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Daddy Pharm > Nociception (Exam 2) > Flashcards

Nociception (Exam 2) Flashcards

1
Q

T/F
Transduction always refers to a painful stimulus.

A

False
Transdxn doesn’t necessarily mean painful; refers to converting into electrical impulse

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2
Q

Transduction

A

noxious stimuli (e.g., heat, cold, mechanical distortion)
⬇️
electrical impulse in sensory nerve endings

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3
Q

Whorls

A

spiral shape seen at end of sensory dendrite; deform/compress triggers signal to travel down dendrite to body (senses pressure)

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4
Q

Whorls sense what type of stimulus?

A

pressure

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5
Q

How does increasing T affect receptors?

A

can open and allow NA in&raquo_space; allows stimulation

process of sensing heat

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6
Q

Sensing heat causes an influx of ___

A

Na

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7
Q

Tissue damage results in release of ___ ions, which can open certain receptors.

A

H+

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8
Q

Transmission

A

conduction of these electrical impulses to the CNS

major connections:
-dorsal horn (SC)
-thalamus with projections to the cingulate, insular, and somatosensory cortices.

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9
Q

Process of transmission

A

-Nerves enter dorsal horn (SC)
⬇️
projection pathways (somatosensory pathways)
⬇️
up SC
⬇️
brain
⬇️
branch off in certain places, esp the thalamus

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10
Q

Transmission
major connections:

A

-dorsal horn (SC)
-thalamus with projections to the cingulate, insular, and somatosensory cortices.

(T ➡️ CIS
Thalamus to Cingulate, Insular, Somatosensory)

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11
Q

Relay center for incoming pain signals

A

Thalamus
receive input; synapse to others ie neocortex

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12
Q

Levels of consciousness are found in

A

the cerebral cortex

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13
Q

Which cortices are a/w:
lower brain levels & emotional responses

A

cingulate, insular

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14
Q

Which cortices are a/w:
bringing things into consciousness

A

somatosensory

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15
Q

Modulation
Alters which stage of nociception?

A

altering pain transmission

inhibitory & excitatory mechanisms modulate pain/nociceptive impulse transmission in the PNS and CNS

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16
Q

T/F
mechanisms modulate pain/nociceptive impulse transmission in the PNS and CNS are inhibitory

A

False
inhibitory & excitatory

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17
Q

sensation of pain

A

nociception

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18
Q

Perception
mediated thru…

A

thalamus: central relay station for incoming pain signals

primary somatosensory cortex: discrimination of specific sensory experiences

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19
Q

T/F
Modulation can relieve pain

A

True
Severe sudden pain will shift focus almost 100% to it
Not sustainable
So we modulate pain immediately
Pain relieving in a sense

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20
Q

Perception

A

bringing pain into consciousness to process and make decision

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21
Q

primary somatosensory cortex

A

discrimination of specific sensory experiences

What pain is it? Biggie or no biggie? Where from?

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22
Q

all or nothing response

A

axon only has one choice: fire or dont

signal traveling down axon
axon can only signal down or not

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23
Q

Temporal signaling

A

(down an axon)
firing rate

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24
Q

T/F
There is no required time frame between an axon firing.

A

False
takes time for axon to reset and send another signal
minimum period of time between firing

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25
Q

Cells adjacent to an axon are sensing…

A

a time/signal pattern

a cell may only respond to a certain firing rate/pattern

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26
Q

the only way nerves can signal each other

A

temporal signaling

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27
Q

Very painful stimuli firing rate

A

very rapid
(type 1 neurons)

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28
Q

Firing rates/patterns:
Type I neuron vs. Type II neuron

A

Type I: more linear; can alter firing rate

Type II: have different patterns

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29
Q

discrimination of sensory experience is based on:

A

-which nerves fire
-rate/pattern of firing

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30
Q

Stepping on a lego vs marshmallow
The response is dependent on…

A

temporal signaling
(firing pattern)

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31
Q

The 4 components of Nociception

A

Transduction
Transmission
Modulation
Perception

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32
Q

T/F
Pain can only occur when all 4 components of nociception occur.

A

False
pain can occur without one or more of these steps
(ex: phantom limb pain)

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33
Q

phantom limb “pain”

A

Not always pain; sometimes just sensation

d/t higher processing neurons still responding/firing w/o stimuli
(not getting the stimuli they used to get but still firing)

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34
Q

T/F
phantom limb “pain” is d/t the hypersensitivity of the remaining sensory neurons.

A

False
d/t higher processing neurons still responding/firing w/o the original stimuli

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35
Q

C-fiber afferents

A

(unmyelinated & slowest conduction)
burning
sustained pressure

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36
Q

Type I fibers

A

(some Aβ and some Aδ)
myelinated
“polymodal fibers”
thermal, chemical & mechanical stimuli

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37
Q

T/F
Thermal pain is not the same as burning pain

A

True

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38
Q

Consistent firing in-between transmissions; only “pattern” is speeding up/slowing down (linear)

A

Type I fibers (some Aβ and some Aδ) “polymodal fibers”

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39
Q

T/F
Type I fibers respond to a single stimulus.

A

False
called “polymodal” bc they respond to multiple things

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40
Q

Thermal vs burning pain

A

burning = instantaneous pain

thermal = consistent, longer-term response

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41
Q

Non-linear/ “saddle transmission”

A

Type II fibers (some Aδ fibers; slower)
bizarre patterns
can also speed up and slow down

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42
Q

can signal pain from chemical and cold stimuli

A

Both myelinated and unmyelinated

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43
Q

Type II fibers

A

(some Aδ fibers; slower)
initial pain responses to heat

non-linear
bizarre patterns

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44
Q

Myelination is more critical to (motor/sensory) fxn.

A

motor

Myelinated Motor

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45
Q

“Capsation” receptor is a/w what sensation

A

burning

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46
Q

Capsation/Vanilloid Receptor/ Transient V receptor-1 (TVR1)

structure

A

Voltage gated
4 subunit
similar to NMDA

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47
Q

Capsation/Vanilloid (VR1) Receptor/ Transient V receptor-1 (TVR1)

MoA

A

Na & Ca in; K out
depending on state of neuron

scalding heat and pain

activated/augmented by:
PKC, PKA, Ca

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48
Q

PIP is located in ___ and can be broken down into ….

A

cell membrane

DAG & IP3

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49
Q

T/F
Prostaglandins and bradykinins are known to cause pain

A

False
do not cause
but
worsen/augment pain

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50
Q

substances that transmit pain when released from neurons

A

CGRP (Calcitonin gene-related peptide)
SP (substance P)
glutamate

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51
Q

T/F
Ca release aids in pain transmission

A

True
Ca stimulates NT release into synapse and communicates pain

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52
Q

What stimulates Ca release?

A

-Depolarization (Na influx)
-IP3
-PK3
-PKC

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53
Q

T/F
PKA stimulates Ca release and pain transmission

A

False
stimulates Ca release:
-Depolarization (Na influx)
-IP3
-PK3
-PKC

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54
Q

Role of bradykinin in pain

A

increases IP3&raquo_space; Ca release&raquo_space; NT release

increases DAG&raquo_space; PKC&raquo_space; Ca&raquo_space; NT release

Augments pain, doesn’t cause it

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55
Q

Role of PGE2 in pain

A

(Prostaglandin E2)

increased cAMP > activates PKA > Na influx > depolarization > Ca release > NT release

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56
Q

Activates Na (depolarization)

A

PKC
PKA

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57
Q

Which substances act here to inhibit pain?

A

Endorphins
ACh
cannabinoids

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58
Q

Which act via G protein complexes?
Endorphins
ACh
cannabinoids

A

All

stimulate K channels
K out
hyperpolarize

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59
Q

cAMP role in nociceptive signal transduction

A

Increase cAMP = alter PKA = stimulate Na ion entry = depolarization & passage of signal

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60
Q

increase of cAMP will directly…

A

increase/alter PKA

end result: Na influx & depolarization

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61
Q

released from some sensory nerves as a means of pain transmission

A

Calcitonin gene-related peptide (CGRP)
Substance P (SP)

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62
Q

Substance P (SP)

A

undecapeptide
acts at Neurokinin-1 receptors (NK-1) (amygdala, hypothalamus, & periaqueductal gray)

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63
Q

brings pain into emotional consciousness

A

amygdala

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64
Q

“P” in SP stands for

A

powder

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65
Q

SP is found with ___ in __ __ that respond to painful stimuli

A

glutamate
primary afferents

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66
Q

Neurokinin-1 receptors (NK-1)

A

widely distributed in the brain

in areas a/with pain processing:
amygdala, hypothalamus, & periaqueductal gray

SP acts on this site

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67
Q

specific areas associated with pain processing

A

amygdala, hypothalamus, and periaqueductal gray

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68
Q

An NK-1 receptor antagonist would block…

A

Substance P

SP: undecapeptide that acts at Neurokinin-1 receptors (NK-1)

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69
Q

Aside from nociceptive pain transduction, CGRP causes ___

A

vasodilation
decreases BP

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70
Q

CGRP antagonist
MoA

A

attenuates the increase in BP (that causes migraine) and block pain

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71
Q

Gi/o receptor

A

“G inhibitory”
Inhibitory opioid receptor

inhibitory actions at pain receptors

Causes receptor hyperpolarization by increasing potassium conductance (K out)

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72
Q

T/F
Endorphin, cannabinoid, and acetylcholine receptors are examples of Transient V receptor-1 (TVR1)

A

False
Gi/o receptor system

hyperpolarization by increasing potassium conductance

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73
Q

Provides sensations of scalding heat and pain

A

Transient V receptor-1 (TVR1)

“Capsaicin/Vanilloid receptor”

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74
Q

Transient V receptor-1 (TVR1)/ Vanilloid/ Capcasin
when it is open….

A

K out
Na, Ca in

similar to NMDA

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75
Q

Increasing K conductance means…

A

more K flows OUT

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76
Q

Bradykinin is considered a..

A

inflammatory mediator

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77
Q

increasing Bradykinin results in

A

increased DAG & IP3
increases overall response of system

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78
Q

T/F
CNS neurons can be sensitized for pain transmission by many inflammatory mediators

A

False
peripheral

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79
Q

released in response to tissue damage

A

bradykinin

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80
Q

Chronic pain occurs when

A

inflammatory effects do not resolve
leading to hyperalgesia due to sensitization

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81
Q

T/F
Hyperalgesia is a result from nerve understimulation.

A

False
hyperalgesia is due to sensitization/overstimulation

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82
Q

Allodynia

A

perception of pain from normally non-painful stimuli

body’s response to sensitization

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83
Q

T/F
Allodynia can occur without a stimuli

A

False
It is specifically pain from a nonpainful stimuli

84
Q

Where is adenosine released from?

A

damaged tissue

85
Q

Pain inhibitory receptors

A

Mu (endorphins)
GABA A
M2 (ACh)
GIRK
SSTR2a

86
Q

Endorphins act on ____ receptors

A

Mu

87
Q

Which propagate pain? Which are inhibitory?
NMDA
GABA
AMPA

A

propagate: NMDA & AMPA

inhibit: GABA

88
Q

Substance P
MoA

A

act on NK1 > G Prtn > cAMP & PKA >VR1/NMDA (increases + [ ]/depolarization)

89
Q

Glutamate MoA

A

act on AMPA
Na in
depolarization/pain nociception

90
Q

GABA MoA (pain)

A

increases Cl- conductance
hyper polarizes
signal harder to propagate

91
Q

Dorsal Horn Synapse
Afferent substances

A

SP
glutamate

92
Q

White and grey matter
SC vs brain

A

SC: grey inside; white outside

brain: grey outside; white inside

93
Q

White matter vs grey matter
whats in it?

A

White matter: myelinated axons; pathways/tracts

Grey matter: cell bodies/cellular region

94
Q

Stimulation of ___ ___ causes the anger a/w pain

A

insular cortex

95
Q

Amygdala transmit signals to

A

insular cortex

96
Q

Lower level pain structures

A

Rostral ventral medulla
Periaqueductal Gray (PAG)

-respiration
-BP
-emotion
-lizards

97
Q

insular cortex

A

brings into consciousness
specifically conscious emotion
ie: anger

98
Q

T/F
nociceptors synapse once at the spinal cord

A

False
can have 1 or more

99
Q

The thalamus relays info to

A

somatosensory cortex

100
Q

T/F
In the brain, most pathways are outside and transmit to cells in the inner region.

A

False
most brain pathways are INSIDE
&
transmit to cells the outer regions

101
Q

Where do nociceptors enter the spinal cord?

A

Dorsal spinal column

102
Q

functions as a relay center for nociceptive and other sensory activity

A

spinal dorsal horn

103
Q

periaqueductal gray (PAG)-RVM (rostral ventromedial medulla) system may either depress or facilitate the integration of painful information in the ______

A

spinal dorsal horn

104
Q

Primary afferent nociceptors convey noxious information to

A

projection neurons within the dorsal horn (SC)

105
Q

make up the great majority of the neuronal population throughout the dorsal horn

A

interneurons

106
Q

Ascending pathway

A
107
Q

Ascending information also accesses neurons of the ___ and ___ to engage descending feedback systems that regulate the output from the spinal cord.

A

rostral ventromedial medulla (RVM)

midbrain periaqueductal gray (PAG)

108
Q

T/F
Cell bodies are usually found in the dorsal horn.

A

false
dorsal root

109
Q

Which fibers enter thru the dorsal root?

A

AB, Ad, C

110
Q

Dorsal root fibers & their laminae

A
111
Q

Processing neurons
augment or inhibit depending on…

A

the level the information comes in on

112
Q

Gate Theory of Pain

A

Pain information is transmitted to the brain if the gate is open but not if the gate is closed by inhibitory stimulation

113
Q

Explains how fibers can augment/modulate pain

A

Gate Theory of Pain

114
Q

T/F
A neuron must synapse on another neuron’s terminal to inhibit the passage of pain signals.

A

False
does not have to synapse only here

115
Q

The mechanism of rubbing skin when in pain

A

activates large myelinated afferents (Aβ) (“faster” than Aδ & C fibers that convey pain)

Aβ fibers deliver pressure & touch info to dorsal horn
↓
overrides some pain messages (Aδ & C fibers) by activating the inhibitory interneurons in the dorsal horn.

116
Q

T/F
Rubbing skin stimulates additional mechanical inputs which inhibit the gate through A-delta fibers and diminishes pain transmission to the brain

A

False
inhibit the gate through Aβ fibers

rubbing activates large myelinated afferents (Aβ) (“faster” than Aδ & C fibers that convey pain)

Aβ fibers deliver pressure & touch info to dorsal horn
↓
overrides some pain messages (Aδ & C fibers) by activating the inhibitory interneurons in the dorsal horn.

117
Q

Which fibers tend to be stimulating? Which are inhibitory?
Adelta
C
AB

A

Stimulating: Ad & C (small)

inhibiting: AB (large)

118
Q

The gate is seen as an (excitatory/inhibitory) mechanism

A

inhibitory

119
Q

How does a very strong pain stimulus affect Ad & C fiber modulation?

A

High degrees of pain can enhance the stimulating effect of Ad & C fibers

-block Ab fibers
-enhance pain by inhibiting the closing of the gate

esp if many fibers are affected

120
Q

The neurologic “gate” is in….

A

the spinal dorsal horn

121
Q

GCT
painful information is projected to the ____ brain regions if the gate is open, although painful stimulus is not felt if the gate is closed by….

A

supraspinal

simultaneous inhibitory impulses (ie: rubbing skin)

122
Q

large-diameter myelinated afferent fibers

A

AB

123
Q

How we harvest Opium

A

-Slice poppies open
-Collect dried resin (morphine & other natural opioids)
-Modify via chemical treatment to make diff compounds (semi-synthetics; heroin)

124
Q

Opium first known use

A

100 AD rome

125
Q

alkaloids

A

naturally occurring compound in plants

126
Q

Codeine and Papaverine and examples of

A

alkaloids (naturally occurring compounds in plants)

127
Q

Morphine chemically isolated in

A

1806

128
Q

Papaverine

A

no pain relief activity

activity on GIT

TB: papverine & noscapine lack analgesic activity

129
Q

Does codeine relieve pain?

A

Yes, but not as potent as morphine.

130
Q

Meperidine is an example of…

A

Synthetic congeners
(fully synthetic)

131
Q

T/F
Heroin is a synthetic product of morphine.

A

False
semi-synthetic

132
Q

How we make semi-synthetic opioids

A

-Collect dried resin (morphine & natural opioids)
-chemical treatment to make diff compounds = semi-synthetic

ie: heroin

133
Q

T/F
Opiates refers to all agents acting on morphine receptors, including antagonists.

A

False
Opiates = derived from opium

Opioids: all agents acting on morphine receptors, including antagonists

134
Q

T/F
All opioids have pain-relieving properties.

A

False
Opioids = all agents acting on morphine receptors, including antagonists.

135
Q

T/F
Stupor specifically refers to opioids.

A

False
anything that produces stupor in theory could be considered a narcotic

136
Q

Opioid Receptors
major families

A

m, d, k, Nociceptin

“Four”

137
Q

Four major families (m, d, k, Nociceptin) all belong to ….

A

the G protein-coupled class of receptors.

138
Q

Endogenous ligands for opioid receptors are ___ with ___ for each receptor type

A

peptides

varying affinities

139
Q

T/F
All opioid receptor activity is inhibitory

A

False
very low doses are actually excitatory (increases intracellular cAMP)

140
Q

Opioids exhibit inhibitory activity by…

A

decreasing adenylate cyclase
↓
decreases intracellular cAMP

141
Q

T/F
Excitatory responses to opioids can be seen with clinical doses.

A

False
this is seen in a testing/lab environment; usually not seen in pts

142
Q

converts ATP to cAMP

A

adenylate cyclase

(Adenylyl cyclase = adenylate cyclase)

143
Q

Which are excitatory?
Which are inhibitory?

Go
Gi
Gs

A

excite: Gs
inhibit: Gi Go

“stimulate”
Gi = inhibit

144
Q

Ca and K conductance that will increase action potential

A

Decrease K cndxn
Increase Ca cndxn

“Keep my K. Ca, come in!”

145
Q

T/F
Opioid Receptors are found all over the body.

A

true

146
Q

Opioid Receptor Locations:
mu, kappa, delta

A

Mu: brainstem & thalamus; some SC; GIT

K: dorsal H; some Bstem medullary retic.

d: limbic

147
Q

Which opioid receptors are mainly a/w lower level fxns?

A

Kappa
Delta (lower lvl consciousness & emotion)

“My K:D is a lower level”

148
Q

Opioid Receptor Functions
Mu

A

analgesia
resp depression
euphoria
miosis
physical dependence
decreased GI motility

Mu = euphoria “Muphoria”

149
Q

physical dependence

A

overstimulation = tolerance

body craves more to stimulate same pathway

150
Q

Mu receptor [ ] is highest in…

A

the GIT

151
Q

T/F
physical dependence is the reason for opioid abuse

A

False
euphoria leads to abuse

152
Q

Opioid Receptor Functions
Kappa

A

supraspinal analgesia
sedation
dysphoria (psychoses)

153
Q

Opioid Receptor Functions
Delta

A

analgesia (spinal?)

D Does 1 thing = analgesia

154
Q

a/w recovery effects in long term addicts (craving/dependence)

A

Kappa receptor dysphoria (psychoses)

155
Q

Endogenous Opioids are derived from

A

precursor polypeptides

156
Q

Endogenous Opioids
agents

A

endorphins
dynorphins
enkephalins

157
Q

Endogenous Opioids
All differ in ____, but share the same …

A

chain length

first few AA’s (61-65)

158
Q

smallest unit that produces response at opioid receptors

A

Met-Enkephalin
(AA 61-65)

159
Q

How we cleave to obtain the different endogenous opioids

A

B-endorphin (61-91)
y-endorphin (61-77)
A-endorphin (61-76)
Met-Enkephalin (61-65)

160
Q

ACTH & B-LPH

A

both: neurohumoral control

ACTH: control adrenaline release

not pain relieving!

161
Q

Met-Enkephalin (61-65) is a ___ unit structure

A

5

smallest unit that produces response at opioid receptors

162
Q

Endomorphines

A

newly discovered mu-receptor selective tetrapeptides

163
Q

T/F
Endomorphines come from the same peptide structure as the endorphins, dynorphins, and enkephalins.

A

False

164
Q

Endomorphines role in pain

A

Act as NTs, neuromodulators, or neurohormones

decrease signal strength or block completely)

Body’s pain modulators

165
Q

Opioid Receptor Homology

A

~65% homology exists among m, d, k

Open circles are AA’s that differ among each receptor type.

166
Q

T/F
The opioid G receptor proteins are more similar in terms of their ligands rather than how they work.

A

False
more homologous in terms of intracellular side, which controls how it works

external portion (binding site) is less homologous

167
Q

Analgesia mediated via receptors located in…

A

-dorsal horn (SC)
-periaqueductal gray matter
-thalamus

168
Q

PAG process information & brings it to ___ levels of the brain.

The thalamus, brings info to ___ levels.

A

PAG → lower levels

thalamus → higher levels

169
Q

Ventral brainstem receptors mediate effects on…

A

coughing
vomiting
respiration
pupillary diameter

170
Q

Can create substances to augment pain

A

hypothalamus

171
Q

Neuroendocrine functions controlled via the ___.

A

hypothalamus

172
Q

amygdala is a/w

A

Mood and behavioral effects

173
Q

associated mainly with the GI tract

A

Peripheral mu receptors

174
Q

Opioid ligands can interact with opioid receptors in 4 primary ways:

A

-agonist (can be inhibitory!)
-antagonist
-partial agonist
-Mixed agonist/antagonist

175
Q

T/F
An opioid agonist can inhibit the opioid receptor.

A

True
Agonist: binds & activates receptor.
Agonists CAN be INHIBITORY

“can be inhibitory in its agonist activity”

176
Q

binds to the receptor but does not activate it

A

antagonist

177
Q

Partial Agonist

A

-binds but produces a submaximal response

-Lacks intrinsic activity

178
Q

Mixed Agonist/Antagonist

A

binds to more than 1 type of opioid receptor

acting as an agonist at one, and an antagonist at others

179
Q

Stimulating a G protein receptor typically leads to a ___ action

A

inhibitory

180
Q

T/F
If we give higher doses of a partial agonist/antagonist, it is possible to achieve maximal effect.

A

False
partial agonist/antagonist lacks intrinsic activity

181
Q

Opioids are (bases/acids) and bind to receptors in (ionized/nonionized) form.

A

opioids = bases & bind in ionized form

ionized form = + charge
(bases accept protons)

182
Q

Opioid MoA
CNS activity primarily in…

A

brainstem/spinal cord

183
Q

Opioid MoA
Non-CNS activity

A

peripheral afferent neurons

184
Q

Opioids
Primary action

A

decreased neurotransmission by presynaptic inhibition of neurotransmitter release (NE, ACh, DA, SubP)
↓
increased potassium conductance and/or calcium channel inactivation

185
Q

Opioid action is (mostly/all/rarely) pre-synaptic.

A

mostly pre-synaptic

some post-synaptic inhibition

186
Q

Central Opioid Effects

A

↓ Neuronal activity

Analgesia – ↑ perception threshold & tolerance

Resp dprsn – ↓ CO2 sensitivity (Cheyne-Stokes)

Mood – clouded state (agonists); euphoria

Sedation – agonist dependent

Miosis
N/V
antitussive
endocrine

187
Q

Opioids
Endocrine effects MoA

A

inhibits LHRH secretion

188
Q

Cheyne-Stokes resp

A

rapid RR, apnea, repeat

not sensing CO2 during apnea
CO2 builds up to a higher extent triggers rapid RR
CO2 drops
apnea restarts

189
Q

Peripheral Opioid Effects

A

Histamine release – peripheral arteriole & venous dilatation

Venous dilatation – direct opioid receptor action.

Smooth muscle contraction – biliary and bladder sphincter muscles. (↓ bile & urine)

Inhibit ACh release – mesentery: constipation.

190
Q

Codeine has (high/low) Mu activity.

A

low

191
Q

Histamine release w/ opioids

A

innate response
can occur on the first dose
Don’t give large doses without resp support

192
Q

Opioids constipation MoA

A

Inhibition of ACh release in mesentery
↓
decreases peristalsis
↓
constipation

193
Q

T/F
constipation can cause infection

A

True
bacteria can multiply & move up intestines

30-50% fecal matter = bacteria

194
Q

opioids + ___ ___ = worsened constipation

A

bowel manipulation/surgery

195
Q

Therapeutic Opioid Uses

A

Analgesia – acute & chronic

Pre-op sedation, anesthesia, epidural analgesia.

Diarrhea (Lomotil)

Cough suppression(codeine)

Opioid withdrawal

Opioid overdose (antagonist)
Remember opioids can be antagonists too

196
Q

Why do we give opioid w/drawl pts more opioids?

A

Trying to block internal response (N/V)

give opioid w/ more targeted action

197
Q

“MOR”

A

Mu opioid receptor complex

198
Q

MORs can be found (2)

A

PAG
Dorsal horn (SC)

199
Q

Opiate analgesia pathway

A

Start → finish
Medulla
dorsal raphe
PAG
Locus coeruleus
spinal cord

200
Q

MOR PAG Opiate action

A

MOR activation = Inhibits GABA release
↓
PAG outflow & signal passage
↓
activates forebrain, spinal & monoamine rcptrs
↓
input to higher centers & mood

201
Q

MOR Spinal Opiate Action

A

second order dorsal horn:

Pre & Post synaptic MOR

Pre: block Ca
Post: ↑K cndxn (hyperpolarize)
Result: hyperpolarize POST synaptic membrane

202
Q

_____ MOR are a/w K+ & Ca++ channels

A

Spinal/2nd order DH

203
Q

Opiate receptor binding is highly expressed in the

A

superficial spinal dorsal horn (substantia gelatinosa)

presynaptic C fibers (small aff)

204
Q

Opiate agonist acting @ spinal sites serves to…

A

Lessen afferent excitation of the second order neuron

205
Q

small primary afferent fibers

A

C fibers

“C small af”

Daddy Pharm (13 decks)

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