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Psych 478 > Neuropeptides > Flashcards

Neuropeptides Flashcards

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1
Q

What are neuropeptides similar to?

A

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

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2
Q

What are neuropeptides similar to?

A

Many pituitary and GI hormones

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3
Q

Where are neuropeptides’ sites of action?

A

selective sites in the CNS

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4
Q

How are neuropeptides compared to NTs?

A

NP > classical NTs

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5
Q

Describe general neuropeptide characteristics

A
  • Over 100 identified neuroactive peptides currently identified
  • At least 10 families, over 90 genes, many responsible for
    expression of multiple neuropeptides
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6
Q

Describe peptide formation

A

formed from cleavage of
polypeptides

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7
Q

What are the function of inactive peptides?

A

Inactive proteins that function
exclusively as precursors to peptides

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8
Q

What are the common names for precursors?

A

propeptides or pre-propeptides

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9
Q

Describe characteristics of precursors

A
  • Contain 2 or more amino acids linked by a peptide bond
  • Smaller than proteins
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10
Q

What are the shared characteristic between proteins, peptides and pre-propeptides?

A

have a specific sequence of amino acids

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11
Q

What are the terminal names?

A
  • N- and C-terminus
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12
Q

How are peptides synthesized?

A
  • Peptides are synthesized as polypeptide
    precursors
  • Same general process as protein biosynthesis
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13
Q

Where does synthesis occur?

A

only in cell body

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14
Q

describe peptide metabolism

A
  • Metabolism to active peptide is tissue specific
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15
Q

Describe pre-propeptide processing and transport

A
  • Pre-propeptides typically contain a series of hydrophobic amino acids at the N-terminus
  • Signal sequence targets the transcribed polypeptide to the endoplasmic reticulum
  • In the ER the signal sequence is cleaved by a signal peptidase
  • Cleavage of the signal sequence produces an inactive propeptide
  • Propeptides are packaged into large dense- core vesicles (LDCV) for transport to the nerve terminal
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16
Q

Describe prepropeptide cleavage to active peptide

A
  • Pro-opiomelanocortin (POMC) gene
    produces a propeptide for:
  • α-
    , β-, and γ-melanocyte stimulating
    hormones (MSH)
  • adrenocorticotropic hormone (ACTH)
  • β-endorphins
  • β- and γ-lipoproteins (LPH)
  • Corticotropin-like intermediate peptide
    (CLIP)
  • Propeptide cleavage to
    active peptides occurs
    inside trafficking vesicles by
    synthesizing peptidases.
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17
Q

Describe signal peptidases

A
  • Signal peptidases (ER)
  • Cleave signal sequence from pre-propeptide to generate
    propeptide
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18
Q

Describe neurotransmitters

A
  • Synthesized in the nerve terminal
  • Synthetic machinery transported to nerve terminal from
    soma
  • Released from small synaptic vesicles by exocytosis
  • Closely coupled to Ca2+
    -channels
  • Relatively low Ca2+
    -sensitivity
  • Ca2+ from external sources
  • Recycled at the nerve terminal
  • High concentrations at nerve terminal
  • Receptors respond to relatively high concentrations of
    NT
  • Release occurs at synapse
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19
Q

Describe neuropeptides

A
  • Synthesized only in the cell body
  • Propeptides transported to nerve terminal from soma
  • Released from LDCV by exocytosis
  • Distant from sites of Ca2+
    -entry
  • Highly sensitive to Ca2+
  • Ca2+ from internal or external sources
  • Degraded after release
  • Low concentrations at nerve terminal
  • Receptors respond to relatively low concentrations of
    neuropeptides
  • Release can be extrasynaptic
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20
Q

Why do neuropeptides do this?

A
  • Neuropeptides are proposed to function as modulators of classic
    neurotransmitter systems
  • Neuropeptide release can strengthen or prolong actions of primary
    neurotransmitters
  • Correspondingly, most neuropeptide receptors are G-protein coupled
    receptors
  • There are more receptors than peptides (subtypes exist for most
    neuropeptides)
  • Receptors are often found at sites distal to synapses
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21
Q

Describe neuropeptide functions

A
  • Neuropeptides may act at many sites
  • Direct action on postsynaptic cell
  • Presynaptic sites on the releasing cell (autocrine function)
  • On adjacent cells (juxtacrine functions)
  • On close cells (paracrine effects)
  • At distant sites requiring transport through circulatory
    system (endocrine effects)
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22
Q

Describe neuroactive peptides

A
  • Tachykinin peptides
  • Substance P
  • Cholecystokinin peptides
  • CCK & Gastrins
  • Cocaine- and amphetamine regulated transcript (CART)
  • Orexigenic peptides
  • Neuropeptide Y, ghrelin, orexin
  • Oxytocin / vasopressin
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23
Q

Describe Substance P

A
  • One of the earliest neuroactive peptides
    identified
  • 1931 Ulf von Euler and John Gaddum
    identified a tissue extract that caused
    intestinal contraction in an ex vivo
    preparation
  • Named Substance P
  • 1970 Nobel Prize for von Euler
  • Identified as an 11-amino acid peptide in 1971
  • Tachykinin family has at least 7 peptides
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24
Q

Describe tachykinin genes

A
  • Two pre-protachykinin genes express
    all known tachykinin peptides
  • TAC1
  • Substance P
  • All are GPCR that signal through
    Gq
  • PLC → IP3 and DAG → Ca2+
    release and PKC activation
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25
Q

Describe nociception

A

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

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26
Q

Describe the link between Substance P and pain

A
  • Substance P is used in nociception
  • Substance P is co-released from glutamatergic sensory afferents
  • Transmission of information from damaged tissues to peripheral nerves
  • Regulates sensitization of pain fibers (C fibers)
  • Proposed to be involved in fibromyalgia and neuropathic pain
  • NK2 and NK3 agonists reduce the response threshold for noxious stimuli
  • Antagonists for NK1 and NK2 are being explored as possible targets for
    analgesic drugs
27
Q

Describe capsaicin

A
  • Active component of chili
    peppers
  • Produces intense burning
    sensation on contact with
    tissues
  • Analgesic effect in topical
    application
  • Depletes Substance P
28
Q

Describe Substance P in the vomit centre

A
  • The chemoreceptor trigger zone (CTZ)
    of the area postrema (medulla)
    senses toxins in the bloodstream
  • BBB permeable area
  • Also detects excess 5HT from the gut via
    5HT3 channels
  • The tachykinin receptor NK1 is
    expressed in late, convergent steps of
    the vomit pathway
  • Substance P release in the CTZ is a
    final triggering step of the vomit reflex
  • Apripitant is an NK1 substance P
    antagonist used as an anti-emetic for
    chemotherapy and post-operative
    nausea
29
Q

Describe role of tachykinins in psych. 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
  • NK1 antagonists have antidepressant effects in animal models
  • NK1 knockout mice show decreased voluntary alcohol consumption and NK1
    antagonists decreased alcohol cravings in preclinical trials of detoxified
    alcoholic inpatients
  • NK2 antagonists have anxiolytic and antidepressant effects in animal models
  • NK3 antagonists have antipsychotic effects in clinical trials (with very limited
    side effects)
30
Q

Describe CCK peptides

A
  • Cholecystokinin (CCK) family includes CCK
    and gastrins
  • Derived from two pre-proCCK, pre-proGastrin
    genes
  • Gastrointestinal peptide hormones that
    normally triggers digestion of fat and protein
  • Triggers release of digestive enzymes and bile
    from the pancreas and gallbladder,
    respectively
  • Acts as a hunger suppressant in response to
    presence of fat/protein rich foods
31
Q

Describe CCK expression

A

widely expressed in the CNS

32
Q

Describe effects of CCK administration

A

nausea and emesis,
satiety

33
Q

Describe the proposed method of CCK function

A

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

34
Q

Describe the role of CCK in abnormal behaviour

A

CCKR polymorphisms are associated with panic disorder and
schizophrenia

35
Q

Describe CCK antagonist similarity with benzos

A
  • CCK receptor antagonists share structure and affinity with
    benzodiazepine
36
Q

Describe effects of benzodiazepine treatment on CCK

A
  • Chronic benzodiazepine treatment decreases neural
    responsiveness to CCK
37
Q

Describe effects of benzodiazepines withdrawal

A
  • CCK receptor density is upregulated
38
Q

Describe brain regions impacted

A

Esp. hippocampus and frontal cortex

39
Q

Describe CCK receptor antagonists

A
  • CCK receptor antagonists produce anxiolytic effects in animal
    models
40
Q

Describe proglumide

A
  • Proglumide is a CCKA and CCKB antagonist used to treat stomach
    ulcers
41
Q

Describe effects in animal models

A
  • Anxiolytic in animal models
42
Q

Describe effects of opioids and role in tolerance

A
  • Increases the analgesic effect of opioids and decreases the development of
    opioid analgesic tolerance in humans
  • Prevents the development of analgesic tolerance to other pain treatments
    e.g. transcutaneous electrical nerve stimulation (animal models)
43
Q

What is the nocebo effect?

A

opposite phenomenon to the placebo effect

Expectation of symptom worsening leads to negative outcome

44
Q

What were the results of nocebo research?

A

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

45
Q

Describe the link between HPA axis and pain

A

Decreased pain threshold is associated with increased activation of the HPA axis (stress response leading to
cortisol release)

46
Q

Describe the role of diazepam

A

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

47
Q

Describe the role of proglumide

A

blocked the hyperalgesia of verbally induced nocebo but
not the HPA axis activity

48
Q

Describe CCK and anxiety

A

Suggests CCK affects nocebo independent or downstream of anxiety

49
Q

What does CART stand for?

A

Cocaine- and amphetamine-regulated
transcript

50
Q

What type of peptide is CART?

A

Endogenous psychostimulant and anorexic peptide

51
Q

Describe upregulatory agents of CART

A

cocaine or amphetamine (?*)

52
Q

Describe the proposed functions of CART

A

some central effects of psychostimulants

53
Q

What are CART’s effects when admin. alone?

A

induces locomotor hyperactivity

54
Q

What are CART’s effects when admin. with cocaine?

A

inhibits motor hyperactivity

55
Q

Where is CART expressed?

A
  • Highly expressed in the hypothalamus
56
Q

Describe modifiers of expression

A

modified by alcohol, nicotine, opioids

57
Q

Describe the role of CART in addiction

A

prevents reinstatement of abuse (animal models)

58
Q

Describe CART’s role in hunger suppression

A

Inhibits known orexigenic pathways

  • CART signals downstream of 5HT in supressing appetite in the
    hypothalamus
59
Q

What are the effects of CARt deficit

A
  • Deficits in CART expression have been associated with binge eating
    (animal models)
  • Treatments for binge-eating (rimonabant) increase CART expression
60
Q

What do synthesizing peptidases do?

A
  • Synthesizing peptidases (LDCV)
  • Cleave propeptides to generate neuroactive peptides
61
Q

What do catabolic peptidases do?

A
  • Catabolic peptidases (extracellular)
  • Cleave active peptides to inactivate signalling
62
Q

Describe exopeptidases

A

Exopeptidases cleave single amino acid residues from either end of a peptide (catabolic)

63
Q

Describe endopeptidases

A

Endopeptidases cleave peptides within the sequence of the peptide (2 s peptidases)

Psych 478 (28 decks)

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