Question 1

What is the difference between barbiturates and benzodiazepines?

Accepted Answer

A)  Barbiturates act on NMDA receptors and benzodiazepines act on GABAA receptors. 
B)  Barbiturates act on GABAB receptors and benzodiazepines act on GABAA receptors. 
C)  Barbiturates can independently activate GABAA receptors whereas benzodiazepines augment the action of intrinsic GABA. 
D)  Barbiturates block NMDA receptors whereas benzodiazepines activate GABA receptors. 
A)  Barbiturates act on NMDA receptors and benzodiazepines act on GABAA receptors. 
B)  Barbiturates act on GABAB receptors and benzodiazepines act on GABAA receptors. 
C)  Barbiturates can independently activate GABAA receptors whereas benzodiazepines augment the action of intrinsic GABA. 
D)  Barbiturates block NMDA receptors whereas benzodiazepines activate GABA receptors. C

Question 2

To better understand how MeCP2 regulates neuronal function, a mouse model was generated in which the Mecp2 gene was knocked out. The abnormal phenotype of this mouse could be rescued by conditional expression of MeCP2 in young mice. Why is this an important finding? Select all that apply.

Accepted Answer

A)  It shows that the defects seen in the mice are due to the dysfunction of MeCP2. 
B)  It shows that Rett syndrome is due to a dysfunctional Mecp2 gene. 
C)  It shows that Mecp2 is expressed in all neurons. 
D)  It indicates that the symptoms are reversible and therefore the disease can be treated by restoring MeCP2. 
A)  It shows that the defects seen in the mice are due to the dysfunction of MeCP2. 
B)  It shows that Rett syndrome is due to a dysfunctional Mecp2 gene. 
C)  It shows that Mecp2 is expressed in all neurons. 
D)  It indicates that the symptoms are reversible and therefore the disease can be treated by restoring MeCP2. A,D

Question 3

Figure  illustrates how many drugs of abuse enhance dopamine action on its postsynaptic targets, specifically the nucleus accumbens and prefrontal cortex.   Figure Q11-29
A. What are two mechanisms nicotine uses that result in increased dopamine release on its postsynaptic targets?
B. How does cocaine increase dopamine in the postsynaptic targets of VTA dopaminergic neurons?
C. How do cannabinoids increase dopamine in the postsynaptic targets of VTA dopaminergic neurons?

Accepted Answer

A.Nicotine excites the presynaptic terminals of prefrontal cortex neurons onto VTA dopaminergic neurons. This increases the release of glutamate and increases the activity of the VTA dopaminergic neurons. Nicotine also directly excites VTA neurons. The increased activity of the VTA neurons releases more dopamine onto the postsynaptic targets.
B. Cocaine blocks dopamine reuptake at the presynaptic terminal of the VTA dopaminergic neurons in both the prefrontal cortex and the nucleus accumbens. This results in more dopamine in the synapses.
C. Cannabinoids inhibit inhibitory VTA neurons which results in increased activity in dopaminergic VTA neurons (disinhibition of these neurons) and increased dopamine release in the postsynaptic targets.

Question 4

What are presenilins?

Accepted Answer

A)  Proteins that aggregate in amyloid plaques 
B)  Proteins that aggregate in neurofibrillary tangles 
C)  Proteins that are part of the γ-secretase complex 
D)  One of the cleaved proteins from APP 
A)  Proteins that aggregate in amyloid plaques 
B)  Proteins that aggregate in neurofibrillary tangles 
C)  Proteins that are part of the γ-secretase complex 
D)  One of the cleaved proteins from APP

Question 5

Why has it been difficult to develop effective drugs for psychiatric disorders?
Neurodevelopmental Disorders

Accepted Answer

(1) Many genes contribute to psychiatric

Question 6

If α-synuclein knock-out mice and mice with normal α-synuclein were injected with α-synuclein in the substantia nigra, which mice would develop symptoms of Parkinson's disease and why?

Accepted Answer

A)  The wild type mice would develop symptoms of Parkinson's as the α-synuclein would be able to cause mitochondrial dysfunction in the substantia nigra. 
B)  The α-synuclein knock-out mice would develop symptoms of Parkinson's as the α-synuclein would be able to cause mitochondrial dysfunction in the substantia nigra. 
C)  The α-synuclein knock-out mice would develop symptoms of Parkinson's because the α-synuclein protein would aggregate and spread cell to cell. 
D)  The α-synuclein wild type mice would develop symptoms of Parkinson's because the injected α-synuclein protein would recruit native α-synuclein and the aggregates could spread cell to cell. 
A)  The wild type mice would develop symptoms of Parkinson's as the α-synuclein would be able to cause mitochondrial dysfunction in the substantia nigra. 
B)  The α-synuclein knock-out mice would develop symptoms of Parkinson's as the α-synuclein would be able to cause mitochondrial dysfunction in the substantia nigra. 
C)  The α-synuclein knock-out mice would develop symptoms of Parkinson's because the α-synuclein protein would aggregate and spread cell to cell. 
D)  The α-synuclein wild type mice would develop symptoms of Parkinson's because the injected α-synuclein protein would recruit native α-synuclein and the aggregates could spread cell to cell.

Question 7

One protein implicated in intellectual disability (ID) is oligophrenin. How does this protein influence neurons during development? Choose all that apply.

Accepted Answer

A)  Enhances Rho-GTP levels 
B)  Decreases spine length 
C)  Impairs synaptic transmission 
D)  Enhances Rho-GTPase activity 
A)  Enhances Rho-GTP levels 
B)  Decreases spine length 
C)  Impairs synaptic transmission 
D)  Enhances Rho-GTPase activity

Question 8

Activation of type 1 mGluRs induces LTD through protein translation. What do you predict would happen to LTD if you could selectively increase PP2A phosphatase that regulates FMRP phosphorylation?

Accepted Answer

A)  mGluR activation would result in FMRP phosphorylation and repression of protein translation. This would enhance LTD. 
B)  mGluR activation would result in FMRP dephosphorylation and repression of protein translation. This would decrease LTD. 
C)  mGluR activation would result in an increase in phosphorylated FMRP which would increase repression of protein translation. This would decrease LTD. 
D)  mGluR activation would result in an increase in dephosphorylated FMRP which would decrease repression of protein synthesis. This would enhance LTD. 
A)  mGluR activation would result in FMRP phosphorylation and repression of protein translation. This would enhance LTD. 
B)  mGluR activation would result in FMRP dephosphorylation and repression of protein translation. This would decrease LTD. 
C)  mGluR activation would result in an increase in phosphorylated FMRP which would increase repression of protein translation. This would decrease LTD. 
D)  mGluR activation would result in an increase in dephosphorylated FMRP which would decrease repression of protein synthesis. This would enhance LTD.

Question 9

Pink1 and Parkin mutant flies both die prematurely, have degeneration of dopamine neurons, and have mitochondria with abnormal morphology and function. What happened when Parkin was overexpressed in Pink1 mutant flies?

Accepted Answer

A)  They still died, but their dopamine neurons were not degenerated. 
B)  The defects appeared earlier and so the Drosophila died even younger. 
C)  The Parkin flies were rescued. 
D)  There was no change. 
A)  They still died, but their dopamine neurons were not degenerated. 
B)  The defects appeared earlier and so the Drosophila died even younger. 
C)  The Parkin flies were rescued. 
D)  There was no change.

Question 10

Benzodiazepines help reduce anxiety but they also cause sedation. A more effective drug would reduce anxiety without causing sedation. The experiment shown in Figure was performed in which the histidine was replaced by an arginine on either the α1 or α2 subunit of GABAA receptors. This substitution causes the subunit to become insensitive to benzodiazepines while retaining its sensitivity to GABA.   Figure Q11-28
A. What happened to the α1(H101R) mice when they were given diazepam and what conclusion can be drawn about the α1 subunit?
B. What happened to the α2(H101R) mice when they were given diazepam and what conclusion can be drawn about the α2 subunit?
C. What does this tell you about designing a drug for anxiety?

Accepted Answer

The α1 mice were no longer sedated by di

Question 11

Why is Rett syndrome found only in human females?

Accepted Answer

A)  It is a recessive mutation located on the X chromosome and two copies are required to show the disease. 
B)  It is a dominant mutation on the X chromosome and you need both copies of the mutation to show the disease. 
C)  It is caused by a loss-of-function mutation of MeCP2 that is only expressed in females because it is silenced in males. 
D)  It is caused by a loss-of-function mutation of MeCP2, and X-linked gene, and when this is silenced in males, they often die prenatally or as infants. 
A)  It is a recessive mutation located on the X chromosome and two copies are required to show the disease. 
B)  It is a dominant mutation on the X chromosome and you need both copies of the mutation to show the disease. 
C)  It is caused by a loss-of-function mutation of MeCP2 that is only expressed in females because it is silenced in males. 
D)  It is caused by a loss-of-function mutation of MeCP2, and X-linked gene, and when this is silenced in males, they often die prenatally or as infants.

Question 12

What is ApoE? Select all that apply.

Accepted Answer

A)  A component of high-density lipoproteins 
B)  A molecule involved in lipid transport 
C)  A molecule that binds to Aβ 
D)  A molecule that triggers the accumulation of the tau protein 
E)  A molecule that triggers microglia accumulation
F) A molecule that is part of the γ-secretase complex 
A)  A component of high-density lipoproteins 
B)  A molecule involved in lipid transport 
C)  A molecule that binds to Aβ 
D)  A molecule that triggers the accumulation of the tau protein 
E)  A molecule that triggers microglia accumulation
F) A molecule that is part of the γ-secretase complex

Question 13

In the 1990s, drug users started developing Parkinson's like symptoms. It was found that a contaminant, called MPTP, was in an opioid-like drug. How does MPTP cause Parkinson's like symptoms?

Accepted Answer

A)  MPP+ inhibits mitochondrial function in dopaminergic neurons. 
B)  MPTP inhibits mitochondrial function in dopaminergic neurons. 
C)  MPTP increases the enzymatic activity of monoamine oxidase with increases the number of free radicals in dopaminergic neurons. 
D)  MPP+ blocks the release in dopamine from dopaminergic neurons, specifically from the substantia nigra. 
A)  MPP+ inhibits mitochondrial function in dopaminergic neurons. 
B)  MPTP inhibits mitochondrial function in dopaminergic neurons. 
C)  MPTP increases the enzymatic activity of monoamine oxidase with increases the number of free radicals in dopaminergic neurons. 
D)  MPP+ blocks the release in dopamine from dopaminergic neurons, specifically from the substantia nigra.

Question 14

What is the link between Down syndrome and familial Alzheimer's disease?

Accepted Answer

A)  The APP gene is located on Chromosome 21, which has an extra copy in Down syndrome. 
B)  The APP gene is located on Chromosome 14, which is the duplicated chromosome in Down syndrome. 
C)  The presenilin 1 and 2 gene is located on Chromosome 21, which is the duplicated chromosome in Down syndrome. 
D)  The presenilin 1 and 2 gene is located on Chromosome 14, which is the duplicated chromosome in Down syndrome. 
A)  The APP gene is located on Chromosome 21, which has an extra copy in Down syndrome. 
B)  The APP gene is located on Chromosome 14, which is the duplicated chromosome in Down syndrome. 
C)  The presenilin 1 and 2 gene is located on Chromosome 21, which is the duplicated chromosome in Down syndrome. 
D)  The presenilin 1 and 2 gene is located on Chromosome 14, which is the duplicated chromosome in Down syndrome.

Question 15

Match between columns
                        Premises: Prion disease
Huntington's disease
Alzheimer’s disease
Amyotrophic lateral sclerosis
Parkinson’s disease

Accepted Answer

The Answer of APP and polyQ repeats and motor neuron is...

Question 16

Figureshows several molecules that have been targeted for Alzheimer's therapy. Explain the rational for targeting each molecule:   Figure Q11-9
A. α-secretase
B. Microglia
C. ApoE

Accepted Answer

α-secretase cleaves the APP protein in t

Question 17

Both Prp+/+ and Prp-/- mice were inoculated intracerebrally with prions. Which mice developed symptoms of prion disease and why?

Accepted Answer

The Prp^+/+ mice (wild type) developed sympt

Question 18

How is the Aβ protein produced? Include the name of the precursor protein.

Accepted Answer

A)  The APP protein is cleaved by α-secretase, which is then cleaved by β-secretase. 
B)  The APP protein is cleaved by β-secretase and then by α-secretase. 
C)  The APP protein is cleaved by α-secretase and then γ-secretase. 
D)  The APP protein is cleaved by β-secretase and then γ-secretase. 
A)  The APP protein is cleaved by α-secretase, which is then cleaved by β-secretase. 
B)  The APP protein is cleaved by β-secretase and then by α-secretase. 
C)  The APP protein is cleaved by α-secretase and then γ-secretase. 
D)  The APP protein is cleaved by β-secretase and then γ-secretase.

Question 19

The text lists three treatments for Parkinson's disease: l-dopa administration, deep brain stimulation, and cell-replacement therapy. Choose one of these and discuss the theory behind how it works and the limitations of its success and effectiveness.

Accepted Answer

l-dopa is the precursor to dopamine. Dop

Question 20

What does this tell you about the relation between these two gene products?

Accepted Answer

A)  They are in independent pathways. 
B)  Parkin is downstream of Pink1. 
C)  Pink1 is downstream of Parkin. 
D)  Both gene products act on a common target. 
A)  They are in independent pathways. 
B)  Parkin is downstream of Pink1. 
C)  Pink1 is downstream of Parkin. 
D)  Both gene products act on a common target.

What is the difference between barbiturates and benzodiazepines?

To better understand how MeCP2 regulates neuronal function, a mouse model was generated in which the Mecp2 gene was knocked out. The abnormal phenotype of this mouse could be rescued by conditional expression of MeCP2 in young mice. Why is this an important finding? Select all that apply.

What are presenilins?

Why has it been difficult to develop effective drugs for psychiatric disorders? Neurodevelopmental Disorders

If α-synuclein knock-out mice and mice with normal α-synuclein were injected with α-synuclein in the substantia nigra, which mice would develop symptoms of Parkinson's disease and why?

One protein implicated in intellectual disability (ID) is oligophrenin. How does this protein influence neurons during development? Choose all that apply.

Activation of type 1 mGluRs induces LTD through protein translation. What do you predict would happen to LTD if you could selectively increase PP2A phosphatase that regulates FMRP phosphorylation?

Pink1 and Parkin mutant flies both die prematurely, have degeneration of dopamine neurons, and have mitochondria with abnormal morphology and function. What happened when Parkin was overexpressed in Pink1 mutant flies?

Why is Rett syndrome found only in human females?

What is ApoE? Select all that apply.

In the 1990s, drug users started developing Parkinson's like symptoms. It was found that a contaminant, called MPTP, was in an opioid-like drug. How does MPTP cause Parkinson's like symptoms?

What is the link between Down syndrome and familial Alzheimer's disease?

Figureshows several molecules that have been targeted for Alzheimer's therapy. Explain the rational for targeting each molecule: Figure Q11-9 A. α-secretase B. Microglia C. ApoE

Both Prp^+/+ and Prp^-^/^- mice were inoculated intracerebrally with prions. Which mice developed symptoms of prion disease and why?

How is the Aβ protein produced? Include the name of the precursor protein.

The text lists three treatments for Parkinson's disease: l-dopa administration, deep brain stimulation, and cell-replacement therapy. Choose one of these and discuss the theory behind how it works and the limitations of its success and effectiveness.

What does this tell you about the relation between these two gene products?

An Invitation to Neurobiology

Signaling Within Neurons

Signaling Across Synapses

Vision

Wiring of the Visual System

Olfaction, Taste, Audition, and Somatosensation

Wiring of the Nervous System

Motor and Regulatory Systems

Sexual Behavior

Memory, Learning, and Synaptic Plasticity

Evolution of the Nervous System

Ways of Exploring

Filters

Exam 11: Brain Disorders

What is the difference between barbiturates and benzodiazepines?

To better understand how MeCP2 regulates neuronal function, a mouse model was generated in which the Mecp2 gene was knocked out. The abnormal phenotype of this mouse could be rescued by conditional expression of MeCP2 in young mice. Why is this an important finding? Select all that apply.

What are presenilins?

Why has it been difficult to develop effective drugs for psychiatric disorders? Neurodevelopmental Disorders

If α-synuclein knock-out mice and mice with normal α-synuclein were injected with α-synuclein in the substantia nigra, which mice would develop symptoms of Parkinson's disease and why?

One protein implicated in intellectual disability (ID) is oligophrenin. How does this protein influence neurons during development? Choose all that apply.

Activation of type 1 mGluRs induces LTD through protein translation. What do you predict would happen to LTD if you could selectively increase PP2A phosphatase that regulates FMRP phosphorylation?

Pink1 and Parkin mutant flies both die prematurely, have degeneration of dopamine neurons, and have mitochondria with abnormal morphology and function. What happened when Parkin was overexpressed in Pink1 mutant flies?

Why is Rett syndrome found only in human females?

What is ApoE? Select all that apply.

In the 1990s, drug users started developing Parkinson's like symptoms. It was found that a contaminant, called MPTP, was in an opioid-like drug. How does MPTP cause Parkinson's like symptoms?

What is the link between Down syndrome and familial Alzheimer's disease?

Figureshows several molecules that have been targeted for Alzheimer's therapy. Explain the rational for targeting each molecule: Figure Q11-9 A. α-secretase B. Microglia C. ApoE

Both Prp+/+ and Prp-/- mice were inoculated intracerebrally with prions. Which mice developed symptoms of prion disease and why?

How is the Aβ protein produced? Include the name of the precursor protein.

The text lists three treatments for Parkinson's disease: l-dopa administration, deep brain stimulation, and cell-replacement therapy. Choose one of these and discuss the theory behind how it works and the limitations of its success and effectiveness.

What does this tell you about the relation between these two gene products?

An Invitation to Neurobiology

Signaling Within Neurons

Signaling Across Synapses

Vision

Wiring of the Visual System

Olfaction, Taste, Audition, and Somatosensation

Wiring of the Nervous System

Motor and Regulatory Systems

Sexual Behavior

Memory, Learning, and Synaptic Plasticity

Evolution of the Nervous System

Ways of Exploring

Filters

Both Prp^+/+ and Prp^-^/^- mice were inoculated intracerebrally with prions. Which mice developed symptoms of prion disease and why?