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Neuro-pharmacology > Neuropeptides > Flashcards

Neuropeptides Flashcards

1
Q

Neuropeptides

A

Similar in design and function to many peptide hormones of
pituitary or gastrointestinal systems

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2
Q

Many pituitary and GI hormones are

A

neuroactive and used at
selective sites in the CNS

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3
Q

Far more neuropeptides than

A

classical neurotransmitters

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4
Q

Far more neuropeptides than classical neurotransmitters Over

A

100 identified neuroactive peptides currently identified

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5
Q

Far more neuropeptides than classical neurotransmitters how many families and how many genes

A

At least 10 families, over 90 genes, many responsible for
expression of multiple neuropeptides

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6
Q

Neuroactive peptides derive from

A

proteins

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7
Q

Peptides formed from

A

cleavage of
polypeptides

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8
Q

Specific polypeptide precursors are
termed

A

propeptides or pre-propeptides

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9
Q

Peptides formed from cleavage of
polypeptides inactive proteins that function
exclusively as

A

precursors to peptides

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10
Q

Neuroactive peptides derive from proteins Contain 2 or more

A

amino acids linked
by a peptide bond

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11
Q

Neuroactive peptides derive from proteins Smaller than

A

proteins

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12
Q

Peptide structures * Like proteins, peptides and pre-propeptides
have a

A

specific sequence of amino acids

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13
Q

Like proteins, peptides and pre-propeptides
have a specific sequence of amino acids

A
  • N- and C-terminus
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14
Q

Peptides with similar structure often have very

A

different functions

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15
Q

Jellyfish, hydras, and corals often use

A

e peptides
rather than classical neurotransmitters

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16
Q

Peptides are

A

Phylogenetically old

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17
Q

Peptides are synthesized as

A

s polypeptide
precursors, generally at least 90 amino acids

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18
Q

Peptide synthesis Same general process as

A

protein biosynthesis

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19
Q

Peptide synthesis Occurs only in

A

cell body

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20
Q

Metabolism to active peptide is

A

tissue specific

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21
Q

Metabolism to active peptide is tissue specific Most precursors are

A

expressed in more than
one tissue and the processing is yields tissue
specific peptide

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22
Q

Pre-propeptides typically contain a series of

A

hydrophobic amino acids at the N-terminus

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23
Q

Pre-propeptides typically contain a series of
hydrophobic amino acids at the N-terminus signaling

A

sequence targets the transcribed
polypeptide to the endoplasmic reticulum

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24
Q

In the ER the signal sequence is

A

s cleaved by a
signal peptidase

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25
Q
  • Cleavage of the signal sequence produces
    an
A

inactive propeptide

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26
Q

Propeptides are packaged into

A

large densecore vesicles (LDCV) for transport to the
nerve terminal

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27
Q

Propeptide cleavage to active peptide Pro-opiomelanocortin (POMC) gene
produces a propeptide for

A
  1. α-, β-, and γ- (MSH)
  2. adrenocorticotropic hormone (ACTH)
  3. β-endorphins
  4. β- and γ-lipoproteins (LPH)
  5. Corticotropin-like intermediate peptide
    (CLIP)
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28
Q

Propeptide cleavage to
active peptides occurs
inside

A

trafficking vesicles by
synthesizing peptidases.

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29
Q

Signal peptidases (ER)

A

Cleave signal sequence from pre-propeptide to generate
propeptide

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30
Q

Synthesizing peptidases (LDCV)

A

Cleave propeptides to generate neuroactive peptides

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31
Q

Catabolic peptidases (extracellular)

A
  • Cleave active peptides to inactivate signalling
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32
Q

Exopeptidases

A

cleave single amino acid residues from either end of a peptide

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33
Q

Endopeptidases

A

cleave peptides within the sequence of the peptide

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34
Q

Catabolic peptidases are typically

A

exopeptidases
Signalling

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35
Q

synthesizing peptidases are typically

A

endopeptidases

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36
Q

Neurotransmitter Synthesized in

A

n the nerve terminal

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37
Q

Neurotransmitter Synthetic machinery transported to

A

nerve terminal from
soma

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38
Q

Neurotransmitter Released from small

A

synaptic vesicles by exocytosis

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39
Q

Neurotransmitter Released from small synaptic vesicles by exocytosis Closely coupled to

A

Ca2+
-channels

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40
Q

Neurotransmitter Released from small synaptic vesicles by exocytosis Relatively low

A

Ca2+
-sensitivity

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41
Q

Neurotransmitter Released from small synaptic vesicles by exocytosis Ca2+ from

A

external sources

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42
Q

Neurotransmitter Recycled at the

A

nerve terminal

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43
Q

Neurotransmitter High concentrations at

A

nerve terminal

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44
Q

Neurotransmitter High concentrations at nerve terminal

A

Receptors respond to relatively high concentrations of
NT

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45
Q

Neurotransmitter * Release occurs at

A

synapse

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46
Q

Neuropeptide Synthesized only in the

A

cell body

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47
Q

Neuropeptide Synthesized only in the cell body

A

Propeptides transported to nerve terminal from soma

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48
Q

Neuropeptide Released from

A

LDCV by exocytosis

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49
Q

Neuropeptide Released from LDCV by exocytosis Distant from sites of

A

Ca2+
-entry

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50
Q

Neuropeptide Released from LDCV by exocytosis Highly sensitive to

A

Ca2+

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51
Q

Neuropeptide Released from LDCV by exocytosis Ca2+ from

A

internal or external sources

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52
Q

Neuropeptides Degraded after

A

release

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53
Q

Neuropeptide Low concentrations at

A

nerve terminal

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54
Q

Neuropeptide Low concentrations at nerve terminal

A
  • Receptors respond to relatively low concentrations of
    neuropeptides
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55
Q

Neuropeptide Release can be

A

extrasynaptic

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56
Q
  • Neuropeptides are proposed to function as
A

modulators of classic
neurotransmitter systems

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57
Q
  • Neuropeptide release can
A

strengthen or prolong actions of primary
neurotransmitters

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58
Q

Correspondingly, most neuropeptide receptors are

A

G-protein coupled
receptors

59
Q

Neuropeptides are proposed to function as modulators of classic
neurotransmitter systems
There are more receptors than

A

peptides

60
Q

Neuropeptide Receptors are often found at sites

A

distal to synapses

61
Q

Neuropeptide functions Neuropeptides may act at many sites Direct action on

A

postsynaptic cell

62
Q

Neuropeptide functions Neuropeptides may act at many sites Presynaptic sites on the

A

releasing cell (autocrine function)

63
Q

Neuropeptide functions Neuropeptides may act at many sites * On adjacent cells

A

(juxtacrine functions)

64
Q

Neuropeptide functions Neuropeptides may act at many sites On close cells

A

(paracrine effects)

65
Q

Neuropeptide functions Neuropeptides may act at many sites At distant sites requiring transport through circulatory
system

A

(endocrine effects)

66
Q

Neuroactive peptides Tachykinin peptides

A

Substance P, neurokinins, neuromedins, neuropeptides K & γ

67
Q

Neuroactive peptides Cholecystokinin peptides

A

CCK & Gastrins

68
Q

Neuroactive peptides Cocaine- and amphetamine regulated transcript

A

(CART)

69
Q

Neuroactive peptides Orexigenic peptides

A

Neuropeptide Y, ghrelin, orexin

70
Q

Neuroactive peptides Oxytocin / vasopressin

A

same

71
Q

Tachykinin Peptides – Substance P

A

One of the earliest neuroactive peptides
identified intestinal contractions

72
Q

Tachykinin Peptides – Substance P Identified as an

A

11-amino acid peptide

73
Q

Tachykinin family has at least

A

7 peptides

74
Q

Tachykinin genes Two pre-protachykinin genes express
all known tachykinin peptides

A

TAC1, TAC3

75
Q

TAC1

A

Substance P, neurokinin A, neuropeptide
K, neuropeptide γ

76
Q
  • TAC3
A

Neuromedin K, neurokinin B

77
Q

Three mammalian tachykinin
receptors

A

NK1
* NK2
* NK3

78
Q

All are GPCR that signal through

A

Gq

79
Q

All are GPCR that signal through
Gq

A
  • PLC → IP3 and DAG → Ca2+
    release and PKC activation
80
Q

Nociception

A

Substance P is
involved in pain
transmission at the
level of the spinal cord – involved in pain
sensitization.

81
Q

Substance P and pain

A
  • Substance P is used in nociception
82
Q

Substance P is co-released from

A

glutamatergic sensory afferents

83
Q

Substance P is used in nociception Transmission of information from

A

damaged tissues to peripheral nerves

84
Q

Substance P is used in nociception Regulates sensitization of

A

pain fibers (C fibers)

85
Q

Substance P is used in nociception Proposed to be involved in

A

fibromyalgia and neuropathic pain

86
Q

NK2 and NK3 agonists reduce the

A

response threshold for noxious stimuli

87
Q

Antagonists for NK1 and NK2 are being explored as possible targets for

A

analgesic drugs

88
Q

Capsaicin

A

Active component of chili
peppers Produces intense burning
sensation on contact with
tissues

89
Q

Capsaicin Analgesic effect in

A

topical
application

90
Q

Capsaicin Analgesic effect in topical
application

A

Depletes Substance P

91
Q

Substance P in the vomit center

A
  • The chemoreceptor trigger zone (CTZ)
    of the area postrema (medulla)
    senses toxins in the bloodstream
92
Q

The chemoreceptor trigger zone (CTZ)
of the area postrema (medulla)
senses toxins in the bloodstream
BBB

A

BBB permeable area

93
Q

The chemoreceptor trigger zone (CTZ)
of the area postrema (medulla)
senses toxins in the bloodstream Also detects excess

A

5HT from the gut via
5HT3 channels

94
Q

The tachykinin receptor NK1 is
expressed in late,

A

convergent steps of
the vomit pathway

95
Q

Substance P release in the CTZ is a

A

final triggering step of the vomit reflex

96
Q

Apripitant is an

A

n NK1 substance P
antagonist used as an anti-emetic for
chemotherapy and post-operative
nausea

97
Q

Tachykinins in psychiatric disease

A
  • Pharmaceuticals affecting the tachykinin receptors are being explored in
    psychiatric diseases and suggest a role for tachykinins in depression,
    Schizophrenia, anxiety, and addictions
98
Q

NK1 antagonists have

A

antidepressant effects in animal models

99
Q

NK1 knockout mice show

A

decreased voluntary alcohol consumption

100
Q

NK1
antagonists decreased

A

alcohol cravings in preclinical trials of detoxified
alcoholic inpatient

101
Q

NK2 antagonists have

A

anxiolytic and antidepressant effects in animal models

102
Q

NK3 antagonists have

A

antipsychotic effects in clinical trials (with very limited
side effects)

103
Q

CCK Family peptides Cholecystokinin (CCK) family includes CCK
and gastrins Derived from two pre

A

pre
-proCCK, pre
-proGastrin
genes

104
Q

CCK Family peptides Gastrointestinal peptide hormones that

A

normally triggers digestion of fat and protein

105
Q

CCK Gastrointestinal peptide hormones that
normally triggers digestion of fat and protein

A

Triggers release of digestive enzymes and bile
from the pancreas and gallbladder,
respectively

106
Q

CCK Family peptides Acts as a

A

a hunger suppressant in response to
presence of fat/protein rich foods

107
Q

CCK Family in the CNS CCK peptides are a family designated based on the

A

length in amino acids

108
Q

CCK Family in the CNS CCK peptides commonly found in the CNS

A

CCK4, CCK8, CCK22, CCK33, CCK58

109
Q

CCK receptors are widely expressed in the

A

CNS

110
Q
  • Administration of CCK into systemic circulation triggers
A

nausea and emesis,
as well as satiety

111
Q

Administration of CCK into systemic circulation triggers nausea and emesis,
as well as satiety Thought to act through the

A

vagus nerve as circulating peptides are generally
unable to cross the BBB

112
Q

CCKR polymorphisms are associated with

A

panic disorder and
schizophrenia

113
Q

CCK4 and anxiety CCK4 administration is used as a model of

A

anxiety

114
Q
  • IV administration of CCK4
A

induces anxiety and panic attacks

115
Q

CCK4* Can be used to test

A

anxiolytic drugs in healthy volunteers

116
Q

CCK4 Administration of peptides into systemic circulation elicits very

A

transient effects as the peptides are rapidly metabolised

117
Q

CCK plays some role in

A

nociception

118
Q

CCK may play an important role in

A

anxiety disorders

119
Q

CCK and benzodiazepines

A

CCK receptor antagonists share structure and affinity with
benzodiazepines

120
Q

Chronic benzodiazepine treatment decreases neural
responsiveness to

A

CCK

121
Q
  • CCK receptor density is upregulated during
A

g benzodiazepine
withdrawal

122
Q

CCK receptor density is upregulated during benzodiazepine
withdrawal esp

A

hippocampus and frontal cortex

123
Q
  • CCK receptor antagonists produce
A

anxiolytic effects in animal
models

124
Q

Proglumide

A

is a CCKA and CCKB antagonist used to treat stomach
ulcers

125
Q

Anxiolytic in

A

CCK receptor antagonists

126
Q

CCK receptor antagonists produce Increases the analgesic effect of

A

opioids and decreases the development of
opioid analgesic tolerance in humans

127
Q

CCK receptor antagonists Prevents the development of

A

analgesic tolerance to other pain treatments
e.g. transcutaneous electrical nerve stimulation (animal models)

128
Q

CCK and the ‘nocebo’ effect

A

CCK receptor antagonists (proglumide) blocked the hyperalgesia of verbally induced nocebo but
not the HPA axis activity

129
Q

CCK receptor antagonists (proglumide) blocked the hyperalgesia of verbally induced nocebo but
not the HPA axis activity

A

Suggests CCK affects nocebo independent or downstream of anxiety

130
Q

Diazepam treatment reduces both

A

hyperalgesia and HPA axis activity suggesting anxiety
contributes to the nocebo effect

131
Q

Research models of the nocebo in healthy volunteers uses

A

verbally induced nocebo hyperalgesia
(increased sensitivity to pain on expectancy)

132
Q

Research models of the nocebo in healthy volunteers uses verbally induced nocebo hyperalgesia
(increased sensitivity to pain on expectancy) Decreased pain threshold is associated with

A

increased activation of the HPA axis (stress response leading to
cortisol release)

133
Q

Cocaine- and amphetamine-regulated
transcript (CART)

A
  • Endogenous psychostimulant and anorexic peptide
134
Q

(CART) Upregulated by

A

cocaine or amphetamine

135
Q

(CART May be responsible for some

A

central effects of psychostimulants

136
Q
  • CART alone induces _____ but co-administration with
A

locomotor hyperactivity BUT co-administration with
cocaine inhibits motor hyperactivity

137
Q

CART expression is modified by

A

alcohol, nicotine, opioids

138
Q

CART administration prevents

A

reinstatement of abuse (animal models)

139
Q

(CART) Highly expressed in the

A

hypothalamus

140
Q

(CART) Inhibits known

A

orexigenic pathway

141
Q

CART signals downstream of

A

5HT in supressing appetite in the
hypothalamus

142
Q

Deficits in CART expression have been associated with

A

binge eating

143
Q
  • Treatments for binge-eating (rimonabant) increase
A

CART expression

Neuro-pharmacology (26 decks)

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