Exam II Material Flashcards

1
Q

A possible reason for reduced cortical thickness in schizophrenia patients is
a. Reduced myelination in the cortex
b. Reduced interneuron development in the cortex
c. Excessive excitatory pruning
d. All of the above

A

d. All of the above

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2
Q

Outer radiate white matter is involved in the pathophysiology of which order?

Depression
Autism
Addiction
ADHD
Schizophrenia

A

Autism

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3
Q

Which is a pathophysiological marker of autism?

Enlarged ventricles
Reduced brain volume
Thickened cortex
Spinal lesions

A

Thickened cortex

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4
Q

Autism is associated with a cortical microstructure characterized by

Abnormally low-density minicolumns
Abnormally high density of minicolumns
Reduced cell density
Impaired myelin formation

A

Abnormally high density of minicolumns

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5
Q

Autism is associated with what white matter abnormalities?

Decreased radiate white matter
Increased radiate white matter
Thickened corpus callosum
Abnormally small cerebellum

A

Increased radiate white matter

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6
Q

Autism symptomology is characterized by

Acute awareness of others
Exceptional ability in math
Lacking or absent theory of mind
Blindness

A

Lacking or absent theory of mind

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7
Q

Autism appears to be associated with what white matter structural differences compared to controls?

Enhanced distance but poor local cortical connectivity

Enhanced distant and enhanced local cortical connectivity

Enhanced local and enhanced distant cortical connectivity

Enhanced local and poor distant cortical connectivity

A

Enhanced local and poor distant cortical connectivity

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8
Q

An example of a positive symptom in schizophrenia is

Depression
Catatonia
Hallucinations
Anhedonia

A

Hallucinations

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9
Q

The dopamine hypothesis of schizophrenia was developed because

The discovery that neuroleptics and antipsychotics reduced symptoms

The discovery that amphetamines caused symptoms

The discovery that neuroleptics and antipsychotics caused symptoms

Both A and B

A

Both A and B

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10
Q

In Schizophrenia, the positive symptoms are likely to result from
a. Increased dopamine in the mesolimbic dopamine pathway
b. Decreased dopamine in the mesolimbic dopamine pathway
c. Increase dopamine in the mesocortical dopamine pathway
d. Decreased dopamine in the mesocortical dopamine pathway

A

a. Increased dopamine in the mesolimbic dopamine pathway

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11
Q

In Schizophrenia, the negative symptoms are likely to result from
a. Increased dopamine in the mesolimbic dopamine pathway
b. Decreased dopamine in the mesolimbic dopamine pathway
c. Increase dopamine in the mesocortical dopamine pathway
d. Decreased dopamine in the mesocortical dopamine pathway

A

d. Decreased dopamine in the mesocortical dopamine pathway

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12
Q

The Gs protein-coupled receptor pathway functions by
a. Increasing PKC activation
b. Decreasing Adenylyl cyclase activity
c. Decreasing cAMP concentration
d. Increasing PKA activity

A

a. Increasing PKC activation

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13
Q

Which is not a feature of drug abuse or dependence?
a. Tolerance
b. Withdrawal
c. Sensitization
d. Toxicity

A

d. Toxicity

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14
Q

Bottom-up attention differs from top-down attention in that bottom-up attention is
a. The stimulus, like your homework, that you know needs your attention so you put effort into keeping with it
b. The distracting stimulus that takes you away from the above goals
c. Mediated largely by the frontal cortex
d. Has no evolutionary role in our development as a species

A

b. The distracting stimulus that takes you away from the above goals

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15
Q

The Stroop test, designed to assay inhibition of inappropriate response, asks the participants to
a. Name of the color a word is written in
b. Count the number of words on the screen
c. Read a sentence
d. Start a revolution

A

a. Name of the color a word is written in

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16
Q
  1. Which brain region is identified in imaging studies to be under-activated in individuals with ADHD when inhibiting responses during the Stroop test?
    a. Dorsolateral prefrontal cortex
    b. Cerebellum
    c. Dorsal anterior midcingulate cortex
    d. Inferior vena cava
A

c. Dorsal anterior midcingulate cortex

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17
Q

Which of the following is a likely candidate gene for ADHD?
a. DAT1
b. The serotonin hydroxylase enzyme
c. Estrogen receptor alpha
d. ADHD

A

a. DAT1

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18
Q

The gene identified in question 18 above has a function most related to which neurotransmitter’s function?
a. Serotonin
b. Dopamine
c. Epinephrine
d. PCP

A

b. Dopamine

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19
Q

Which receptor is closely related to addiction?
a. DA
b. D1
c. 5HTT
d. 5HT1a

A

b. D1

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20
Q

Characterize the receptor identified in the previous question
a. Ionotropic
b. Metabotropic
c. Zetatropic
d. Coprophagic

A

b. Metabotropic

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21
Q

The role of the Hippocampus in the stress response is
a. To activate the HPA axis
b. To inhibit the HPA axis
c. To activate the HPG axis
d. To inhibit the HPG axis

A

b. To inhibit the HPA axis

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22
Q

The monoamine hypothesis of depression states that
a. Increasing the monoamine concentration in the brain should cause depression
b. Increasing monoamine concentration in the brain should reduce depression
c. Depression results from increased serotonin concentration
d. Depression results in decreased acetylcholine concentration

A

b. Increasing monoamine concentration in the brain should reduce depression

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23
Q

Monoamine oxidase
a. Is an important enzyme that helps make dopamine
b. Is an important enzyme that breaks down monoamines
c. Is an important enzyme that helps to make monoamines
d. Is an important enzyme that helps make serotonin

A

a. Is an important enzyme that helps make dopamine

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24
Q

Resiliency, or resistance to depression, induced by the social defeat test is associated with
a. Up-regulation of potassium channels in the VTA to reduce the firing rate
b. Increase of glucocorticoid receptors in the hippocampus
c. Loss of feeling in the limbs
d. Intracranial self-stimulation

A

a. Up-regulation of potassium channels in the VTA to reduce the firing rate

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25
Q

Resiliency associated with learned helplessness differs from social defeat in that
a. Involves delta Fos B
b. It involves VTA firing rate
c. It cannot be measured using intracranial self-stimulation
d. Its just not as interesting

A

a. Involves delta Fos B

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26
Q

The delay in treatment efficacy for depression by SSRIs is associated with
a. Raphe nucleus down-regulating 5HT1a receptors
b. The length of time it takes for serotonin to actually build up in synapses
c. Structural changes in the hippocampus including neurogenesis
d. The patient’s motivation to get better

A

c. Structural changes in the hippocampus including neurogenesis

27
Q

What type of hormone is linked to depression and the HPA axis?
a. Adrenalin
b. Glucocorticoids
c. Epinephrine
d. Testosterone

A

a. Adrenalin

28
Q

In response to HPA activation, which of the following hormones helps mediate the stress response?
a. Cholesterol
b. Testosterone
c. Cortisol ( a glucocorticoid)
d. Serotonin (a monoamine)

A

c. Cortisol ( a glucocorticoid)

29
Q

The delay in treatment efficacy for depression by SSRIs is associated with
a. Raphe nucleus down-regulates 5HT la receptors.

b. The length of time it takes for serotonin to actually build up in synapses.

c. Structural changes in the hippocampus including neurogenesis.

d. The patient’s motivation to “get better.”

A

c. Structural changes in the hippocampus including neurogenesis.


30
Q

What is the effect of blocking neurogenesis?
a. It can cause depression
b. It can block relief from depression by SSRIs
c. It can cause hippocampal atrophy
d. All of the above

A

b. It can block relief from depression by SSRIs
c. It can cause hippocampal atrophy
d. All of the above

31
Q

Taking SSRIs for depression is associated with
a. Increased synaptic serotonin concentration
b. Decreased symptoms of depression
c. Increased BDNF expression
d. All of the above

A

d. All of the above

32
Q

Blocking forebrain BDNF
a. Causes depression
b. Blocks recovery from depression
c. Cures depression
d. All of the above

A

b. Blocks recovery from depression

33
Q

The Gs protein-coupled receptor pathway functions in the NAc medium spiny neurons most directly by
a. Increasing PKC activation
b. Decreasing Adenylyl cyclase activity

c. Decreasing cAMP concentration

d. Increasing PKA activity

A

d. Increasing PKA activity

34
Q

Which is not a feature of drug abuse or dependence?
a. Tolerance
b. Withdrawal
c. Sensitization
d. Toxicity

A

d. Toxicity

35
Q

Which is a way that a synapse may adjust to compensate for overstimulation to make the synapse less sensitive?
a. Phosphorylation of AMPA receptors
b. NMDA activation by PKA
c. Receptor internalization
d. Magnesium ejection and calcium influx
e. All of the above

A

c. Receptor internalization

36
Q

Which is a way that a synapse may adjust to make a synapse more responsive or sensitive?
a. Phosphorylation of AMPA receptors
b. NMDA activation by PKA
c. Receptor insertion
d. Magnesium ejection and calcium influx
e. All of the above

A

e. All of the above

37
Q

Which neurotransmitter is most associated with the experience of reward
a. Glutamate
b. Serotonin
c. Norepinephrine
d. GABA

A

d. GABA

38
Q

An SSRI modulates a specific neurotransmitter’s function by
a. Increasing its release
b. Decreasing its release
c. Blocking its reuptake
d. Blocking its degradation

A

c. Blocking its reuptake

39
Q

Which is a way that a synapse may adjust to compensate for overstimulation to make the synapse less sensitive?
a. Phosphorylation of AMPA receptors
b. NMDA activation by PKA
c. Receptor internalization
d. Magnesium ejection and calcium influx

A

c. Receptor internalization

40
Q

The role of the Hippocampus in the stress response is
a. To activate the HPA axis
b. To inhibit the HPA axis
c. To activate the HPG axis
d. To inhibit the HPG axis

A

b. To inhibit the HPA axis

41
Q

The monoamine hypothesis of depression states that
a. Increasing monoamine concentration in the brain should cause depression
b. Increasing monoamine concentration in the brain should reduce depression
c. Depression results from increased serotonin concentration
d. Depression results from decreased acetylcholine concentration

A

b. Increasing monoamine concentration in the brain should reduce depression

42
Q

The need to keep taking a drug in order to avoid experiencing negative effects is called
a. Tolerance
b. Dependence
c. Withdrawl
d. Craving

A

b. Dependence

43
Q

Which of the following is a core symptom of Autism spectrum disorder?
a. Hyperactivity
b. Impaired social interaction
c. Depression
d. Psychosis

A

b. Impaired social interaction

44
Q

Structural MRI studies in autism have found
a. Smaller overall brain volume
b. Corpus callosum enlargement
c. Cortical thinning
d. Increased gray matter

A

d. Increased gray matter

45
Q

Which is a pathophysiological marker of autism
a. Enlarger ventricles
b. Reduced brain volume
c. Thickened cortex
d. Spinal lesions

A

c. Thickened cortex

46
Q

Autism is associated with cortical microstructure characterized by
a. Abnormally low density of minicolumns
b. Abnormally high density of minicolumns
c. Reduced cell density

A

b. Abnormally high density of minicolumns

47
Q

Autism symptomology is characterized by
a. Acute awareness of others
b. Exceptional ability in math
c. Lack absent theory of mind
d. Blindness

A

c. Lack absent theory of mind

48
Q

Identify the difference between top-down and bottom-up attention

A

Top down attention refers to the voluntary, goal-driven process of focusing on specific information based on prior knowledge and expectations, while bottom-up attention is the involuntary shift of focus to stimuli that are highly salient in the environment, like a sudden loud noise or bright color regarless of current expectations

49
Q

Describe two pathopsychological hallmarks of autism and what symptoms they have been hypothesized to underlie

A

Autism patients had higher activation of left posterior temporal gyris (wernicke) hindering speech production.
Relatively lower activation of the left inferior gyrus (broca) hindering language comprehension.
Outer radiate white matter

50
Q

Describe two pathopsychological hallmarks of schizophrenia

A

Enlarge ventricles and gray matter loss

51
Q

List and very briefly describe the phases of onset of schizophrenia

A

Premorbid phase: subtle childhood differences in cognition, motor development, or social functioning
Prodromal phase: gradual emergence of subtle changes, typically in adolescence
Active Phase: full emergence of positive symptoms like hallucinations and delusions
Recovery Phase: acute symptoms begin to subside with treatment and gradually return to baseline functioning
Residual Phase: long-term pattern emerges may have persistent negative symptoms and cognitive deficits

52
Q

Describe the difference between physiological dependence and psychological dependence

A

Physiological dependence is the presence of physical withdrawal symptoms after stopping drug use (i.e. shakes). Psychological dependence is the need to take a drug to reduce negative moods that are caused by stopping drug use.

53
Q

Briefly describe the HPA axis

A

The HPA axis becomes activated due to prolonged threats. It is almost entirely hormonal. The hippocampus activated the paraventricular nucleus of which releases corticotrophin release hormone to the anterior pituitary gland. The anterior pituitary gland release adrenal corticotrophin hormone to the adrenal gland and the adrenal gland releases glucoticoids. Glucocorticoids are released throughout the body to decrease digestion, decrease need to reproduce.

54
Q

Describe the Sally-Anne test and what it test for and how it test for it

A

The Sally-Anne test is used to test for the Theory of the Mind. The scenario is about a character sally hiding a marble in a basket, sadly leaving, and Anne removing the marble from the basket and hiding it in a box. Sally does not know that the ball was moved. Children are asked to answer where will Sally look for the ball and children with autism are not able to ascribe Sally’s perspective.

55
Q

Describe the difference between pharmacodynamics and pharmacokinetic tolerance

A

Pharmacodynamic tolerance is the downregulation of receptors due to chronic or continued presence of drugs. Pharmacokinetic is the response to chronic or continued drug use. Like a person’s liver increase enzyme production to metabolize the drug

56
Q

Briefly, but completely describe the interaction between dopamine and glutamate in the nucleus accumbens after cocaine use (start with the activation of PKA and finish with the transcription of delta FosB)

A

Cocaine-induced dopamine release activates Protein Kinase A (PKA), leading to an increase in extracellular dopamine levels and stimulation of D1-like dopamine receptors on postsynaptic neurons in the nucleus accumbens. This stimulates D1-like dopamine receptors, enhancing neuroplasticity and reward processing. PKA phosphorylates downstream targets, such as cAMP response element-binding protein (CREB), enhancing the transcription of genes critical for neuronal adaptation and plasticity. Additionally, cocaine increases glutamate release from presynaptic terminals, binding to ionotropic and metabotropic glutamate receptors on postsynaptic neurons, promoting synaptic strengthening. The activation of PKA and other signaling pathways leads to the expression of immediate early genes, including delta FosB, a transcription factor that accumulates in response to repeated cocaine exposure. This accumulation induces the transcription of target genes involved in synaptic plasticity, neuronal survival, and adaptation to repeated drug exposure, contributing to long-term changes in the brain’s reward circuitry associated with addiction.

57
Q

What neurobiological systems cause the symptoms observed in schizophrenia(both sets)? Describe the glutamate hypothesis of schizophrenia and reconcile these two sets of symptoms.

A

The positive and negative symptoms of depression which include dopamine and glutamate dysfunction. The glutamate hypothesis helps reconcile these seemingly contradictory dopamine abnormalities. Primary deficit is NMDA receptor hypofunction on GABA neurons. This reduces inhibitory tone leading to excessive glutamate release in some circuits and reduced glutamate signaling in others. Glutamate abnormalities then cause disinhibition of mesolimbic dopamine and reduces mesocortical dopamine. This model explains how a single underlying pathology can produce both dopamine excess in subcortical regions and dopamine deficits in cortical regions generating the full spectrum of symptoms.

58
Q

Describe the role of the hippocampus and neurogenesis in depression.

A
  • Neurogenesis hypothesis of depression postulated that a decrease in new granule cells related to the pathophysiology of depression and recovery of neurogenesis is related to treatment
  • Clinical observations of decreased hippocampal volume led to the discovery and study of DG
59
Q

Describe the HPA axis and its role in depression; how might this relate to the hippocampus?

A
  • The hippocampus has high levels of glucocorticoid receptors
  • Chronic activation of the HPA axis leads to chronic activation of the glucocorticoid and mineralocorticoid receptors
  • This leads to a decrease in action on the hippocampus and the inability of the hippocampus to negative feedback on the HPA axis
60
Q

What factors are involved in making resilience to depression more likely? Be sure to discuss the animal models used and what mechanisms have been identified that mediate resilience too.

A

Refers to the capacity of an individual to avoid negative social, psychological, and biological consequences of extreme stress
Recent reports indicate that resilience represents an active process rather than the absence of pathological responses. Some examples of this was shown in the reward pathway identified by studies done on mice, delta Fos B accumulation in the nucleus accumbens and HPA Axis regulation. Resilience was also shown in the learned helplessness modeled by mice. Some key mechanisms are the stress response system and neurotrophic factors

61
Q

Describe the interaction between dopamine and glutamate in the nucleus accumbens after cocaine use (identified in class as the early or short-term effects of cocaine)

A

Cocaine and other drugs of addiction have distinct phases of action
Short term – chemical changes that lead to the subjective “high”
Intermediate term: changes in gene expression
Long-term: changes in nerve cell structure
Dopamine in the NAc acts on D1 Receptors
D1 Glutamate Receptors enhance glutamate signaling in the NAc

62
Q

Describe the role of the Hippocampus in depression

A
  • hippocampus is one of the biggest regions involved in depression not yet mentioned
  • structural studies indicate reduced volume of the hippocampus in individuals with depression
  • functional studies with fMRI and PET implicate the amygdala and cingulate
  • nucleus accumbens implicated with results of deep brain stimulation s as well as the VTA
  • some of these structures appear to play specific roles in the presentation of depression
63
Q

Diagram the reward pathway as described in Kandel and Schwartz. There are five brain regions you need to include. Be sure to draw all pathways and indicate the direction (from what structure to what structure) as well as what the pathway releases neurotransmitters.

A