy for disgust.

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13
Q

• Separate roles of the cingulate, prefrontal, and orbitofrontal cortex in emotion *

A

The cingulate monitors conflicts between goals.
Prefrontal cortex processes information about goals.
Orbitofrontal cortex processes information about rewards (left side) and punishments (right side) related to our actions

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14
Q

• How is voting behavior affected by orbitofrontal damage?

A

More likely to vote for someone based on their attractiveness instead of whether they look competent.

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15
Q

Depression - •Rates in population

•Gender difference

A
  • Affects 5% of population at any given time
  • Increased rate in teens and elderly
  • Affects twice as many women as men
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16
Q

• Genetic contributions to depression

A
  • More severe depression seems more genetic.

- If parents 1st episode occurs before age of 20, risk in offspring doubles

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17
Q

• Evidence for each neurochemical hypothesis of depression*

A

Depression due to a lack of norepinephrine (NE). Evidence:
-Some antidepressant drugs (tricyclics) block NE reuptake into terminals and increase synaptic levels of NE.
-Some antidepressants act as MAO inhibitors that prevent MAO breakdown of NE and increase synaptic NE.
Depression due to a lack of serotonin (5HT).
-Evidence:
Some antidepressant drugs block NE and 5HT reuptake.
All MAO-I antidepressants prevent break down of 5HT by MAO.
Tryptophan (amino acid from which 5HT is formed) depletion produces depression in some subjects.

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18
Q

• Immediate vs. therapeutic effects of antidepressants

A

The biological effects of the drugs on the brain are immediate but clinical improvement takes 4- 6 weeks to emerge.

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19
Q

• How does ketamine work to relieve depression?

A

Blocks NMDA receptors on GABA terminals.

Loss of GABA inhibition leads to greater glutamate release and AMPA receptor stimulation in cortical neurons.

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20
Q

• Frontal cortex and depression*

A

Prefrontal cortex (PFC):
Less activation of left PFC in depression
If the right PFC is more active before treatment, then the person is LESS likely to respond to treatment.
Anterior cingulate (ACC):
Less activity in dorsal ACC (cognitive part) in depression.
If the ventral ACC (emotional part) is more active before treatment, then the person is MORE likely to respond to treatment.

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21
Q

• What is the default mode network and how does it respond in people with depression?

A

DMN- A group of brain regions that are active at rest and inactive during tasks.

  • Depressed people ruminate more and may have a more active DMN.
  • Depressed people do not suppress activity in the DMN during visual tasks.
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22
Q

Schizophrenia - • How many people have it and when do they first present with symptoms?

A

Affects 1% of population in world

Begins in late adolescence or early adulthood

23
Q

• Symptom clusters in schizophrenia

A

Positive symptoms: hallucinations and delusions
Negative symptoms: flat affect, lack of motivation
Cognitive symptoms: Impaired attention, memory, and thought

24
Q

• Differences in brain structure and activity in schizophrenia *

A
  • No single anatomical change in ppl with or without it
  • Most reliable difference is enlargement of the lateral ventricle.
  • also sometimes see reductions in the size of temporal lobe structures
  • Frontal cortex does not activate completely during cognitively challenging tasks
25
Q

• Schizophrenia- Developmental influences and frontal anatomy in high risk individuals*

A
  • People with SCZ are more likely to have had gestational complications, (doubles risk)
  • Prenatal malnutrition is associated with higher rates of SCZ (doubles risk)
  • Prenatal exposure to flu is associated with higher rates of SCZ (doubles risk)
  • Winter Birth
  • People at high risk for SCZ who become ill show greater progressive loss of prefrontal (PFL) gray matter.
26
Q

• Schizophrenia- Genes – concordance rates in fraternal vs. identical twins

A

-fraternal: 17% Identical: 48%

A single gene for schizophrenia has not been isolated

27
Q

• Rare variant, common disease hypothesis (For schizophrenia)

A

says that Schizophrenia may be linked to genetic mutations called copy number variants. (A CNV is a change in the number of whole copies of a gene)

  • not many ppl probably share the same gene mutation
  • a rare gene mutation alone can cause a common disease like schizophrenia; but very few people with schizophrenia share the same rare gene mutation.
28
Q

• Describe each neurochemical hypothesis of schizophrenia and the evidence for it: Dopamine, Serotonin, and Glutamate *

A

Dopamine - too much dopamine (DA)

  • DA agonists (amphetamine) produce psychosis.
  • All antipsychotic drugs block dopamine receptors.

Serotonin - too much serotonin

  • Some serotonin (LSD) agonists produce hallucinations.
  • Some antipsychotics block serotonin receptors (reduce negative symptoms).

Glutamate- too little glutamate in the brain in SCZ.
-Drugs that block glutamate receptors (e.g., PCP) produce all three symptoms of schizophrenia.

29
Q

• Dementia vs. Alzheimer’s disease

A

Alzheimer’s: a subtype of dementia. Afflicts 5.3 million Americans a year. By age 85, 20% of people have AD.

Dementia affects 5% of people over age of 65 (Half of these people have AD)

30
Q

• Normal aging or disease process (Alzheimer’s)

A

AD is probably not an inevitable part of aging, but an active disease process.

31
Q

• How is Alzheimer’s disease ultimately diagnosed?

A

Diagnosis confirmed at autopsy by presence of amyloid plaques in brain.

32
Q

• What are plaques and how are they made? *

A

-Mass of degenerating axons and dendrites that surround a “core” of amyloid.
Making good amyloid:
1. APP inserts itself into the neuronal cell membrane.
2.A portion of APP located outside of the cell is then cut. (Done by protease)
3.The portion that is cut is AB-1-40

Making bad amyloid: (APP is cut too long)
-due to a problem with protease, faulty construction of APP protein, or an overproduction of APP in the brain

33
Q

• Genes that affect plaque formation*

A

-APP encoded by a gene on chromosome 21.
(Some familial, early-onset forms of AD have alterations in this APP gene.)
-Trisomy is an extra copy of chromosome 21.
(Most people with Down’s syndrome get AD; they have an extra APP gene.)
-Other forms of early-onset, familial AD have been linked to mutations in two other genes called presenilin 1 and 2 (PS1 & PS2)

34
Q

• What are NFT’s and tau?*

A

-NFT-neurofibrillary tangles- also found in autopsy
-NFTs are basically dead axons and dendrites.
-They come from within neurons.
(From tau proteins)
-In AD, the tau proteins become too sticky or hyper-phosphorylated (Clump together instead of binding to and stabilizing the microtubule.)

35
Q

• What comes first – plaques, tangles, brain volume loss, or memory impairment?

A

Plaques, then tangles, then brain structure, then memory

-Plaques and tangles may already be maximally expressed at early stages.

36
Q

• Head injury as a risk factor (Alzheimer’s disease)

A

Previous head injury doubles the risk of AD, risk increases with severity of injury

37
Q

• Role of APOE allelic variations in Alzheimer’s disease*

A

ApoE gene
-Codes for a protein involved in cholesterol breakdown in the bloodstream.
-Gene is located on chromosome 19.
-People carry one of three forms of the gene: E2, E3, and E4
-E4 allele is over-represented in AD.
(In sporadic AD, 33% of people have one E4 allele.
In familial, late onset AD, 52% of people with AD have an E4 allele.)
-In the brain, ApoE helps bring together Ab.
(E2 and E3 bind to AB)

38
Q

• Drug therapies for Alzheimer’s disease*

A
  • Drugs that block the breakdown of acetylcholine (ACh) (by inhibiting acetylcholinesterase) improve memory in AD.
  • NMDA receptor antagonists are also being used to treat moderate to severe AD. (There may be too much glutamate released, which is neurotoxic.)
39
Q

• Therapy with B-amyloid – how does it work and is it effective?

A

If APP mutant mice are injected with bad amyloid or Ab1-42, antibodies are internally generated that attack the preexisting amyloid plaques in the brain.
If immunized prior to 6 months, they have far fewer plaques.
If immunized from 6-12 months, plaque development is arrested.
-Ab therapy decreases plaques in some people (humans) with mid-stage AD but does not improve behavioral outcome.
(Maybe try therapy at earlier stage before plaques ravage brain. )

40
Q

Serotonin and aggression

A

In a study with monkeys it was seen that those with lower serotonin had increased risk taking and aggressive behaviors. It appears that serotonin exerts a controlling influence on risky behavior, including aggression.

41
Q

Role of frontal cortex in moral decision making

A

vmPFC (also involved in emotional reactions) activated when ppl are presented with a moral dilemma
people with vmPFC lesions are not as conflicted (they do not get a strong unpleasant emotional reaction when thinking of moral dilemmas)

42
Q

Parkinson’s disease –neurotransmitters involved

A

accumulation of a-synuclein and destruction of dopaminergic neurons (not enough dopamine)
increasing GABA in sub-thalamic nucleus relives symptoms too

43
Q

Neurotransmitters and brain regions involved in anxiety disorders and OCD

A

amygdala, cingulate, prefrontal and insular cortex are involved in anxiety disorders (low Serotonin and GABA involved in anxiety)
OCD= damage or disfunction of the basal ganglia, cingulate gyrus, and prefrontal cortex.
increased levels of activity in frontal lobes and caudate nucleus.
serotonin may help.

44
Q

Autism - causes*

A
  • heritable
  • rubella during pregnancy
  • prenatal thalidomide
  • encephalitis caused by herpes virus
  • tuberous sclerosis
  • abnormalities in development of brains in children with autism: grows abnormally quickly 2-3 years of age it is 10% larger than a normal brain
45
Q

Heritability of substance abuse disorders *

A
  • genetics strongly determines whether a person will stay addicted or not
  • a study of male twin pairs found a strong common genetic factor for the use of all categories of drugs
  • evidence that gene responsible for production of alcohol dehydrogenase plays a role in susceptibility to alcoholism
46
Q

Which of the following lists of brain regions best matches the following list of language functions? Word recognition, word meaning, speech production.

A

Wernicke’s area, posterior language area, Broca’s area

47
Q

Which brain regions are involved in sight or whole-word reading?

A

the posterior-inferior temporal cortex and the fusiform cortex

48
Q

Damage to the ______ is associated with reductions in fear, and increases in the neurotransmitter _______ within this same brain region have also been associated with reduced anxiety.

A

amygdala; GABA

49
Q

Which of the following sequences best fits with the Schacter-Singer theory of emotional processing?

A

Perception – autonomic arousal/appraisal of current context – subjective emotion

50
Q

Neurochemical imbalances are likely to lead to depression. Which of the following changes in neurotransmitter levels has been strongly implicated in depression?

A

There is a decrease in the level of norepinephrine.

51
Q

Neurochemical hypotheses of schizophrenia hold that schizophrenia is due to:

A

increases in dopamine and serotonin and decreases in glutamate.

52
Q

In people with schizophrenia, what aspect of brain anatomy is enlarged and what brain region remains somewhat inactive during tasks that normally activate it?

A

lateral ventricles; frontal cortex

53
Q

Which of the following statements is true regarding people with autism?

A

By 2-3 years of age, the brains of people with autism are, on average, 10 percent larger than normal.

54
Q

Which brain region is more active in people with depression who are MORE likely to respond to treatment and which brain region is more active in people with depression who are LESS likely to respond to treatment?

A

ventral cingulate cortex and right prefrontal cortex

Biopsychology (5 decks)

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