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Behavioral Pharmacology > Chapter 11: Opioids > Flashcards

Chapter 11: Opioids Flashcards

1
Q

abstinence syndrome

A

Condition characterized by unpleasant symptoms when an individual tries to cease drug use; AKA withdrawal

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2
Q

anesthetic

A

General anesthetics are substances that depress the CNS, decreasing all sensations in the body and causing unconsciousness. Local anesthetics do not cause unconsciousness, but prevent pain signals by blocking Na+ channels.

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3
Q

buprenorphine (buprenex)

A

An opioid partial agonist–antagonist used in opioid treatment programs that may be substituted for methadone and yields similar treatment results; high affinity but low efficacy at the mu opioid receptor as well as antagonist activity at the k-receptor, it has weaker opioid effects and is less likely to result in overdose; has a long duration; can lead to respiratory depression and death when combined with CNS depressants

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4
Q

clonidine

A

An α2-adrenergic agonist that stimulates NE autoreceptors and inhibits noradrenergic cell firing. It is used to reduce symptoms of opioid withdrawal; reverses hyperexcitable state to relieve symptoms (chills, tearing, yawning, stomach cramps, sweating, muscle aches).

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5
Q

Cross-dependence

A

Withdrawal signs occurring in a dependent individual can be terminated by administering drugs in the same class.

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6
Q

cross-tolerance

A

Tolerance to a specific drug can reduce the effectiveness of a another drug in the same class.

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7
Q

δ-receptor

A

A type of opioid receptor primarily in the forebrain that may help regulate olfaction, motor integration, reinforcement, and cognitive function.

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8
Q

descending modulatory pathways

A

Bundles of nerve fibers originating at higher brain regions that influence lower brain or spinal cord function. One arises from the PAG in the the midbrain and influences pain signals carried by the spinal cord neurons.

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9
Q

detoxified

A

A drug user undergoing detoxification is considered to be detoxified when signs of the abstinence syndrome end.

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10
Q

endomorphins

A

Group of endogenous opioid peptides in the CNS that selectively bind to the opioid receptor, and eliminate pain.

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11
Q

endorphins

A

Group of endogneous peptides in the brain that stimulate mu and delta opioid receptors, reducing pain and enhancing one’s general mood.

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12
Q

k-receptor

A

An opioid receptor located in the striatum, amygdala, hypothalamus, and pituitary gland that may help regulate pain, perception, gut motility, dysphoria, water balance, hunger, temperature, and neuroendocrine function.

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13
Q

methadone

A

A long-acting opioid drug that may be substituted for other opioids in order to prevent withdrawal symptoms during detox; reduces symptoms to a comfortable level.

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14
Q

methadone maintenance program

A

Most effective treatment program for opioid addicts that involves the substitution of the opioid with methadone to prevent withdrawal symptoms and avoid a relapse.

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15
Q

μ-receptor

A

A subtype of opioid receptor located in the brain and spinal cord that has a high affinity for morphine and certain other opiate drugs.

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16
Q

multidimensional approach

A

Treatment that involves a combination of methods to prevent drug abuse relapse, including detoxification, pharmacological support, and counseling.

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17
Q

narcotic analgesics

A

Class of drugs originally derived from the opium poppy that reduce pain but do not cause unconsciousness. They create a feeling of relaxation and sleep in an individual, but in high doses can cause coma or death.

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18
Q

NOP-R

A

One of the four opioid receptors. It is widely distributed in the CNS and the peripheral nervous system and is activated by the neuropeptide nociceptin/orphanin FQ.

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19
Q

partial agonists

A

Drugs that bind to a receptor but have low efficacy, producing weaker biological effects than a full agonist. Hence they act as agonists at some receptors and antagonists at others, depending on the regional concentration of full agonist. These were previously called mixed agonist-antagonists.

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20
Q

physical dependence

A

Developed need for a drug, such as alcohol or opioids, by the body as a result of prolonged drug use. Termination of drug use will lead to withdrawal symptoms (abstinence).

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21
Q

primers

A

Drug-like effects caused by stress or drug-conditioned stimuli that reinstate drug use after abstinence.

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22
Q

pro-opiomelanocortin (POMC)

A

One of the four large opioid propeptide precursors that are broken down by proteases to form smaller active opioids (endorphins) in the brain.

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23
Q

prodynorphin

A

One of the four large opioid propeptide precursors that are broken down by proteases to form smaller active opioids (dynorphins) in the brain.

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24
Q

proenkephalin

A

One of the four large opioid propeptide precursors that are broken down by proteases to form smaller active opioids (enkephalins) in the brain.

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25
Q

pronociceptin/ orphanin FQ

A

One of the four large opioid propeptide precursors, that is broken down by proteases to form smaller active opioids (nociceptin, orphanin FQ) in the brain.

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26
Q

pure antagonist

A

Drug that produces no pharmacological activity (i.e., no efficacy) and that can prevent or reverse the effects of a drug agonist by occupying the receptor site.

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27
Q

receptor cloning

A

Process used to produce large amounts of identical receptor proteins in a cell line.

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28
Q

sensitization

A

Enhanced response to a particular drug after repeated drug exposure.

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29
Q

spinal interneurons

A

Nerve cells with short axons within the spinal cord.

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30
Q

suraspinal

A

Located above the spinal cord or spine

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31
Q

tolerance

A

Decreased response to a drug as a direct result of repeated drug exposure.

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32
Q

transfection

A

Process used to introduce genetic material into a cell by injecting it with a DNA sequence coding for the desired protein product.

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33
Q

active ingredients of opium

A

morphine, codeine, thebaine, narcotine,

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34
Q

how does codeine differ from morphine?

A

identical except instead of a methoxy (-OCH3) there is a hydroxyl (-OH) group; produces a drug that has less analgesic effects and fewer side effects than morpine

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35
Q

how does heroine differ from morphine?

A

the addition of two acetyl groups; mades it 2-4x more potent when injected and faster acting because the change makes it more lipid soluble –> reaches the brain more quickly

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36
Q

types of opioid receptors

A

μ (mu); δ (delta); κ (kappa); NOP-R

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37
Q

how is morphine usually administered?

A

intramuscularly or orally

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38
Q

how long before opioid metabolites are excreted?

A

most are excreted in the urine within 24 hours

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39
Q

low to moderate doses

A

pain is relieved, respiration is somewhat depressed, pupils are constricted; drowsiness, decreased sensitivity to the environment, impaired ability to concentrate, dreamy sleep, suppressed cough reflex, decreased appetite, drop in body temperature, reduced sex drive

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40
Q

high doses

A

state of euphoria, “rush,” powerful reinforcer, dysphoria, consisting of restlessness and anxiety, nausea, vomiting, effects on chemical trigger zone, unconsciousness, respiratory failure, constipation

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41
Q

binding curve

A

as opioids increase binding also increases and gradually tapers off until the receptors are fully occupied

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42
Q

ileum

A

lowest portion of the small intestine

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43
Q

selectivity

A

a given molecule readily binds to one receptor subtype and has relatively low binding affinity for the others

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44
Q

do opioids bind to NOP-R?

A

no

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45
Q

what brain area of mu receptors plays a role in positive reinforcement?

A

nucleus accumbens

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46
Q

what brain area of mu receptors plays a role in cardiovascular and respiratory depression, cough control, nausea and vomiting?

A

brainstem

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47
Q

what brain area of mu receptors plays a role in sensorimotor integration?

A

thalamus, striatum

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48
Q

what does k receptor have high affinity binding to?

A

ketocyclazocine–an opioid analog that produces hallucinations and dysphoria

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49
Q

what are opioid receptors linked to?

A

the structure of G proteins, which suggest that they mediate metabotrpoic responses

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50
Q

propeptides

A

larger peptides (precursor peptides) that are broken into smaller active opioids; there are four coded for by separate genes

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51
Q

types of propeptides

A

prodynorphin, pro-opiomelanocortin (POMC), proenkephalin, pronociceptin/orphanin FQ

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52
Q

Propeptide production

A

propeptides are manufactured in the soma and must be processed by enzymes (proteases) that are packaged in the Golgi apparatus along with the peptide. These enzymes are responsible for chopping or cleaving the propeptide into individual peptide products that are stored in vesicles and are further processed as they are transported down the axon to be released at the synapse

53
Q

what do each propeptide produce?

A

a number of biologically active opioid and non-opioid peptides

54
Q

where are propeptides found?

A

in the brain, spinal cord, and peripheral autonomic nervous system, concentrated in areas related to pain modulation and mood

55
Q

hypothalamic control of ACTH and B-endorphin release

A
  • neuroendocrine cell bodies in the hypothalamus produce corticotropin releasing factor
  • which is released from axon terminals that synapse on the primary plexus of the portal system. CRF travels via the portal veins to the anterior pituitary
  • hormone producing cells in the anterior pituitary respond to the hypothalamic signals by releasing ACTH and B-endorphin
  • ACHT and B-endorphin travel through the bloodstream and regulate endocrine glands
56
Q

opioids and feeding

A
  • modulate the pleasure or palatability associated with food-related stimuli
  • endogenous opioid signaling and u receptor signaling modify the preference of liking of some foods
  • limbic brain regions appear to be the locus of opioid receptor-mediated effects on food palatability
57
Q

are peptides stored by themselves?

A

no, many are co-localized with other neurotransmitters in the same neuron, including ACH, GABA, 5HT, and other peptides

58
Q

what do peptides do to neurotransmitters?

A

modify the function of neurotransmitter or produce changes in ion conductance and membrane potential

59
Q

are peptides selective?

A

no–show only a relative preference

60
Q

ligands for delta receptors

A

derived from proenkephalin (enkephalins) and dynorphin–> are natural k receptor agonists

61
Q

functions of N/OFQ

A

spinal analgesia, supraspinal pronociception, feeding, learning, motor function, neuroendocrine function

62
Q

NOP-R locations

A

cortex, amygdala, hypothalamus, hippocampus, periaqueductal gray, thalamus, substantia nigra, brain stem, spinal cord

63
Q

Endogenous ligand (prohormone source) for NOP-R

A

nociceptin/ orphanin FQ (pronociceptin/ orphanin FQ)

64
Q

Endogenous ligand (prohormone source) for kappa

A

dynorphins (prodynorphin)

65
Q

Endogenous ligand (prohormone source) for delta

A

enkephalin (proenkephalin), endorphins (POMC)

66
Q

Endogenous ligand (prohormone source) for mu

A

endomorphins (unknown), endorphins (POMC)

67
Q

mu locations

A

thalamus, periaqueductal gray, raphe nuceli, spinal cord, striatum, brain stem, nucleus accumbens, amygdala, hippoampus

68
Q

delta locations

A

neocortex, striatum, olfactory areas, substantia nigra, nucleus accumbens, spinal cord

69
Q

kappa locations

A

pituitary, hypothalamus, amygdala, striatum, nucleus accumbens

70
Q

mu functions

A

analgesia, reinforcement, feeding, cardiovascular and respiratory depression, antitussive, vomiting, sensorimotor integration

71
Q

delta functions

A

analgesia, reinforcement, cognitive function, olfaction, motor integration

72
Q

kappa functions

A

neuroendocrine function, water balance, feeding, temperature control, dysphoria, analgesia

73
Q

two actions of G proteins

A
  1. directly stimulate or inhibit the opening of ion channels

2. stimulate or inhibit enzymes to alter second messenger production

74
Q

what are the overall effects of neuropeptides on a nerve cell?

A

the reduction of membrane excitability and subsequent slowing of cell firing and inhibition of neurotransmitter release

75
Q

do opioids and N/OFQ work on both G protein functions?

A

Yes– they work on both to open potassium (K+) channels, close calcium (Ca2+) channels and inhibit adenylyl cyclase activity

76
Q

how do neuropeptides reduce synaptic transmission?

A
  1. by postsynaptic inhibition
  2. axoaxonic inhibition
  3. presynaptic autoreceptors
77
Q

postsynaptic inhibition

A

opioid and N/OFQ receptor-G protein activation opens K+ channels, which increases K+ conductance. Potassium exits the cell, forced by its concentration gradient, causing hyperpolarization. When the receptors are on the soma or dendrites of neurons, the hyperpolarization decreases the cell’s firing rate

78
Q

axoaxonic inhibition

A

opioid and N/OFQ also produce an inhibitory effect by closing voltage-gate Ca2+ channels. Receptors on the presynaptic terminal activate G proteins, which in turn close the ca2+ channels. Reducing the amount of Ca2+ entering during an action potential proportionately decreases the amount of neurotransmitter released

79
Q

presynaptic autoreceptors

A

opioid autoreceptors also produce inhibatory effects. Somatodendritic autoreceptors hyperpolarize cells in the locus coeruleus by enhancing K+ conductance and subsequently reducing cell firing. Presynaptic autoreceptors reduce the release of co-localized neurotransmitters

80
Q

opioid receptors and cAMP

A

all four receptor types are coupled to inhibitory G proteins that inhibit adenylyl cyclase, which normally synthesizes the second messenger cyclic adenosine monophosphate (cAMP). The reduced cAMP and subsequent decreased function of cAMP-dependent protein kinase may be responsible for ion channel changes

81
Q

what detects pain?

A

nociceptors (detectors of noxious stimuli)

82
Q

nociceptors

A

networks of free nerve endings that are sensitive to intense pressure, extreme temperature including heat and cold, electrical impulses, cuts, chemical irritants, and inflammation

83
Q

what factors can modify pain?

A

strong emotion, environmental stimuli like stress, hypnosis, acupuncture, and opioid drugs

84
Q

first component of pain

A

immediate sensory component and signals the onset of a noxious stimulus

85
Q

second component of pain

A

has a strong emotional component, the unpleasantness of the sensation; less localized and is often accompanied by autonomic responses

86
Q

what contributes to the types of pain?

A

the types of neuron that carry the signal. Adelta are larger in diameter and are myelinated, so they conduct action potentials more rapidly than the thin and unmyelinated C fibers

87
Q

Adelta neuron pathway

A

have their cell bodies in the dorsal root ganglia and terminate in the gray matter of the dorsal horn of the spinal cord, ending on projection neurons that transmit pain signals to higher brain centers

88
Q

how does early pain travel?

A

is transmitted from the spinal cord via the spinothalamic tractt to the posteroventrolateral (PVL) nucleus of the thalamus before going directly to the primary and then secondary somatosensory cortex.

89
Q

what does the primary somatosensory cortex do?

A

provides sensory discrimination of pain

90
Q

what does the secondary somatosensory cortex do?

A

involved in the recognition of pain and memory of past pain

91
Q

where does late pain go?

A

to the thalamus, hypothalamus, amygdala, anterior cingulate cortex (has a role in pain affect, attention and motor responses)

92
Q

three ways opioids regulate pain

A
  1. within the spinal cord by small inhibatory interneurons
  2. by two significant descending pathways originating in the periaqueductal gray (PAG)
  3. at many higher brain sites, which explains opioid effects on emotional and hormonal aspects of the pain response
93
Q

two ways opioids reduce the transmission of pain signals at the spinal cord

A
  1. small inhibatory spinal interneurons release endorphins that inhibit the activation of the spinal projection neurons. Morphine can act directly o those same opioid receptors to inhibit the transmission of the pain signal to higher brain centers that normally allow us to become aware of the sensory experience
  2. endorphins regulate several modulatory pathways that descend from the brain to inhibit spinal cord pain transmission either by directly inhibiting the projection neuron (A) or the excitatory interneuron (B) or by exciting the inhibitory opioid neuron (C)
94
Q

periaqueductal gray

A

is a brain area rich in endogenous opioid peptides and high concentrations of opioid receptors, particularly mu and kappa

95
Q

overall, how do opioids modulate pain?

A

directly in the spinal cord and by regulating the descending pain inhibitory pathways ending in the spinal cord

96
Q

supraspinal

A

located above the spinal cord

97
Q

where does supraspinal opioid activity take place?

A

limbic structures, hypothalamus, medial thalamus; may be responsible for the emotional component of pain as well as for autonomic and neuroendocrine responses

98
Q

what do endogenous mu opioids modulate?

A

modulate both the sensory and emotional components of pain and that morphine and other opioids act at these sites

99
Q

acupuncture

A

involves inserting a metallic needle into the skin to reach deep structures, such as muscles and tendons; releases endogenous opioids

100
Q

electroacupuncture

A

found to enhance the immune response and reduce gastric acid secretion; activates the satiety center in the hypothalamus

101
Q

one way to increase antinociception (the action or process of blocking the detection of a painful or injurious stimulus by sensory neurons)?

A

enhance the effects of endogenous enkephalin by inhibiting the two peptidase enzymes that degrade it

102
Q

peptidase enzymes

A

dual inhibitors: RB-101, RB-120, RB-3007; others increase the extracellular levels of enkephalin

103
Q

what happens when you inhibit the peptidase enzymes?

A

inhibiting one peptide produces only weak analgesic effects, inhibiting both produces far more robust dose-dependent effects

104
Q

does inhibiting the enzymes work as well as morphine?

A

it never achieves the same effects as morphine (endogenous enkephalin does not saturate opioid receptors and overstimulate them), but they are safer because they do not depress the rate or volume of respiration and induce only a partial tolerance, risk of physical dependence is low

105
Q

gene therapy

A

virus engineered to contain the gene coding for human proenkephalin. The newly synthesized proenkephalin would be expected to be packaged in vesicles, spliced into multiple enkephalin peptides, and ultimately released by the sensory nerve terminals in the dorsal horn of the spinal cord to inhibit pain signal conduction

106
Q

opioid beta-endorphin

A

self administered, mediates opioid reinforcement. beta-endorphin self-administration is blocked by either mu or delta receptor antagonists. both types of receptor are involved in reward processes. K agonists fail to produce self-administration and may induce aversive states

107
Q

opioids in the VTA and DA

A

opioids injected into the VTA increase DA cell firing, which subsequently increase the release of DA within the NAcc.

108
Q

does intraventricular beta-endorphin increase or decrease neuronal firing?

A

increases neuronal firing.

109
Q

do k agonists increase or decrease neuronal firing?

A

reduce DA neuronal activity and DA turnover (release and metabolism)

110
Q

how do beta-endorphin and opioid drugs increase VTA cell firing?

A

by inhibiting the inhibitory GABA cells found in the VTA. they can decrease the release of GABA by opening K+ channels or reducing Ca2+ influx on GABA terminals. the inhibition of inhibitory neurons leads to increased firing and greater DA release in the NAcc. the endogenous peptide dynorphin, which acts on k receptors can reduce the release of DA

111
Q

does tolerance occur across receptor types?

A

kind of– selective agonists for the mu receptor reduce the effectiveness of other mu receptor agnonists, but only minimally reduce k agonists diminishes the effects of other k agonists but not mu agonists

112
Q

The role of sensitization

A

the motivation (inventive) to approach (craving)/desire for the drug undergoes sensitization. However, the high, or liking remains unchanged or decreases as tolerance develops

113
Q

rebound during abstinence syndrome

A

opioids in general depress the CNS function and thus during opioid withdrawal there is rebound hyperactivity

114
Q

is opioid withdrawal life threatening?

A

no–consists of pain, dysphoria, restlessness, fearfulness, flu-like symptoms; the longer the duration of action of the opioid, the more prolonged is the abstinence syndrome but the lower the intensity of the syndrome

115
Q

in what systems is there a rebound effect?

A

GI tract, autonomic nervous ystem

116
Q

what brain areas are most prominent in withdrawal symptoms?

A

locus coeruleus and the PAG are sensitive to the antagonist in terms of precipitating withdrawal; may mediate withdrawal induced anxiety

117
Q

Role of the NAcc in withdrawal?

A

may be important in the aversive stimulus effects or motivational aspects of opioid withdrawal

118
Q

what is Oxycodone and OxyContin?

A

Oxycodone is a semi-synthetic opioid; Percodan is usedto treat acute pain

119
Q

rebound effect

A

The acute effects of opioids acting at the mu-receptors consists of hyperpolarization and reduce rate of firing. Repeated exposure to opioids produced a gradual increase in firing rates of locus coeruleus cells as tolerance developed. Administration of an opioid antagonist after chronic opioid treatment induced a significant rise in firing rate to levels well above pretreatment levels, reflecting a rebound withdrawal that gradually returned to normal

120
Q

tolerance of analgesic effects

A

results because environmental cues regularly paired with drug administration begin to elicit the compensatory response of hyperalgesia, which diminishes the analgesic effect of the drug

121
Q

increased drug taking and environment

A

environmental factors –if euphoria is associated with certain stimuli, those aspects of the environment will act as secondary reinforcers, strengthening the drug-taking behavior; increased metabolic activity in the amygdala and anterior cingulate during cue induced craving suggests the importance of emotional memory (amygdala) and emotional expectation (anterior cingulate) to conditioning

122
Q

can abstinence symptoms be conditioned?

A

yes, classically.

123
Q

biopsychosocial model of drug treatment

A
  1. the physiological effects of the drug on nervous system functioning (opioid activation of mesolimbic pathway)
  2. psychological status of the individual and their unique neurochemical makeup and history of drug use
  3. environmental factors that provide salient cues for drug taking and powerful secondary reinforcement
124
Q

what can NMDA antagonists do?

A

seem to prevent the acquisition of tolerance and physical dependence to morphine

125
Q

using electoacupuncture (EA) to prevent withdrawal

A

restored low levels of prodynorphin mRNA to normal in the spinal cord, hypothalamus, and PAG, which suggests that withdrawal is suppressed by increasing dynorphin synthesis

126
Q

risks associated with methadone treatment?

A

accidental overdosing because of its long half life

127
Q

benefits of methadone

A
  1. it can prevent more severe withdrawal
  2. cross-tolerance that develops with repeated exposure means that normal euphoric effects of heroin are reduced or prevented
  3. its oral administration leads to little or no euphoria
  4. is relatively long-acting and produces a constant blood level
  5. medically safe
128
Q

use of naltrexone

A

antagonist treatment will block effects of self-administered opioids; longer duration than naloxone; does not stop cravings

Behavioral Pharmacology (11 decks)

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