Chapter 3 Workbook Questions Flashcards

1
Q

What events occur in the presynaptic terminal when an action potential reaches the presynaptic terminal?

A

The membrane of the presynaptic terminal depolarizes; voltage-gated calcium ion (Ca+2) channels open; Ca+2 influxes into the nerve terminal; synaptic vesicles move toward a release site in the membrane, fuse with the membrane, then rupture to release a neurotransmitter into the synaptic cleft.

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2
Q

How does the binding of a neurotransmitter to a receptor result in the opening of a ligand-gated ion channel?

A

The associated membrane channel changes shape, allowing it to open

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3
Q

What is a postsynaptic potential?

A

local change in ion concentration across the postsynaptic membrane.

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4
Q

What is an excitatory postsynaptic potential (EPSP)?

A

local depolarization of a postsynaptic membrane from an influx of positively charged ions (Na and Ca)

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5
Q

What is an inhibitory postsynaptic potential (IPSP)?

A

local hyperpolarization of a postsynaptic membrane from an influx of chloride ion (Cl–) or an efflux of potassium ion (K+).

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6
Q

What happens when acetylcholine (ACh) binds to receptors associated with membrane channels on a muscle cell?

A

When ACh binds to the receptor, Na+ channels open and the influx of Na+ initiates a series of events that produce a mechanical contraction of the muscle cell

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7
Q

What are the three types of synaptic connections between neurons?

A
  1. axoaxonic (communication occurs at axon of postsynaptic neuron)
  2. axodendritic (communication occurs at the dendrites)
  3. axosomatic (communication occurs at cell body)
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8
Q

What is the effect of presynaptic facilitation on the action potential produced by the second axon at an axoaxonic synapse?

A

The action potential is longer in duration, allowing increased Ca+2 into the second synaptic terminal, and more neurotransmitter vesicles than usual move to the cell membrane and rupture. The facilitated neuron releases more transmitter than normal.

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9
Q

How are neurotransmitters removed from the synapse, allowing inactivation of ligand-gated channel receptors?

A

The three mechanisms of receptor inactivation are:

  1. neurotransmitter diffusion away from the synaptic cleft
  2. enzymatic degradation of the neurotransmitter in the synaptic cleft; or
  3. neurotransmitter reuptake by the presynaptic axon terminal.
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10
Q

What is a guanine nucleotide–binding protein (G-protein)–mediated receptor?

A

A receptor that has an associated G-protein. When the receptor is bound by a neurotransmitter, the G-protein is activated and may alter the opening of membrane ion channels or may produce long-lasting changes in the neuron.

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11
Q

What is the first step in the sequence of action in the G protein?

A

Neurotransmitters bind with the receptor.

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12
Q

What is the second step in the sequence of action in the G protein?

A

Receptor protein changes shape.

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13
Q

What is the third step in the sequence of action in the G protein?

A

Alpha (α) chain separates to act as a cytoplasmic shuttle.

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14
Q

What is the fourth step in the sequence of action in the G protein?

A

The α chain activates a target protein.

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15
Q

The second messenger in a second messenger system is a(n):

A. G-protein

B. α chain of the G-protein

C. Enzyme inside the neuron that can trigger responses within the neuron

D. Neurotransmitter

E. Gene

A

C: The G-protein–mediated second-messenger system involves:

(1) binding of a neurotransmitter (first messenger) to a G-protein–associated membrane receptor
(2) activation of an effector enzyme (second messenger)
(3) increased levels of the second second messenger that elicits responses within the neuron.

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16
Q

Second messengers may initiate the:

A. Opening of membrane ion channels

B. Activation of genes, causing increased synthesis of specific cellular products

C. Modulation of Ca+2 levels inside the cell

D. A, B, and C

E. None of the above

A

D: Second messengers activate responses inside the cell. In these cases, a single neurotransmitter might turn on a molecular pathway that ends with a change in gene expression, the opening of ion channels, and/or phosphorylation of a structural protein.

17
Q

Which one of the following can serve as the postsynaptic cell of a synapse?

A. Smooth muscle cell in an artery

B. Hepatocyte in the liver

C. Neuron in the thalamus

D. Muscle cell in the triceps

E. All of the above

A

E: A postsynaptic cell is any cell of an organ, gland, blood vessel, neuron, or muscle cell that synapses with a neuron.

18
Q

ACh receptor subtypes include:

A. Adrenergic and noradrenergic.

B. Nicotinic and muscarinic

C. Alpha and beta

D. Alpha and gamma

E. None of the above

A

B: Receptors that bind ACh fall into two categories: nicotinic and muscarinic. These receptors are distinguished by their ability to bind certain drugs. Nicotine, derived from tobacco, selectively activates the nicotinic receptors. Muscarine, a poison derived from mushrooms, activates only the muscarinic receptors.

19
Q

How does onabotulinumtoxinA (BOTOX) therapeutically produce paresis in overactive muscles?

A. Acts as an antagonist by binding to the ACh receptor on the postsynaptic membrane

B. Rapidly degrades ACh in the synaptic cleft

C. Facilitates the reuptake and sequestration of ACh into the presynaptic cell

D. Disrupts the protein structure of the muscle cell receptor, thus preventing ACh from binding

E. Inhibits the release of ACh from the presynaptic terminal at the neuromuscular junction.

A

E: Botulinum toxin is naturally produced by a family of bacteria and, when ingested, causes widespread paralysis by inhibiting the release of ACh at the neuromuscular junction. When small doses of BOTOX are therapeutically injected directly into an overactive muscle, the inhibition of ACh release reduces or prevents contraction of the injected muscle.

20
Q

N-methyl-D-aspartate (NMDA) receptors

A. Are involved in long-term potentiation

B. Bind glutamate

C. Have been implicated in pathologic changes in the nervous system

D. A, B, and C

E. None of the above

A

D: The ligand-gated ion channels that bind glutamate are alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, and NMDA receptors. The NMDA receptor is unique because glutamate must be bound to the receptor and, simultaneously, the membrane must depolarize to open the ion channel. Thus the NMDA receptor is both voltage and ligand-gated. Activation of an NMDA receptor causes the associated channel to open and close very slowly, resulting in prolonged ionic changes inside the postsynaptic neuron. This produces long-term potentiation (LTP), a prolonged increase in the size of the postsynaptic response to a given stimulus. Abnormal NMDA receptor activity has been implicated in epilepsy, chronic pain, Parkinson’s disease, stroke, and schizophrenia.

21
Q

Myasthenia gravis:

A. Is caused by the destruction of gamma-aminobutyric acid (GABA) receptors on the postsynaptic membrane of muscles

B. Results in the decreased release of ACh at the neuromuscular junction

C. Is an autoimmune disease that destroys ACh receptors on the postsynaptic membrane of muscles, thus interferes with ACh binding for repetitive muscle contractions

D. Is successfully treated with removal of the pituitary gland

E. All of the above

A

C: Myasthenia gravis is an autoimmune disease during which antibodies attack and destroy nicotinic receptors on muscle cells. Normal amounts of ACh are released into the cleft, but few receptors are available for binding, resulting in increasing weakness with repetitive muscle contractions.

22
Q

What local membrane potential is created when a Sodium (Na) channel opens on the postsynaptic membrane?

A

EPSP (Excitatory Postsynaptic Potential)

23
Q

What local membrane potential is created when a Calcium (Ca) channel opens on the postsynaptic membrane?

A

EPSP (Excitatory Postsynaptic Potential)

24
Q

What local membrane potential is created when a Chloride (Cl) channel opens on the postsynaptic membrane?

A

IPSP (Inhibitory Postsynaptic Potential)

25
Q

What local membrane potential is created when a Potassium (K) channel opens on the postsynaptic membrane?

A

IPSP (Inhibitory Postsynaptic Potential)

26
Q

What is the purpose of Neurotransmitters and neuromodulators?

A

chemicals that convey information among neurons

27
Q

Neurotransmitters are released by what type of neuron?

A

released by presynaptic neuron and acts directly on postsynaptic ion channels or activates proteins made inside the postsynaptic neuron

28
Q

Neuromodulators are released into what space?

A

released into extracellular fluid and adjust activity of many neurons.

29
Q

Neurotransmitters that effect the postsynaptic neuron directly are called what?

A

ionotropic

30
Q

Neurotransmitters that effect the postsynaptic neuron indirectly are called what?

A

metabotropic

31
Q

ionotropic neurotransmitters or neurotransmitters that act directly on the postsynaptic neuron are classified as what?

A

fast-acting: effects are extremely short lived (less than 1/1000 of a second)

32
Q

metabotropic neurotransmitters or neurotransmitters that act indirectly on the postsynaptic neuron are classified as what?

A

slow-acting: transmission takes 1/10 of a second to minutes

33
Q

How to slow-acting neurotransmitters regulate fast acting neurotransmitters?

A
  1. control the amount of neurotransmitter released from presynaptic terminal
  2. can influence the actions of fast-acting neurotransmitters on the postsynaptic membrane
34
Q

how long can a neuromodulators effects last?

A

minutes to days: neuromodulators cellular effects may take seconds to be initiated, but the changes they create can last from minutes to days

35
Q

What is the fifth step in the sequence of action in the G protein?

A

Membrane channels open, or intracellular target proteins are activated.