SDL-1 Synaptic Transmission I & II Flashcards Preview

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Flashcards in SDL-1 Synaptic Transmission I & II Deck (77):
1

Axodendritic synapses typically convey (inhibitory/excitatory) signals.

Excitatory

2

Axosomatic synapses typically convey (inhibitory/excitatory) signals.

Inhibitory

3

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

Presynaptic inhibition.
Modulates neurotransmitter release

4

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

Presynaptic density

5

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

Postsynaptic density

6

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

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

7

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

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

8

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

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.

9

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

Nerve terminal

10

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

Soma

11

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

True

12

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

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

13

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

Phosphorylation of enzymes

14

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

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.

15

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

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

16

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

Ionotropic

17

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

Metabotropic

18

Nicotinic receptors tend to be (ionotropic/metabotropic).

Ionotropic

19

Muscarinic receptors tend to be (ionotropic/metabotropic).

Metabotropic

20

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

Ionotropic

21

(Ionotropic/Metabotropic) receptors have a longer duration.

Metabotropic

22

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

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

23

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

Depolarization

24

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

Hyperpolarization

25

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

Epilepsy

26

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

Anesthesia; coma

27

What are the four general groups used to classify neurotransmitters?

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

28

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

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

29

Acetylcholine acts on what receptors in the body?

I. Nicotinic
II. Muscarinic

30

Dopamine acts on what receptors in the body?

I. D1
II. D2

31

Norepinephrine acts on what receptors in the body?

I. α receptors
II. β receptors

32

Epinephrine acts on what receptors in the body?

I. α receptors
II. β receptors

33

Histamine acts on what receptors in the body?

I. H1
II. H2

34

Glutamate acts on what receptors in the body?

I. Ionotropic
II. Metabotropic

35

GABAa acts on what receptors in the body?

Ionotropic

36

GABAb acts on what receptors in the body?

Metabotropic

37

What are three examples of opioid peptides?

I. Beta-endorphin
II. Enkephalin
III. Dynorphin

38

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

Tyrosine hydroxylase

39

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

Sympathomimetics

40

The amino acid precursor for catecholamines is ____________.

Tyrosine

41

The amino acid precursor for serotonin and histamine is _____________.

Tryptophan

42

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

Choline

43

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

The uptake and reuptake of choline

44

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

Choline Acetyl Transferase (CAT)

45

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

Acetylcholinesterase (AChE)

46

____________ 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.

Axoaxonal

47

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

Postsynaptic muscle cell

48

The precursor for the amino acid neurotransmitter Glutamate is __________.

Glutamine

49

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).

Reuptaken by an axon and recycled for future use

50

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

Excitatory; depolarization

51

NMDA receptors are (ionotropic/metabotropic) receptors.

Ionotropic

52

NMDA receptors are important in _________ and _________.

Learning and memory

53

NMDA receptors require co-activation by ________ and ________.

Glutamate and glycine

54

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

Non-specific

55

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

Inhibitory; hyperpolarization

56

The amino acid precursor of GABA is __________.

Glutamate

57

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

Ionotropic; opening of Cl- channels

58

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

Metabotropic; opening of K+ channels

59

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

Inhibitory; hyperpolarization

60

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

Opening of Cl- channels

61

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

Retrograde; postsynaptic to presynaptic

62

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

Relaxation of smooth muscle, resulting in vasodilation

63

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

α-bungarotoxin

64

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

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

65

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

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

66

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

Organophosphates

67

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

Atropine

68

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

Baclofen; K+ channels

69

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

Barbiturates; increase the DURATION of Cl- channel openings

70

___________ 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.

Botulinum toxin (used clinically as Botox)

71

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

Cocaine (is a hell of a drug)

72

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

Curare

73

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

Morphine

74

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

Neostigmine

75

_________ functions as an NMDA glutamate receptor blocker.

Phencyclidine (PCP; angel dust)

76

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

Strychnine

77

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

Tricyclic antidepressants (SSRIs, NRIs)