SDL-1 Synaptic Transmission I & II Flashcards

1
Q

Axodendritic synapses typically convey (inhibitory/excitatory) signals.

A

Excitatory

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2
Q

Axosomatic synapses typically convey (inhibitory/excitatory) signals.

A

Inhibitory

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3
Q

Axoaxonic synapses typically convey signals for (presynaptic/postsynaptic) inhibition.

A

Presynaptic inhibition.

Modulates neurotransmitter release

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4
Q

Synaptic vesicles carrying neurotransmitter congregate in the ___________ before release into the synaptic cleft.

A

Presynaptic density

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5
Q

Neurotransmitter receptors congregate in the ______________ following release of neurotransmitter into the synaptic cleft.

A

Postsynaptic density

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6
Q

What are three important attributes of electrical synapses when compared to chemical synapses?

A

I. Electrical synapses use gap junctions
II. Electrical synapses make use of bidirectional communication
III. Electrical synapses are faster than chemical synapses

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7
Q

What are three important attributes of chemical synapses when compared to electrical synapses?

A

I. Chemical synapses use a chemical synapse. Neurotransmitter is released into cleft and then taken up by the postsynaptic cell
II. Chemical synapses use unidirectional communication
III. Chemical synapses are slower than electrical synapses

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8
Q

A chemical needs to meet what four criteria to be considered a neurotransmitter?

A

I. Localization: It is present at the synapse.
II. Release: It is released following an action potential at a nerve terminal.
III. Mimicry: Structure should be able to elicit same response in a post-synaptic cell in a laboratory setting if reproduced artificially.
IV. Inactivation: Chemical should be inactivated by a specific mechanism.

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9
Q

Relatively small neurotransmitter molecules such as acetylcholine and norepinephrine are made in the (soma/nerve terminal).

A

Nerve terminal

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10
Q

Peptide neurotransmitters such as opioid peptides are made in the (soma/nerve terminal).

A

Soma

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11
Q

(T/F) Peptide neurotransmitters are first made in the soma, then transported to the nerve terminal for use.

A

True

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12
Q

What are two ways the body increases neurotransmitter assembly by enzymes?

A

I. Increased synthesis of enzyme molecules responsible for neurotransmitter assembly.
II. Phosphorylation of enzymes molecules used in assembly.

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13
Q

(Phosphorylation of enzymes/Increased synthesis of enzymes) is a faster method of increasing production of neurotransmitters.

A

Phosphorylation of enzymes

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14
Q

What is the purpose of an autoreceptor on a presynaptic cell?

A

Released neurotransmitter may bind to its corresponding autoreceptor on the presynaptic cell, modulating release and uptake of the neurotransmitter. This allows the body to maintain control in how much neurotransmitter is present at a synapse.

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15
Q

In what four ways is the action of a neurotransmitter terminated?

A

I. Extracellular degradative enzymes
II. Specific reuptake proteins
III. Diffusion of neurotransmitter away from synapse
IV. Internalization of ligand-receptor complex

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16
Q

A(n) (ionotropic/metabotropic) receptor is a ligand-gated receptor that acts as an ion channel into the cell upon activation.

A

Ionotropic

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17
Q

A(n) (ionotropic/metabotropic) receptor is a G protein-coupled receptor that elicits its response through secondary mediators upon activation.

A

Metabotropic

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18
Q

Nicotinic receptors tend to be (ionotropic/metabotropic).

A

Ionotropic

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19
Q

Muscarinic receptors tend to be (ionotropic/metabotropic).

A

Metabotropic

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20
Q

(Ionotropic/Metabotropic) receptors tend to elicit their responses faster.

A

Ionotropic

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21
Q

(Ionotropic/Metabotropic) receptors have a longer duration.

A

Metabotropic

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22
Q

(T/F) Excitation and inhibition are largely dependent on the neurotransmitter released at the synapse.

A

False. It is the RECEPTOR that accounts for the difference, never the neurotransmitter.

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23
Q

Excitation consists of (hyperpolarization/depolarization) of the membrane potential.

A

Depolarization

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24
Q

Inhibition consists of (depolarization/hyperpolarization) of the membrane potential.

A

Hyperpolarization

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25
Q

Too much repeated excitation or too little inhibition of a receptor may result in a condition known as _____________.

A

Epilepsy

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26
Q

Too little excitation or too much inhibition of a receptor may result in ____________ or ___________.

A

Anesthesia; coma

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27
Q

What are the four general groups used to classify neurotransmitters?

A

I. Amines (Acetylcholine, Dopamine, Norepinephrine)
II. Amino Acids (Glutamate, GABA, Glycine)
III. Neuropeptides (Opioids)
IV. Gases (Nitric Oxide)

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28
Q

In what ways are peptide neurotransmitters different when compared to classical neurotransmitters such as acetylcholine?

A

I. Peptide neurotransmitter synthesis is directed by mRNA
II. Peptide neurotransmitters usually exist as an inactive precursor first
III. Peptide NTs are made in the soma and transported to the nerve terminal (vs. being synthesized at the nerve terminal)
IV. Peptide NTs become activated during transport by peptidases that cleave them

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29
Q

Acetylcholine acts on what receptors in the body?

A

I. Nicotinic

II. Muscarinic

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30
Q

Dopamine acts on what receptors in the body?

A

I. D1

II. D2

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31
Q

Norepinephrine acts on what receptors in the body?

A

I. α receptors

II. β receptors

32
Q

Epinephrine acts on what receptors in the body?

A

I. α receptors

II. β receptors

33
Q

Histamine acts on what receptors in the body?

A

I. H1

II. H2

34
Q

Glutamate acts on what receptors in the body?

A

I. Ionotropic

II. Metabotropic

35
Q

GABAa acts on what receptors in the body?

A

Ionotropic

36
Q

GABAb acts on what receptors in the body?

A

Metabotropic

37
Q

What are three examples of opioid peptides?

A

I. Beta-endorphin
II. Enkephalin
III. Dynorphin

38
Q

____________ is the enzyme responsible for adding the second hydroxyl (-OH) group to tyrosine, transforming it into a catechol ring.

A

Tyrosine hydroxylase

39
Q

Pharmaceutical agents that mimic the actions of the sympathetic nervous system are referred to as ______________.

A

Sympathomimetics

40
Q

The amino acid precursor for catecholamines is ____________.

A

Tyrosine

41
Q

The amino acid precursor for serotonin and histamine is _____________.

A

Tryptophan

42
Q

The non-amino acid precursor of acetylcholine (ACh) is __________.

A

Choline

43
Q

The rate-limiting step in the synthesis of acetylcholine at the nerve terminal is _______________________.

A

The uptake and reuptake of choline

44
Q

___________ is the biosynthetic enzyme responsible for the synthesis of acetylcholine.

A

Choline Acetyl Transferase (CAT)

45
Q

__________ is the degradative enzyme that acts upon acetylcholine to form an acetyl group and choline, terminating the action of the neurotransmitter.

A

Acetylcholinesterase (AChE)

46
Q

____________ synapses mediate presynaptic inhibition by decreasing the size of the action potential through activation of K+ or Cl- channels in the presynaptic membrane, or by reduction in the opening of Ca2+ channels in the presynaptic terminal.

A

Axoaxonal

47
Q

Nicotinic receptors at a neuromuscular junction are located on the (presynaptic neuron/postsynaptic muscle cell).

A

Postsynaptic muscle cell

48
Q

The precursor for the amino acid neurotransmitter Glutamate is __________.

A

Glutamine

49
Q

After glutamate has completed its function, it is (broken down by an enzyme into smaller functional groups/reuptaken by an axon and recycled for future use).

A

Reuptaken by an axon and recycled for future use

50
Q

Glutamate is considered an (excitatory/inhibitory) neurotransmitter because all of its receptors lead to (hyperpolarization/depolarization).

A

Excitatory; depolarization

51
Q

NMDA receptors are (ionotropic/metabotropic) receptors.

A

Ionotropic

52
Q

NMDA receptors are important in _________ and _________.

A

Learning and memory

53
Q

NMDA receptors require co-activation by ________ and ________.

A

Glutamate and glycine

54
Q

Activation of NMDA receptors results in the opening of (highly specific/non-specific) cation channels.

A

Non-specific

55
Q

GABA is considered an (excitatory/inhibitory) neurotransmitter because all of its receptors lead to (hyperpolarization/depolarization).

A

Inhibitory; hyperpolarization

56
Q

The amino acid precursor of GABA is __________.

A

Glutamate

57
Q

GABAa, a(n) (metabotropic/ionotropic) receptor, results in the opening of (Cl-/K+) channels and subsequent hyperpolarization of the membrane potential.

A

Ionotropic; opening of Cl- channels

58
Q

GABAb, a(n) (metabotropic/ionotropic) receptor, results in the opening of (Cl-/K+) channels and subsequent hyperpolarization of the membrane potential.

A

Metabotropic; opening of K+ channels

59
Q

Glycine is considered an (excitatory/inhibitory) neurotransmitter because all of its receptors lead to (hyperpolarization/depolarization).

A

Inhibitory; hyperpolarization

60
Q

Glycine receptor activation leads to opening of (K+/Cl-) channels and subsequent hyperpolarization.

A

Opening of Cl- channels

61
Q

Nitric oxide acts in a(n) (anterograde/retrograde) manner, moving from (presynaptic/postsynaptic) to (presynaptic/postsynaptic).

A

Retrograde; postsynaptic to presynaptic

62
Q

Nitric oxide’s predominant effect is ___________________, resulting in ______________.

A

Relaxation of smooth muscle, resulting in vasodilation

63
Q

___________ is a toxin that blocks binding of ACh to its nicotinic receptor in the parasympathetic nervous system.

A

α-bungarotoxin

64
Q

_________ are sedatives that increase the FREQUENCY of GABAa (Cl-/K+) channel openings, subsequently hyperpolarizing neurons.

A

Benzodiazepines (e.g. Valium); increase FREQUENCY of Cl- channel openings

65
Q

A(n) __________________ is an example of a drug that inhibits reuptake of neurotransmitter, extending its presence in the synaptic cleft, and prolonging its effect.

A

Selective Serotonin Reuptake Inhibitor (SSRI) (e.g. Zoloft)

66
Q

______________ are chemicals that IRREVERSIBLY bind to and block the effects of AChE, prolonging the effect of ACh in the synaptic cleft.

A

Organophosphates

67
Q

__________ is a muscarinic receptor blocker used clinically to block postganglionic parasympathetics.

A

Atropine

68
Q

_________ is a GABAb agonist used clinically to treat spasticity and some forms of epilepsy by hyperpolarization of neurons through opening of (Cl-/K+) channels.

A

Baclofen; K+ channels

69
Q

_________ are sedatives that increase the DURATION of GABAa (Cl-/K+) channel openings, subsequently hyperpolarizing neurons.

A

Barbiturates; increase the DURATION of Cl- channel openings

70
Q

___________ is a toxin that prevents the release of synaptic vesicles containing neurotransmitters (primarily ACh). May be used clinically for aesthetic reasons under the right supervision.

A

Botulinum toxin (used clinically as Botox)

71
Q

__________ functions by blocking the dopamine transporter (DAT1), a monoamine reuptake transporter, which prolongs the effect of monoamines at nerve synapses.

A

Cocaine (is a hell of a drug)

72
Q

_________ blocks binding of ACh to its nicotinic receptor on skeletal muscles, resulting in muscle relaxation and eventually paralysis in greater doses.

A

Curare

73
Q

________ mimics the action of opioid peptides at their associated receptors to produce analgesia.

A

Morphine

74
Q

________ REVERSIBLY inhibits AChE activity, prolonging the action of ACh in the synaptic cleft.

A

Neostigmine

75
Q

_________ functions as an NMDA glutamate receptor blocker.

A

Phencyclidine (PCP; angel dust)

76
Q

________ functions as a glycine receptor blocker and is an active ingredient in rat poisons.

A

Strychnine

77
Q

________ acts by blocking monoamine reuptake and is used clinically in treatment of depressed individuals.

A

Tricyclic antidepressants (SSRIs, NRIs)