Ch17 The Molecular And Cellular Biology Complete Test Bank

Chapter 17: The Molecular and Cellular Biology of Synaptic Plasticity

Test Bank

Type: multiple choice question

Title: Chapter 17 - Question 01

1. Long term potentiation is associated with _______ of dendritic spines.

Feedback: Subhead: Structural plasticity: In Vivo Studies on Spine Dynamics

Learning Objective: Explain why measurements of spine volume and dynamics provide an excellent indication of synaptic strength.

Bloom’s Level: 2. Understanding

a. a change in shape

b. shrinkage

c. no change

d. a decrease in number

e. growth

Type: multiple choice question

Title: Chapter 17 - Question 02

2. Long term depression is associated with _______ of dendritic spines.

Feedback: Subhead: Structural plasticity: In Vivo Studies on Spine Dynamics

Learning Objective: Explain why measurements of spine volume and dynamics provide an excellent indication of synaptic strength.

Bloom’s Level: 2. Understanding

a. a change in shape

b. shrinkage

c. no change

d. a decrease in number

e. growth

Type: multiple choice question

Title: Chapter 17 - Question 03

3. In adult mouse hippocampus, synaptic elimination of spines has been shown to be related to microglial cell actions. What is the resultant behavioral result?

Feedback: Subhead: Structural plasticity: In Vivo Studies on Spine Dynamics

Learning Objective: Explain why measurements of spine volume and dynamics provide an excellent indication of synaptic strength.

Bloom’s Level: 3. Applying

a. Learning a novel motor skill task.

b. Shivering motion of entire animal

c. Forgetting of learned contextual fear conditioning task

d. Loss of autonomic system function.

e. Consolidation of lasting motor memories.

Type: multiple choice question

Title: Chapter 17 - Question 04

4. Which was a necessary development to undertake in vivo longitudinal imaging studies of identified spins?

Feedback: Subhead: Structural plasticity: In Vivo Studies on Spine Dynamics

Learning Objective: Describe the experimental evidence that motor learning enhances spine dynamics in the mouse motor cortex.

Bloom’s Level: 3. Applying

a. Whole cell patch clamp

b. Voltage clamp

c. CRISPR cas-9

d. Transcranial two-photon microscopy

e. Transgenic labeling with GFP

Type: multiple choice question

Title: Chapter 17 - Question 05

5. All of the following lead to enduring changes in the efficacy of synaptic transmission except

Feedback: Subhead: Synaptic Protein Turnover and the Transition from Short- to Long-Term Synaptic Plasticity

Learning Objective: Explain what determines enduring changes in the molecular composition of synapses that support long-term changes in the efficacy of synaptic transmission.

Bloom’s Level: 2. Understanding

a. long lifetime of synaptic related proteins that matches duration of plasticity

b. protein traffic into and out of the synapse

c. rates of synthesis and degradation of protein.

d. activity dependent traffic of receptors

e. All processes are strongly activity-dependent.

Type: multiple choice question

Title: Chapter 17 - Question 06

6. Which is found after calcium entry through synaptic NMDA receptors?

Feedback: Subhead: Signaling from Synapses to the Nucleus Activates de Novo Transcription

Learning Objective: Identify the key messenger(s) that integrates synaptic activation, action potential firing, and gene transcription in the nucleus.

Bloom’s Level: 2. Understanding

a. Activation of cell death pathway.

b. Inactivation of CREB activity

c. Activation leading to mitochondrial dysfunction.

d. Induction of cyclic AMP response element binding protein (CREB) activity

e. Inactivation of brain derived neurotrophic factor (BDNF) gene expression.

Type: multiple choice question

Title: Chapter 17 - Question 07

7. Which leads to transcription of immediate early genes (IEGs)?

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how the rapid transcription of IEGs is achieved, on synaptic and neuronal stimulation.

Bloom’s Level: 2. Understanding

a. Paired pulse facilitation.

b. L-LTP

c. S-LTP

d. PTP

e. L-LTD

Type: multiple choice question

Title: Chapter 17 - Question 08

8. How fast does gene expression of immediate early genes (IEGs) occur?

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how the rapid transcription of IEGs is achieved, on synaptic and neuronal stimulation.

Bloom’s Level: 2. Understanding

a. Milliseconds

b. Seconds

c. Minutes

d. Hours

e. Days

Type: multiple choice question

Title: Chapter 17 - Question 09

9. Synaptic activity triggers _______ that relieve the transcriptional repression of IEGS.

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Name two different types of proteins that are encoded by IEGs.

Bloom’s Level: 2. Understanding

a. opening of ion-specific channels

b. cytoskeletal modifications

c. late response genes

d. membrane potential events

e. calcium-regulated signaling events

Type: multiple choice question

Title: Chapter 17 - Question 10

10. Some IEGs encode effector proteins, like _______, that directly regulate synaptic function.

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Name two different types of proteins that are encoded by IEGs.

Bloom’s Level: 2. Understanding

a. CREB

b. Arc/Arg3-1

c. c-fos

d. channel proteins

e. microtubule-associated protein

Type: multiple choice question

Title: Chapter 17 - Question 11

11. BDNF promoter IV is bound to several transcriptional factors that recruit repressor complexes. When calcium influx occurs the transcription factors are turned into

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how BDNF and Arc help regulate synaptic function.

Bloom’s Level: 2. Understanding

a. an inactive transcriptional state

b. dephosphorylated molecules

c. an active transcriptional state.

d. repressors

e. introns

Type: multiple choice question

Title: Chapter 17 - Question 12

12. Which of the following is the technique that allows one to determine which neuronal populations that have been activated by two distinct experiences?

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how BDNF and Arc help regulate synaptic function.

Bloom’s Level: 3. Applying

a. Cellular compartment analysis of temporal activity by fluorescent in sit hybridization (catFISH)

b. In situ hybridization

c. Transcranial two photon microscopy

d. Repetitive photolysis of caged glutamate

e. Paired recordings of unitary IPSC.

Type: multiple choice question

Title: Chapter 17 - Question 13

13. Which of the following leads to the induction and activation of Npas4?

Feedback: Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how BDNF and Arc help regulate synaptic function.

Bloom’s Level: 2. Understanding

a. Repression of transcription complex

b. Release of CREB

c. Activation of Arc

d. Neuronal activity in both excitatory and inhibitory neurons

e. Repression of IEGs

Type: multiple choice question

Title: Chapter 17 - Question 14

14. Neuroepigenetics is

Feedback: Subhead: Neuroepigenetics: Stabilizing Activity-Dependent Transcriptional Changes

Learning Objectives: Define neuroepigenetics.

Bloom’s Level: 2. Understanding

a. Distribution of chromosomes during mitosis in a neuron

b. A persistent modification of the organization of the chromatin without altering the genome sequence in a neuron.

c. Distribution of mutations on the genomic sequence of a neuronal cell

d. Repression of modification of chromatin in a neuron

e. A persistent modification of the proteome in a neuron.

Type: multiple choice question

Title: Chapter 17 - Question 15

15. Synaptic activity dependent calcium signals regulate which of the following epigenetic mechanisms?

Feedback: Subhead: Neuroepigenetics: Stabilizing Activity-Dependent Transcriptional Changes

Learning Objectives: State two canonical epigenetic mechanisms.

Bloom’s Level: 3. Applying

a. Creation and distribution of mutations in a neuron

b. Post-translational modifications of histone proteins and DNA methylation

c. Induction of DNA replication and mitosis in a neuron

d. Repression of promoters and late gene activation

e. RNA splicing and translation

Type: multiple choice question

Title: Chapter 17 - Question 16

16. Evidence for local protein synthesis has been supported from findings of electron microscopic evidence for _______ in distal dendrites of dentate gyrus granule cells.

Feedback: Subhead: Early Evidence for Decentralized Protein Synthesis in Neurons

Learning Objective: Describe the conceptual basis for postulating the existence of decentralized protein synthesis in neurons.

Bloom’s Level: 2. Understanding

a. polyribosomes

b. nuclei

c. vesicles

d. neurofilaments

e. microtubules

Type: multiple choice question

Title: Chapter 17 - Question 17

17. Using in situ hybridization, researchers have detected dendritic mRNAs, such as

Feedback: Subhead: Early Evidence for Decentralized Protein Synthesis in Neurons

Learning Objective: Describe the experimental evidence that local protein synthesis can occur at postsynaptic and presynaptic sites.

Bloom’s Level: 2. Understanding

a. voltage gated K⁺ channels

b. tau

c. IEGs

d. synapsin

e. CaMKII

Type: multiple choice question

Title: Chapter 17 - Question 18

18. Which of the following is involved in targeting mRNA to dendrites and axons?

Feedback: Subhead: mRNA Targeting to Dendrites and Axons

Learning Objective: Explain how mRNAs are targeted to dendrites and axons.

Bloom’s Level: 3. Applying

a. a spliceosome

b. ligases

c. ribonucleoprotein (mRNP) granule

d. IEGs

e. late-response genes

Type: multiple choice question

Title: Chapter 17 - Question 19

19. Since mRNAs appear to not rest but continuously patrol the dendrites, how are they functionally regulated?

Feedback: Subhead: mRNA Targeting to Dendrites and Axons

Learning Objective: Describe some of the molecules that associate to mRNAs to control their targeting and local translation.

Bloom’s Level: 3. Applying

a. They travel in an active state but specific signal molecules located in the dendrites and axons allow them to localize.

b. The mRNA has a signal sequence that directs it to these locations

c. Polysomes are found in the key target areas.

d. They attach to actin and follow them to the dendrites and axons.

e. They travel in a repressed state but synaptic activity releases mRNAs from their translationally repressed state.

Type: multiple choice question

Title: Chapter 17 - Question 20

20. In experiments the use of anysomicin leads to which of the following?

Feedback: Subhead: Postsynaptic Protein Synthesis and Synaptic Plasticity

Learning Objective: Explain how local protein synthesis is involved in maintaining synaptic plasticity.

Bloom’s Level: 3. Applying

a. Induction of both chemical and electrical LTD is blocked

b. There is no effect on phosphorylation of internal proteins

c. Blockage of IEGs produced

d. Inactivity of mGluRs

e. No effect on induction

Type: multiple choice question

Title: Chapter 17 - Question 21

21. Which of the following is involved with depolarization –induced suppression of inhibition (DSI) and long term depression (iLTD)?

Feedback: Subhead: Postsynaptic Protein Synthesis and Synaptic Plasticity

Learning Objectives: Explain what depolarization-induced suppression of inhibition (DSI) and inhibitory long-term depression (iLTD) are.

Bloom’s Level: 2. Understanding

a. Glutaminergic synapses

b. Cholinergic synapses

c. GABAergic synapses

d. Serotoninergic

e. Glycine synapses

Type: multiple choice question

Title: Chapter 17 - Question 22

22. Which will block iLTD?

Feedback: Subhead: Postsynaptic Protein Synthesis and Synaptic Plasticity

Learning Objectives: Explain what depolarization-induced suppression of inhibition (DSI) and inhibitory long-term depression (iLTD) are.

Bloom’s Level: 3. Applying

a. Protein synthesis inhibitor injected into the postsynaptcic cell

b. Antagonist of NMDA receptor

c. Protein synthesis inhibitor injected into the presynaptic cell

d. Antagonist of cholinergic receptor

e. Inhibitor of CaMKII

Type: multiple choice question

Title: Chapter 17 - Question 23

23. What controls the formation of the translation initiation complex?

Feedback: Subhead: Biochemical Mechanisms of Translational Control in Long-Lasting Synaptic Plasticity

Learning Objectives: Name three sensitive points for the regulation of translation initiation by synaptic activity.

Bloom’s Level: 3. Applying

a. Phosphorylation of the eukaryotic initiation factor 2a

b. MTOR signaling and phosphorylation of its downstream translation effectors

c. Phosphorylation of the cytoplasmic polyadenylation element binding protein (CPEB)

d. Phosphorylation of MAPK

e. Methylation of mRNA

Type: multiple choice question

Title: Chapter 17 - Question 24

24. Which of the following controls polyadenylation of dendritic mRNAs?

Feedback: Subhead: Biochemical Mechanisms of Translational Control in Long-Lasting Synaptic Plasticity

Learning Objectives: Name three sensitive points for the regulation of translation initiation by synaptic activity.

Bloom’s Level: 3. Applying

a. Phosphorylation of the cytoplasmic polyadenylation element binding protein (CPEB)

b. MTOR signaling and phosphorylation of its downstream translation effectors

c. Methylation of mRNA

d. Phosphorylation of CREB

e. Eukaryotic initiation factor 2a

Type: multiple choice question

Title: Chapter 17 - Question 25

25. Which of the following is likely to occur following a disruption of FMRP ?

Feedback: Subhead: Biochemical Mechanisms of Translational Control in Long-Lasting Synaptic Plasticity

Learning Objectives: Describe how biochemical signaling cascades couple neurotransmission to protein synthesis regulatory factors.

Bloom’s Level: 3. Applying

a. A decrease in Arc translation

b. Increased amount of constitutive translation and loss of synaptic activity-induced translation

c. An increase in AMPA receptors to the post synaptic membrane leading to potentiation

d. Major changes in NMDA receptor-dependent LTP

e. No major changes in mGluR-dependent LTD

Type: multiple choice question

Title: Chapter 17 - Question 26

26. What is the most likely proteome scenario that synapses need to provide in terms of maintaining L-LTP?

Feedback: Subhead: Degradation of Synaptic Proteins

Learning Objective: Describe the role of protein degradation in maintaining protein homeostasis in relation to synaptic activity.

Bloom’s Level: 3. Applying

a. Increased production of “positive” proteins during synaptic activity

b. Increased degradation of “negative” proteins during rest.

c. Increase in movement of proteosomes toward the dendritic shaft during potentiation.

d. Decreased movement of polyribosomes in potentiated spines during LTP.

e. A coordinated balance between protein synthesis of “positive” proteins and degradation of “negative” proteins.

Type: multiple choice question

Title: Chapter 17 - Question 27

27. During synaptic activity, proteosomes are

Feedback: Subhead: Degradation of Synaptic Proteins

Learning Objective: Describe the role of protein degradation in maintaining protein homeostasis in relation to synaptic activity.

Bloom’s Level: 2. Understanding

a. relocated back to the soma.

b. fused with vesicles that contain molecules to inactivate the enzymes.

c. relocated to the pre-synaptic terminal.

d. relocated from the dendritic shaft into the spine.

e. moving in opposite direction of the polyribosomes.

Type: multiple choice question

Title: Chapter 17 - Question 28

28. Which best describes the relationship between microRNAs (miRNA) and synaptic plasticity?

Feedback: Subhead: MicroRNAs and Synaptic Plasticity

Learning Objective: Describe the role of microRNAs (miRNAs) in regulating local protein synthesis and synaptic plasticity.

Bloom’s Level: 3. Applying

a. miRNA replaces mRNA during synaptic plasticity

b. Portions of the miRNA attach to the mRNA and extend the length of the mRNA

c. miRNA directs translational repression or mRNA degradations depending on the degree of complementarity between the miRNA and the sequences on target mRNAs

d. miRNA carry the sequence for proteins needed to maintain potentiated spines

e. MiRNA regulate local protein degradation.

Type: multiple choice question

Title: Chapter 17 - Question 29

29. MOV10 is located at synapses in the mouse. It is degraded in response to

Feedback: Subhead: MicroRNAs and Synaptic Plasticity

Learning Objective: Describe the role of microRNAs (miRNAs) in regulating local protein synthesis and synaptic plasticity.

Bloom’s Level: 2. Understanding

a. increased transcription of IEGs.

b. decreased AMPA receptor synthesis.

c. resting conditions in the neuron.

d. synaptic activity.

e. increased axonal transport of neurofilaments.

Type: multiple choice question

Title: Chapter 17 - Question 30

30. Which of the following is not a property of a synaptic tag?

Feedback: Subhead: The Identity of the Synaptic Tag

Learning Objective: Describe the main properties that characterize a synaptic tag.

Bloom’s Level: 2. Understanding

a. It lasts for seconds

b. It is protein synthesis independent

c. It is immobile

d. It is set by weak as well as by strong inducing stimulations

e. It allows the tagged synapses to capture the PRPs generated by the strong stimulation of the other synapse of the same neuron.

Type: multiple choice question

Title: Chapter 17 - Question 31

31. Which of the following is support that BDNF and TrkB mRNA might form a local autocrine loop in hippocampal and cortical neurons?

Feedback: Subhead: The Identity of the Synaptic Tag

Learning Objective: Explain why a signaling pathway that links synaptic activity to local translation can be considered a synaptic tag and provide an example.

Bloom’s Level: 2. Understanding

a. They are both found in the soma in hippocampal and cortical neurons

b. They are both found to be transported via fast transport

c. They are both transcribed at similar times.

d. They are both transcribed at similar rates.

e. They are co-localized and they are targeted to the dendrites and locally translated in hippocampal and cortical neurons.

Type: multiple choice question

Title: Chapter 17 - Question 32

32. Which of the following is an example of an inverse synaptic tag?

Feedback: Subhead: Inverse Synaptic Tagging

Learning Objective: Explain what inverse synaptic tagging is, and give an example of it.

Bloom’s Level: 2. Understanding

a. CREB

b. MOV10

c. RISC

d. Arc

e. CPEP

Type: multiple choice question

Title: Chapter 17 - Question 33

33. The transient expression of IEGs in response to neuronal and synaptic activity provides a route for labeling neurons activated by a behavioral task. This is called

Feedback: Subhead: Genetically Tagged Active Neurons

Learning Objective: Explain what activity mapping is and how it can help identifying cell assemblies involved in a memory trace.

Bloom’s Level: 2. Understanding

a. cortical mapping.

b. activity mapping.

c. connectome.

d. in situ hybridization.

e. western blot.

Type: multiple choice question

Title: Chapter 17 - Question 34

34. Which of the following techniques has been essential to better establishing a causal link between neuronal activity, synaptic plasticity, and memory associated behaviors?

Feedback: Subhead: Genetically Tagged Active Neurons

Learning Objective: Explain what activity mapping is and how it can help identifying cell assemblies involved in a memory trace.

Bloom’s Level: 2. Understanding

a. Genetically tag and manipulate neurons

b. Whole cell patch clamp of neurons

c. Knock outs of specific genes

d. In situ hybridization

e. Radioactive tagging of specific molecules

Type: multiple choice question

Title: Chapter 17 - Question 35

35. Which is a reporter gene that is inserted to tag a molecule of interest?

Feedback: Subhead: Genetically Tagged Active Neurons

Learning Objective: Explain what activity mapping is and how it can help identifying cell assemblies involved in a memory trace.

Bloom’s Level: 2. Understanding

a. Arc

b. BDNF

c. CREB

d. CPEP

e. LacZ

Type: multiple choice question

Title: Chapter 17 - Question 36

36. How can researchers provide a time window in experiments trying to link gene expression with a specific time window?

Feedback: Subhead: Genetically Tagged Active Neurons

Learning Objective: Describe the experimental work that showed that learning and memory of a fear conditioning task activate largely the same set of neurons.

Bloom’s Level: 3. Applying

a. Use of promoter for LacZ which encodes B-galactosidase

b. Use of BDNF which then induces release of B-galactosidase

c. Use of doxycycline (DOX) will inhibit the transcription factor iTA

d. Promotion of Arc

e. Use of de-phosphorylated form of FMRP.

Type: multiple choice question

Title: Chapter 17 - Question 37

37. What type of learning was examined in experiments where doxycycline (DOX) was used with TetTag transgenic mice which expressed a LacZ reporter gene which resulted in neurons tagged with B-galactosidase.

Feedback: Subhead: Genetically Tagged Active Neurons

Learning Objective: Describe the experimental work that showed that learning and memory of a fear conditioning task activate largely the same set of neurons.

Bloom’s Level: 3. Applying

a. Fear conditioning task

b. Startle response

c. Visual cues to arm movement

d. Olfactory cues to learn maze

e. Morris water navigation task

Type: multiple choice question

Title: Chapter 17 - Question 38

38. How were researchers able to observe active neurons in experiments in learning where doxycycline (DOX) was used with TetTag transgenic mice?

Feedback: Subhead: Genetically Tagged Active Neurons

Learning Objective: Describe the experimental work that showed that learning and memory of a fear conditioning task activate largely the same set of neurons.

Bloom’s Level: 2. Understanding

a. Antibodies for doxycycline

b. B-galactosidase staining

c. Fluorescent rhodamine beads

d. Nissl stain

e. MAP-2 antibody

Type: multiple choice question

Title: Chapter 17 - Question 39

39. Which of the following processes involves a subset of neurons that are induced to have plastic changes for memory encoding?

Feedback: Subhead: Necessity and Sufficiency of Memory Trace Cells
Learning Objective: Distinguish between the memory allocation and the tag-and-manipulate strategies to investigate the properties of engram cells.

Bloom’s Level: 2. Understanding

a. Synaptic tagging and capture

b. Facilitation at CNS synapses

c. Degradation of proteins at synapses

d. Capture of plasticity related particles

e. Memory allocation

Type: multiple choice question

Title: Chapter 17 - Question 40

40. Which of the following brain structures has been used to examine fear conditioning and increased expression of CREB?

Feedback: Subhead: Necessity and Sufficiency of Memory Trace Cells
Learning Objective: Distinguish between the memory allocation and the tag-and-manipulate strategies to investigate the properties of engram cells.

Bloom’s Level: 1. Remembering

a. Hypothalamus

b. Substantia nigra

c. Lateral amygdala

d. Pineal gland

e. Putamen nucleus

Type: multiple choice question

Title: Chapter 17 - Question 41

41. Associative fear leaning is thought to occur through LTP at cortico-amygdala synaptic connections. To further study the involvement of synaptic plasticity in memory, experiments have used optogenetic stimulation of post synaptic neurons at the time of tone delivery and this results in

Feedback: Subhead: Learning and Memory by Ensembles of Potentiated Synapses

Learning Objective: Discuss how the synaptic plasticity and memory hypothesis differs from the neuron-centric view of memory formation and how it can be experimentally tested.

Bloom’s Level: 3. Applying

a. formation of an artificial fear memory without the need for a foot shock.
b. erasure of a fear memory
c. erasure of an olfactory triggered memory
d. inability for synapses of cortico-amygdala axons to induce LTP
e. inability for synapses of cortico-amygdala axons to induce LTD.

Type: essay/short answer question

Title: Chapter 17 - Question 42

42. Devise an experiment that would show whether or not activity dependent RNA transcription is needed for long term potentiation.

Feedback: Provide a strong tetanic stimulation in the CA3-CA1 synapse in hippocampal slices and determine response when using actinomycin D, which inhibits transcription, and apply prior to LTP induction. Compare these results with a control run when same stimulus is given but not actinomycin D. If LTP is blocked this would support idea that activity dependent RNA transcription is needed for long lasting LTP.

Subhead: Signaling from Synapses to the Nucleus Activates de Novo Transcription

Learning Objective: Explain how activity-dependent RNA transcription supports long-term plasticity.

Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 17 - Question 43

43. Identify different ways that calcium links and integrates synaptic activation, action potential firing, and gene transcription in the nucleus.

Feedback: Calcium can regulate transcription by directly entering the nucleus or indirectly by activating signally pathways. Synaptic NMDA receptor-mediated depolarization and metabotropic glutamate receptors can trigger internal release of calcium stores. Regenerative waves of calcium – induced calcium release travel from synapse to nucleus which will elevate the level of calcium in the nucleus. This then can lead to gene expression.

The way that calcium travels and enters will influence which signaling pathways are activated.

Subhead: Signaling from Synapses to the Nucleus Activates de Novo Transcription

Learning Objective: Identify the key messenger(s) that integrates synaptic activation, action potential firing, and gene transcription in the nucleus.

Bloom’s Level: 3. Applying

Type: essay/short answer question

Title: Chapter 17 - Question 44

44. How is the speed of transcription of immediate early genes (IEGs) possible?

Feedback: The speed of activation is quick since in rest conditions a complex transcriptional machinery is permanently assembled on their promotors and ready to work. It is preassembled and ready to work. At rest this unit is repressed by association of histone deacetylases and a closed chromatin structure.

Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how the rapid transcription of IEGs is achieved, on synaptic and neuronal stimulation.

Bloom’s Level: 3. Applying

Type: essay/short answer question

Title: Chapter 17 - Question 45

45. Describe the two types of proteins that are encoded by IEGS and their function.

Feedback: IEGs encode “DNA binding proteins” which function as transcription factors and regulate the gene expression of late-response genes which will influence long term consolidation of plasticity changes. A second type of molecules encoded by IEGs are “effector proteins” which directly regulate synaptic function.

Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Name two different types of proteins that are encoded by IEGs.

Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 17 - Question 46

46. What is peculiar about the mammalian BDNF gene?

Feedback: It has multiple promoters that drive the expression of a common exon coding the whole BDNF protein.

Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how BDNF and Arc help regulate synaptic function.

Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 17 - Question 47

47. Describe a way that scientists dissect the distinct biological functions of the constitutive versus the activity dependent pool of BDNF protein. What are the expected findings?

Feedback: Using knock-in mice mutant transgenic mice to disrupt the expression of BDNF from promotor IV but not the other promoters. They have similar basal levels of BDNF, but reduced levels of BDNF promoter IV-dependent mRNA transcripts following synaptic stimulation. The mice exhibit a reduction in the strength and number of GABAergic synapses and an impaired inhibitory but not excitatory cortical synaptic transmission.

Subhead: Early Genomic Targets of Synaptic Activity

Learning Objective: Explain how BDNF and Arc help regulate synaptic function.

Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 17 - Question 48

48. How do new proteins become available at post synaptic sites?

Feedback: There is an initial wave of early local synthesis and then a second wave of newly transcribed mRNAs that reaches synapses and is available to be translated on synaptic activation.

Subhead: Postsynaptic Protein Synthesis and Synaptic Plasticity

Learning Objective: Describe the two waves in which new proteins become available at postsynaptic sites.

Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 17 - Question 49

49. Describe how mRNA polyadenylation control regulates translation initiation by synaptic activity.

Feedback: Dormant translationally repressed mRNAs at the post synaptic site have a short polyA tail at rest. Activation of NMDA receptor by synaptic activity leads to CaMKII activation which then leads to phosphorylation of CPEB. This action leads to the extension of the polyA tail of the repressed mRNAs rand this relieves the repression of a subset of dendritic mRNAs.

Subhead: Biochemical Mechanisms of Translational Control in Long-Lasting Synaptic Plasticity

Learning Objectives: Describe how biochemical signaling cascades couple neurotransmission to protein synthesis regulatory factors.

Bloom’s Level: 3. Applying

Type: essay/short answer question

Title: Chapter 17 - Question 50

50. Describe the role of fragile X mental retardation protein (FMRP) in translation dependent synaptic plasticity.

Feedback: When mGluR are stimulated this activates protein phosphatase 2A which leads to the dephosphorylation of FMRP. This process leads to translation of FMRP-bound mRNAs like Arc. Arc will then lead to internalization of AMPA receptors which will increase the likelihood of long term depression, such as seen in mGluR-dependent LTD.

Subhead: Biochemical Mechanisms of Translational Control in Long-Lasting Synaptic Plasticity

Learning Objectives: Describe how biochemical signaling cascades couple neurotransmission to protein synthesis regulatory factors.

Bloom’s Level: 3. Applying

Type: essay/short answer question

Title: Chapter 17 - Question 51

51. Describe how you would examine the mechanism underlying the input specificity that occurs during LTP.

Feedback: By using the “two pathways” LTP experiment, one can examine input specificity. One stimulating electrode is placed on one input to the hippocampal CA1 neuron and a second stimulating electrode is placed on a distinct pathway also to that neuron. This set up allows independent stimulation of each pathway and the determination of occurrence of synaptic plasticity at the CA1 neuron.

Subhead: Synaptic Tagging and Capture

Learning Objective: Explain the basic setup of a two-pathway LTP experiment.

Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 17 - Question 52

52. Explain how the induction of plasticity related products (PRPs) can lead to input specificity of L-LTP.

Feedback: During the induction phase of LTP, strong or weak stimulation creates a local synaptic tag. In addition, a strong stimulation also induces the transcription of plasticity related products (PRPs) in the soma which then are transported throughout the neuron. The weak stimulated synapse can also capture the PRPs. The synaptic tagging and capture model (STC) allows experimenters to make testable predictions in regards to the association and cooperative nature of LTP. If the PRPs become limited, tagged synapses may compete for these molecules.

Subhead: Synaptic Tagging and Capture

Learning Objective: Discuss what is postulated by the synaptic tagging and capture (STC) model, and why the model is so useful to investigators.

Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 17 - Question 53

53. Explain how local autocrine loops might be considered a synaptic tag.

Feedback: BDNF and TrkB mRNAs are co expressed in hippocampal and cortical neurons and are targeted to dendrites for translation. Experimental evidence of this loop has been shown within a single dendritic spine. Glutamate uncaging induces a rapid, NMDA receptor

increase in BDNF and a concomitant TrkB activation in the stimulated spine but not in the neighboring spines. This activated BDNF-TrkB signaling can activate local protein synthesis and act in a self-perpetuating manner. This pathway has the “properties of a synaptic tag.

Subhead: The Identity of the Synaptic Tag

Learning Objective: Explain why a signaling pathway that links synaptic activity to local translation can be considered a synaptic tag and provide an example

Bloom’s Level: 3. Applying

Type: essay/short answer question

Title: Chapter 17 - Question 54

54. List the two experimental models used to investigate the cellular basis of memory.

Feedback: Neuronal activation model and the synaptic plasticity and memory model.

Subhead: The Cellular Basis of Memory

Learning Objective: Discuss the two models that are being experimentally investigated to understand the molecular and cellular basis of memory traces.

Bloom’s Level: 2. Understanding

Type: essay/short answer question

Title: Chapter 17 - Question 55

55. Design an experimental procedure that would allow you to determine if learning and memory were carried out by the same set of neurons.

Feedback: You would use a line of TetTag transgenic mice that are able to express a reporter gene, Lac Z (encoding for B-galactosidase which labels the cell) due to the placement of promoter sequences. When the neurons are stimulated with electrical activity the c-fos promoter drives the transcription of iTA which binds to TetO DNA sequence and activates transcription of LacZ reporter. ITA is inhibited by doxycycline (DOX). You can then raise mice in their home cage on a DOX diet that blocks reporter gene activity and there will be no labeling during this time period. When DOX is removed the mice are moved to a new home where they receive a foot shock which is known to activate a series of neuron circuits related to fear conditioning. This learning will lead to mice with neurons expressing the Lac-Z gene and tagged by B-galactosidase. After this the mice are placed back into their home cage on the Dox diet. In a few days the mice are moved back to the foot shock chamber and tested for fear memory of the task. When examined these mice had IEG which was labeled using antibodies for IEG. Neurons identified during the task (B-galactosidase positive) were reactivated during its recall (double positive for B-galactosidase and antibody for IEG). This shows learning a task and its retrieval activate roughly the same set of neurons. behavioral expression of the fear memory.
Subhead: Genetically Tagged Active Neurons

Learning Objective: Describe the experimental work that showed that learning and memory of a fear conditioning task activate largely the same set of neurons.

Bloom’s Level: 4. Analyzing

Type: essay/short answer question

Title: Chapter 17 - Question 56

56. Design an experiment to show how PTSD patients may be treated in the future by erasing memories.

Feedback: Determination of molecules that are expressed during memory formation is key to understanding how memories are formed but also important for erasing those memories when they are doing clinical harm. To understand how cells can be located for this erasure, transgenic mice are developed to express diphtheria toxin receptors in neurons in which high levels of CREB are induced. When mice are given the toxin it will selectively kill active high-CREB neurons. These mice can be tested for expression of the fear memory to see if there is causal link between the activation of a specific set of neurons and a fear memory.

Subhead: Necessity and Sufficiency of Memory Trace Cells
Learning Objective: Explain how experimental approaches can cause specific memories to be erased or recalled in mice

Bloom’s Level: 3. Applying