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
Describe nociception
Substance P is involved in pain transmission at the level of the spinal cord – involved in pain sensitization.
26
Describe the link between Substance P and pain
* 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
Describe capsaicin
* Active component of chili peppers * Produces intense burning sensation on contact with tissues * Analgesic effect in topical application * Depletes Substance P
28
Describe Substance P in the vomit centre
* 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
Describe role of tachykinins in psych. disease
* 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
Describe CCK peptides
* 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
Describe CCK expression
widely expressed in the CNS
32
Describe effects of CCK administration
nausea and emesis, satiety
33
Describe the proposed method of CCK function
act through the vagus nerve as circulating peptides are generally unable to cross the BBB
34
Describe the role of CCK in abnormal behaviour
CCKR polymorphisms are associated with panic disorder and schizophrenia
35
Describe CCK antagonist similarity with benzos
* CCK receptor antagonists share structure and affinity with benzodiazepine
36
Describe effects of benzodiazepine treatment on CCK
* Chronic benzodiazepine treatment decreases neural responsiveness to CCK
37
Describe effects of benzodiazepines withdrawal
* CCK receptor density is upregulated
38
Describe brain regions impacted
Esp. hippocampus and frontal cortex
39
Describe CCK receptor antagonists
* CCK receptor antagonists produce anxiolytic effects in animal models
40
Describe proglumide
* Proglumide is a CCKA and CCKB antagonist used to treat stomach ulcers
41
Describe effects in animal models
* Anxiolytic in animal models
42
Describe effects of opioids and role in tolerance
* 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
What is the nocebo effect?
opposite phenomenon to the placebo effect Expectation of symptom worsening leads to negative outcome
44
What were the results of nocebo research?
Research models of the nocebo in healthy volunteers uses verbally induced nocebo hyperalgesia (increased sensitivity to pain on expectancy)
45
Describe the link between HPA axis and pain
Decreased pain threshold is associated with increased activation of the HPA axis (stress response leading to cortisol release)
46
Describe the role of diazepam
reduces both hyperalgesia and HPA axis activity suggesting anxiety contributes to the nocebo effect
47
Describe the role of proglumide
blocked the hyperalgesia of verbally induced nocebo but not the HPA axis activity
48
Describe CCK and anxiety
Suggests CCK affects nocebo independent or downstream of anxiety
49
What does CART stand for?
Cocaine- and amphetamine-regulated transcript
50
What type of peptide is CART?
Endogenous psychostimulant and anorexic peptide
51
Describe upregulatory agents of CART
cocaine or amphetamine (?*)
52
Describe the proposed functions of CART
some central effects of psychostimulants
53
What are CART's effects when admin. alone?
induces locomotor hyperactivity
54
What are CART's effects when admin. with cocaine?
inhibits motor hyperactivity
55
Where is CART expressed?
* Highly expressed in the hypothalamus
56
Describe modifiers of expression
modified by alcohol, nicotine, opioids
57
Describe the role of CART in addiction
prevents reinstatement of abuse (animal models)
58
Describe CART's role in hunger suppression
Inhibits known orexigenic pathways * CART signals downstream of 5HT in supressing appetite in the hypothalamus
59
What are the effects of CARt deficit
* Deficits in CART expression have been associated with binge eating (animal models) * Treatments for binge-eating (rimonabant) increase CART expression
60
What do synthesizing peptidases do?
* Synthesizing peptidases (LDCV) * Cleave propeptides to generate neuroactive peptides
61
What do catabolic peptidases do?
* Catabolic peptidases (extracellular) * Cleave active peptides to inactivate signalling
62
Describe exopeptidases
Exopeptidases cleave single amino acid residues from either end of a peptide (catabolic)
63
Describe endopeptidases
Endopeptidases cleave peptides within the sequence of the peptide (2 s peptidases)
Psych 478
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