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BOT 380 > Plants and Pain > Flashcards

Plants and Pain Flashcards

1
Q

Plants used for halucinogenic modulating effects

A
  1. psilocibin - serotonin agonist
  2. ayahuasca - monoamine oxidase inhibitory (increase synaptic serotonin levels)
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2
Q

Plants used for Stimulant modulating effects

A
  1. coca leaves - dopamine reuptake inhibitor (increase synaptic dopamine levels)
    - tobacco - cholinergic agonist nicotinic receptors
    - coffee bean - adenosine receptor antagonist
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3
Q

Analgesic drugs derived from plants include

A
  • salicylic acid (asprin)
  • opiates (morphine, opium, thebaine)
  • cannabis
  • capsaicin
  • menthol
  • salvinorin
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4
Q

Primary Afferents

A
  • sensory neurons in the periphery (skin, organs)
  • two classes: A fibers and C fibers
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5
Q

Nociceptors

A

primary afferents that detect pain

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6
Q

A fibers are:

A
  • myelinated (fast conducting, insulates the axon)
  • end in specialized structures (Ruffini, Pacianian, Meissner)
  • each structure detects specific non-painful stimuli (touch, temp, vibration)
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7
Q

C fibers are:

A
  • unmyelinated (slow conducting)
  • end as free nerve endings in the superficial layers of the skin
  • detect many types of painful stimuli (thermal, mechanical, chemical, electrical)
  • polymodal nociceptor
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8
Q

How are Painful Stimuli Detected?

A
  • on the free nerve nerve endings of C fibres by specialized receptors
  • TRPV1 : ion channel, activated by heat (> 43 degrees) and capsaicin, causes burning pain
  • TRPA1 : allyl isothionate, burning, inflammation
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9
Q

Urishol

A
  • found in poison ivy, crosses the skin and initates and inflammatory reaction that activates NK, BK and cytokine receptors
  • causes itch and pain
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10
Q

How does info get sent up to the brain?

A
  • C fibre primary afferents synapse onto secondary afferents in the dorsal horn of the spinal cord
  • secondary afferents carry nociceptive information up the spinal cord to the brain
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11
Q

Nociception vs. Pain

A
  • nociception does not equal pain
  • nociception: relay of pain signal from periphery to the brain
  • pain: integration of that pain signal with cognitive and emotional context (requires the brain, always a subjective experience)
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12
Q

Define opium, opiates, opioid

A
  • opium : dried latex obtained from the poppy
  • opiates : any drug derived from opium
  • opioid: any drug that binds to an opioid receptor. Includes opiates, as well as synthetic opioid agonists (fentanyl, heroin, oxycontin)
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13
Q

Opioid Receptors in the body and their affect

A
  • brain : many regions are involved in pain perception, emotion, reward and addiction
  • brainstem : can affect breathing by quieting neurons that control respiration
  • spinal cord
  • peripheral neurons
  • intestine
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14
Q

Agonists

A
  • ex. morphine
  • activate opioid receptors, but that activation leads to decreased likelihood that the neuron will fire
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15
Q

What are the 3 classes of opioid receptors?

A

mu, delta, kappa

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16
Q

receptor activation and typical agonists of mu opioid receptors

A
  • receptor activation leads to analgesia euphoria
  • typical agonists: heroin, morphine, oxycodone, fentanyl
17
Q

receptor activation and typical agonists of delta opioid receptors

A
  • receptor activation leads to decrease in anxiety
  • typical agonists: some drugs being developed to treat chronic pain conditions, like migraine (SNC80)
18
Q

receptor activation and typical agonists of kappa opioid receptors

A
  • receptor activation leads to analgesia, dysphoria, hallucinations
  • typical agonists: salvinorin
19
Q

Dopamine

A
  • dopamine is involved in motivated behavior
  • dopamine neurons are located primarily in the VTA
  • opioid recpetors in teh VTA are located on inhibitory GABAergic interneurons
  • opioids inhibit inhibition (disinhibition) leading to dopamine release
20
Q

How do opioid receptors inhibit pain?

A
  1. decreasing nociception at the level of the C fibre, in the spinal cord, and in the thalamus
  2. decreasing the emotional and cognitive aspects of pain (make the pain bother you less)
21
Q

Define Cannabis and Cannabinoids

A
  • cannabis: genus of flowering plant.Contains many bioactive compounds, but most studied are THC and CBD. THC is the primary psychoactive compound in cannabis
  • cannabinoids: class of chemical compounds that act at the cannabinoid receptors
22
Q

CB1 versus CB2 receptors

A
  • CB1 receptors are among the most abundant GPCRs, found in brain, peripheral organs (heart, liver, fat, stomach, testes) and peripheral nerves
    -CB2 receptor distribution mostly on immune cells
23
Q

How Do Cannabinoids Work?

A

-cannabinoid receptors are inhibitory
G-protein coupled receptors (Gi
coupled)
- Cannabinoid receptors are located
on the presynaptic membrane
- cannabinoid receptors leads to decrease in cyclic adenosine
monophosphate (cAMP)
accumulation which inhibits the influx of calcium in the firing neuron and
inhibits neurotransmitter release.
- decrease synaptic transmission,
inhibit neurotransmitter release

24
Q

THC Effects (general, potential therapeutic, and unwanted)

A
  • is a partial agonist at CB1
  • general : euphoria, relaxation, disinhibition, changes in perception, vasodilation, increase pulse rate
  • potential therapeutic: attenuation of nausea, increased appetite, decreased intraocular pressure, chronic pain relief
  • unwanted: memory impairment, dysphoric state, visual hallucinations, depersonalization, psychotic episodes, anxiety
25
Q

CBD Effects

A
  • some preclinical research suggests CBD has therapeutic potential for management of inflammation, anxiety, emesis, nausea, inflammatory pain, and epilepsy
  • strong clinical data lacking for these claims
  • pediatric epilepsy is the only condition in which high quality clinical data (oral CBD significantly reduced frequency of seizures more than placebo)
26
Q

Adverse Effects of THC

A
  • acute effects: panic attacks, severe anxiety, psychosis, paranoia, convulsions, hyperemesis
  • prenatal effects: neuroanatomical and behavioral changes in offspring (dose-response relationship not identified)
  • lung cancer: smoked cannabis
  • driving: increase risk of accident
  • no documented evidence of death - sparsity of CB1 receptors in the brain stem region that controls respiratory and cardiovascular systems
27
Q

Define Psychological Dependence

A

compulsive drug-seeking behavior in which the individual uses the drug receptively for personal satisfaction, often in the face of known risks to health

28
Q

Define Physiological Dependence

A

revealed when withdrawal of the drug produces symptoms and signs that are frequently opposite of those sought by the user

29
Q

Cannabis Withdrawal

A
  • is relatively mild and short-lived
  • symptoms of restlessness, irritability, mild agitation, insomnia, nausea and cramping
  • may be worse in chronic, long-term users and may contribute to continues drug use
30
Q

Define Addiction (Substance use disorder)

A

inability to control the use of legal or illegal substances despite negative consequences

31
Q

The Challenge of Cannabinoid Pharmacology

A
  • smoked cannabis may be effective at treating conditions like chronic pain, chemotherapy induced nausea and others
  • smoked plant not ideal because hard to control dose
  • efforts to design synthetic cannabinoids (CB1 or CB2 agonists) - some success, but not nearly as effective as smoked cannabis

BOT 380 (17 decks)

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