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Neuro > Neuro Elmsie > Flashcards

Neuro Elmsie Flashcards

1
Q

Membrane potential is directly generated by the activity of….

A

ion channels

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2
Q

The force that controls movements of ions across the plasma membrane is the…

A

electrochemical gradient

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3
Q

What are some non-selective ligand gated ion channels?

A

nicotinic ACh channel glutamate (AMPA and NMDA) channels

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4
Q

GABA channel is a selective ligand-gated ion channel for …

A

Cl-

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5
Q

In order for a cell to have a membrane potential, it must have …

A

a Na+ ion gradient across the plasma membrane

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6
Q

Resting Membrane Potential is usually about

A

-70mV

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7
Q

There are ionic pores filled with water in lipid membranes that allow the hydrophilic ions to pass through the hydrophobic membrane. To make one of these ion pores selective, what happens?

A

amino acids line the pore - glutamate is negative, so it attracts Ca2+ and repels Cl- lysine and arginine are positive, so it attracts Cl-

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8
Q

A charged amino acid, separate from those in an ionic pore, to aid in controlling membrane potential could form the channel’s… this sits on the inside of the membrane at rest

A

voltage-sensor

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9
Q

Upon depolarization, the voltage sensor is repelled outward, causing

A

movement that causes the channel to open

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10
Q

At rest, what are the activation gate and inactivation gate doing in regard to ionic gates/channels?

A

activation gate is closed inactivation gate is open

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11
Q

With depolarization, the activation gate…

A

opens rapidly to allow ion movement

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12
Q

With depolarization, the inactivation gate…

A

closes slowly so channel remains open during depolarization and channels accumulate in the inactive state

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13
Q

One effect of hyperpolarization of voltage-dependent Na+ channels is to…

A

open the inactivation gate

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14
Q

How do Calcium Channel Blockers work in regards to voltage-gated ion channels? What channel do they work on specifically?

A

enhance the inactivation of channels Cav1.2 tp arterial smooth muscle

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15
Q

Ligand-gated channels have their gate located…

A

at the narrowest portion of the pore, usually the very middle

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16
Q

Analogous to inactivation, for ligand channels, this causes closure of the channel.

A

desensitization - constant presence of activating ligand

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17
Q

The balance of electrical and chemical forces creates the… of the membrane/cell

A

equilibrium potential

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18
Q

Equilibrium potential is determined by…

A

charge of the ion and concentration of ions across the membrane

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19
Q

Low intracellular Na+ and low extracellular K+ is maintained by..

A

Na-K ATPase

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20
Q

What allows Ca2+ to be an intracellular messenger?

A

exquisite low level and control inside cell, by CaATPase

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21
Q

What is the primary channel responsible for RMP (resting membrane potential)?

A

K2p (2-pore K channel)

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22
Q

What increases activity of K2p? What does this result in?

A

heat, acidic pH, and pressure resulting in hyperpolarization

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23
Q

Membrane potential becomes more positive (depolarizing) with K+ doing what?

A

K+ increasing extracellularly

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24
Q

Equilibrium potentials of K+ Na+ Cl- Ca2+ HCO3-

A

K -86 Na 58 Cl -78 Ca 125 HCO3 -12

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25
Q

Which ion channel dominates conductance at the peak of AP?

A

Na+

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26
Q

The AP repolarization phase is primarily driven by…

A

Nav channel inactivation

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27
Q

Kv opening is slow relative to Nav so peak K+ efflux occurs…

A

during repolarization

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28
Q

Kv transiently hyperpolarizes the membrane potential after the AP. This is called…

A

afterhyperpolarization

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29
Q

immediately following an AP, what percent of Nav are inactivated?

A

90%

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30
Q

Kv channels (except K2p) are closed at rest and remain closed during….

A

depolarization, so Na+ influx is unopposed

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31
Q

What direction does K+ always move?

A

always moving OUTWARD through Kv

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32
Q

A depolarized RMP does what to Nav availibility?

A

decreases

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33
Q

Hyperkalemia causes the RMP to… ultimately doing what?

A

depolarize, causing AP generation to fail

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34
Q

Nav channels are sensitive to what toxin from puffer fish? Is there an exception?

A

sensitive to TTX - tetrodotoxin Nav1.5 - heart (and maybe 1.8 and 1.9 -pain) could be resistant to the toxin

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35
Q

Someone with a mutation in what Nav channel might never feel pain? If this is a gain of function mutation, what would happen?

A

Nav1.7 person in chronic pain

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36
Q

All Nav channels, except…., are involved in AP generation by providing Na influx for depolarization. This other channel is unique because…

A

Nav1.9 it activates too slowly to be part of Na influx but activates at a more negative voltage

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37
Q

If a pt has a neuroma, what channels might be upregulated, causing the pt more pain?

A

Nav1.8 and Nav1.9

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38
Q

What Cav acts as voltage sensors to trigger Ca2+ release from sarcoplasmic reticulum in skeletal muscle?

A

Cav1.1

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39
Q

What is the primary target of calcium channel blockers?

A

Cav1.2 (role in neuronal excitability, but no role in NT release, so CCB do not alter NT)

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40
Q

Cav1.3 channel affects…

A

neurons and cardiac cells in pacemaking - SA and AV nodes

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41
Q

What channel is responsible for all synaptic terminals in the CNS, Ca2+ to trigger NT release at presynaptic NMJ?

A

Cav2.1

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42
Q

Cav2.2 channels are present at all synaptic terminals in the CNS, having less influence on synaptic release, but more geared toward…

A

sympathetic and pain sensory

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43
Q

What drug inhibits Cav2.2 to treat chronic pain? How is it delivered?

A

Ziconotide intrathecal delivery

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44
Q

What channel is in charge of rhythmic electrical activity in the SAN and CNS?

A

Cav3 SAN also Cav1.3

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45
Q

Cav1 and Cav2 have auxillary subunits to modify their gating. What do Cavbeta subunits do?

A

move Cav1 and Cav2 from ER to plasma membrane - regulate membrane levels of Cav - alter speed of inactivation

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46
Q

Cav1 and Cav2 have auxillary subunits to modify their gating. What do Cav-alpha2-delta subunits do?

A

move Cav1 and Cav2 from ER to plasma membrane - shift voltage dependence of channel activation - increase activity with chronic nerve injury

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47
Q

What is the target of gabapentin and pregablin drugs?

A

Cav-alpha2-delta subunit of Cav1 and Cav2

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48
Q

Increasing K+ channel activity will…

A

decrease neuronal or muscle electrical excitability

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49
Q

Anesthesia/volatile anesthetic agents (like sevoflurane) target what channel in order to do what?

A

target K2p in order to hyperpolarize neurons

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50
Q

Calcium can activate some K+ channels (Kca) during the AP. This Kca channel helps to …

A

repolarize the neurons and help produce afterhyperpolarization - sets the number and frequency of APs during burst

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51
Q

Increased Kca channel activity will do what to AP frequency?

A

decrease

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52
Q

What might inhibit Kca channels, resulting in an increase in AP frequency?

A

Apamin - bee venom toxin

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53
Q

What K+ channel helps to hold the membrane potential near RMP?

A

Inward-rectifying K+ channel (Kir)

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54
Q

What sets the membrane potential between AP in the heart?

A

Kir

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55
Q

Activation of GIRK channels by ACh receptors in cardiac muscle (vagal input) causes what to happen?

A

HR to slow

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56
Q

What drug is used in MS to inhibit non-specific Kv channels? How does this work?

A

4-aminopyridine - blocks Kv in demyelinated axons to increase AP conduction and improve coordination

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57
Q

What channels does the drug amiodarone block?

A

Kv11 (Ikr?), Nav1.5, and Cav1.2

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58
Q

What drug activates Kv7 at myelinated axons at the nodes of ranvier to decrease electrical activity and is used as an anti-epileptic?

A

Ezogabine

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59
Q

What is the major excitatory NT in the CNS?

A

glutamate

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60
Q

What channels are fast, excitatory synaptic transmission?

A

AMPA

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61
Q

NMDA channels require what two things to be active?

A

1.glutamate and glycine binding at separate sites 2. previous depolarization of AMPA channel

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62
Q

What does depolarizing AMPA channel have to do with NMDA?

A

depolarized AMPA channel repels Mg2+ that normal blocks NMDA channel, allowing influx of Na+ and Ca2+

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63
Q

What does NMDA channel do in the big picture of function?

A

drives neuronal plasticity involved in learning and memory

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64
Q

What drugs block NMDA channels and why would they be used?

A
  • ketamine - anesthesia - memantine - Alzheimer’s
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65
Q

What is the major inhibitory NT in the CNS?

A

GABA

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66
Q

Epilepsy can be induced by blocking which ligand-gated channel?

A

GABAa

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67
Q

TRPA channels, with gene TRPA1 are found at sensory nerve terminals and respond to what stimulus?

A

painful response to mustard oil, wasabi, or tear gas (acrolein), burning of propofol, extreme cold

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68
Q

TRPV channels, esp TRPV1 are activated by… When might they be a target of a drug?

A

noxious heat and capsaicin - drug target for pain management, such as capsaicin transdermal patch to desensitize nociceptors

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69
Q

TRPM channels, esp TRPM8 is activated by…

A

methanol, cool sensation - signaling cold temp to CNS

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70
Q

In …. propagation, amplitude of the electrical signals do not change with distance from the source and participate as “…..”

A

active all or none there is a threshold for generation

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71
Q

amplitude decreases as it gets farther from its source is part of…

A

passive propagation

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72
Q

Nav channels in the active zone are…

A

activated

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73
Q

Active propagation along axons requires..

A

Nav channels

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74
Q

In the refractory zone, some Kv channels are …

A

open

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75
Q

What is the gating process that causes APs to annihilate each other when they meet in an axon?

A

Nav channel inactivation (refractory zones that follow APs)

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76
Q

synaptic input activated multiple times in a short period would be considered …. and occurs with (passive/active) electrical signals?

A

temporal summation passive electrical signals

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77
Q

simultaneous activation of multiple inputs would be considered… and occurs in passive electrical signals.

A

spatial summation

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78
Q

What are synaptic potentials?

A

EPSP and IPSP traveling along dendrite to soma

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79
Q

Why does amplitude of electrical signal decrease with distance from the source in passive propagation?

A

loss/leak of current along the membrane depending on 1. axial resistance 2. membrane resistance

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80
Q

If the diameter of an axon increases, then the resistance of that axon will…

A

decrease

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81
Q

If there is a higher membrane resistance of an axon, what will happen to the electrical signal? What creates membrane resistance?

A

less leaking, goes farther - created by myelination from Schwann cells in PNS and Oligodendrocytes in CNS

82
Q

In myelinated axons, Nav channels are found only …

A

at Nodes of Ranvier

83
Q

Where are Kv channels in myelinated axons? How do they work?

A

buried in myelin - non-functioning in healthy humans, but as demyelinating disease occurs, Kv channels are exposed and will slow AP propagation

84
Q

In healthy pt, a myelinated axon with an AP is only repolarized by what channels?

A

Nav inactivation and K2p activation

85
Q

small diameter unmyelinated axons have lower AP conduction velocity compared to large myelinated axons because…

A

the distance that passively propagated positive current spreads is shorter

86
Q

What is determined by the number of active channels opposing depolarization vs. driving depolarization?

A

AP threshold

87
Q

What is the mechanism holding the absolute refractory period?

A

Nav channel inactivation mostly - some activity of Kv following APs are generated in unmyelinated axons and neuronal cell bodies

88
Q

a frequency decreasing with continued application of a stimulus would be considered… How does this work?

A

accomodation/adaptation - build up of inactivated Nav channels and activated Kv channels with each AP so strong that AP can be terminated while stimulus is still applied

89
Q

What K+ channel is too slow to participate in AP repolarization? What does the channel do instead?

A

Kv7 - regulate excitability by 1. some open and help set RMP 2. can help terminate a burst

90
Q

Mutation in Kv7 gene can result in … What drug targets Kv7 channel (increasing K+ efflux across neuronal membrane) to combat this?

A

epileptic seizures - Ezogabine

91
Q

for a subthreshold stimulus, the membrane potential is repolarized by the activity of…

A

K2p channels

92
Q

What structures are used by neurons to receive input from other neurons?

A

both soma and dendrite

93
Q

AP invades synaptic terminal and activates what channels that will open a pathway for Ca2+ influx into synaptic terminal?

A

Cav2 channels

94
Q

Ca2+ influx into synaptic terminals will bind to

A

vesicle docking proteins

95
Q

The binding of Ca2+ and vesicle docking proteins in the presynaptic terminal will cause…

A

fusion of synaptic vesicle with presynaptic membrane, ultimately releasing stored NT into the cleft

96
Q

NT will cross the cleft and bind to and activate receptors/ion channels to generate…

A

PSP - post-synaptic potential (either EPSP or IPSP)

97
Q

How are most NTs removed from the cleft?

A

transport proteins

98
Q

Tricyclic antidepressants treat depression by…

A

blocking serotonin reuptake

99
Q

Botulinum toxin produce their clinical effect at the NMJ by…

A

destroying presynaptic vesicle docking proteins

100
Q

Fast synaptic transmission occurs via a combo receptor and channel put into 1 protein. They are called Ionotropic receptors. Examples are…

A

excitatory - glutamate -> AMPA and NMDA channels - ACh -> nicotonic receptors inhibitory - GABA -> GABAa - glycine -> glycineR

101
Q

Slow synaptic transmission goes through..

A

GPCRs or metabotropic receptors

102
Q

What is the primary effect of GIRK?

A

inhibiting neuronal activity, like in opioids

103
Q

Cav2 channels are inhibited by… to inhibit AP signaling by suppressing Ca2+ influx; it inhibits excitatory NT release, even excitatory when inhibiting GABA

A

Beta gamma subunit of GPCRs

104
Q

Ketamine blocks what channel?

A

NMDA

105
Q

Valium enhances what channel?

A

GABA

106
Q

Morphine inhibits pain by bindign to mu-opioid receptors that results in

A

inhibition of presynaptic glutamate release

107
Q

inhibitory synapses are primarily found on the…

A

soma

108
Q

summation of EPSPs enough for AP generation at axon hillocks are considered…

A

synaptic integration

109
Q

IPSP can cancel out EPSP through ….

A

spatial summation

110
Q

If GABAa is inhibited by IPSPs (perhaps by picrotoxin), it will cause…

A

epilepsy

111
Q

What does picrotoxin do?

A

reduces membrane Cl- conductance, causing IPSPs to inhibit GABAa

112
Q

What would you give to terminate seizures?

A

midazolam

113
Q

In healthy muscle, an AP in a motor neuron will…

A

always elicit contraction of the muscle fibers contacted by that motor neuron

114
Q

What neurons are efferent and the only kind of neurons to synapse on skeletal muscle?

A

motor neurons

115
Q

What NT is used by motor neurons?

A

ACh

116
Q

What is a motor neuron + all fibers contacted by it?

A

motor unit

117
Q

fine motor skills require (larger/smaller) motor units

A

smaller

118
Q

Extrafusal fibers are innervated by what types of motor neurons? What do the extrafusal fibers do?

A

alpha and beta MNs generate muscle force

119
Q

What do intrafusal fibers do and what type of MNs innervate them?

A

modulate sensitivity, forming part of the muscle spindle gamma and beta MNs

120
Q

What four things comprise the muscle spindle?

A

intrafusal muscle fibers primary sensory afferent (group Ia) secondary sensory afferent (group II) efferent neurons from beta or gamma MNs

121
Q

The muscle spindle recognizes stretch when …. receptors are activated in afferent nerve terminals called… This will …. the afferent nerve.

A

mechanoreceptors sensory transduction zone depolarize

122
Q

group Ia afferents (Aalpha) are the fastest AP conducting axons innervating the middle section of the spindle and signal…

A

both transient stretch and muscle length

123
Q

group II (Abeta) afferents are moderately fast and signal…

A

only muscle length

124
Q

What is the primary function of intrafusal fiber contraction?

A

maintain spindle sensitivity during extrafusal muscle contraction

125
Q

What prevents there from being slack in a muscle spindle?

A

co-contraction of extrafusal and intrafusal fibers

126
Q

What comprises the Golgi Tendon apparatus?

A

afferent fibers intertwined with collagen fibers of the tendon

127
Q

How does the Golgi tendon signal muscle force?

A

collagen fibers “squeeze” afferent fibers when contraction is occurring, thus increasing force and activating mechanoreceptors.

128
Q

What type of afferent fibers do Golgi Tendon apparatus have? How are they working here?

A

afferent fibers are group Ib - fast AP receptor potential is passively propagated to spike generating zone where APs initiate if receptor potential is greater than threshold.

129
Q

Which type of muscle afferent is activated by the tendon tap?

A

group Ia

130
Q

A load is applied to a muscle, but the muscle does not contract. Which receptor type will be primarily activated?

A

muscle spindles

131
Q

A load is applied to a muscle, and the muscle contracts, but the intrafusal fibers do not contract. Which receptor type will be primarily activated?

A

Golgi tendon organs

132
Q

A fundamental property of MNs is that they…

A

always have some basal AP activity

133
Q

A myotactic unit includes:

A

all extensor and flexor muscles around a joint

134
Q

For reciprocal motor control, an afferent that induces contraction of the muscle in which it resides will also induce…

A

relaxation in the antagonistic muscles in the myotactic unit

135
Q

The stretch reflex is also known as the … reflex. How is this reflex initiated?

A

myotactic reflex initiated by activation of muscle spindle Ia afferents

136
Q

The inverse myotactic reflex is initiated by… What happens with this reflex?

A

activation of Ib afferents from Golgi tendon resident and synergistic muscles relax while antagonist muscle contracts

137
Q

The Ia afferents from muscle spindles make direct excitatory contacts onto motor neurons that innervate

A

both the resident and synergistic muscles

138
Q

To remove the limb from danger, the withdrawal reflex activates…

A

flexor muscle of the injured limb

139
Q

The H-reflex used the circuitry of…

A

stretch reflex

140
Q

What type of pain fibers participate in the crossed extensor reflex?

A

Adelta pain fibers

141
Q

What results from the hyperactivity of the motor neurons in a muscle?

A

cramping

142
Q

What is the mechanism behind treating muscle cramps?

A

a strong force applied activates Golgi tendon and inverse myotactic reflex to inhibit activity of the motor neurons causing cramps

143
Q

What are inhibitory interneurons that are activated by MNs to inhibit the same motor neurons? What would this be called?

A

Renshaw cells feedback inhibition

144
Q

What NT do MNs use to activate Renshaw cells?

A

ACh

145
Q

Based on peripheral motor control, increased activity of gamma MNs without a change in muscle length will…

A

contract the muscle innervated by the gamma MNs

146
Q

What NT do Renshaw cells use to inhibit MNs?

A

glycine

147
Q

Tetanus toxin produces its clinical effects by…

A

preventing glycine release, ultimately decreasing Renshaw cells ability to inhibit MNs and it causes hyperactivity of MNs

148
Q

What fiber type carries ‘fast’ pain, sharp, stabbing, through the dorsal horn, specifically lamina I and V

A

A delta

149
Q

What fibers carry slow pain, burning or aching, through the dorsal horn? What lamina do they go through for their first synapse?

A

C-fibers

lamina I and II

150
Q

Pain fibers, whether A delta or C-fibers, will cross midline and ascend in what tract?

A

spinothalamic

151
Q

In short term sensitization of pain, PKA and PKC will be activated by what? What do PKA and PKC do then?

A

activated by Ca2+, PG, or bradykinin

PKA and PKC will phosphorylate channels like TRPV, MA, Nav, and Kv

152
Q

Activation of what kind of touch receptors can inhibit activity of secondary nociceptors to decrease pain signals using glutamate?

A

Merkel cell touch receptors

153
Q

‘Wind up’ is a spinal mechanism of pain sensitization that is from…

A

increased secondary nociceptor activation induced by repeated or continuous primary nociceptor activity

154
Q

How can wind up be reversed?

A

when primary nociceptor activity returns to normal or with drugs

155
Q

What happens if a primary nociceptor remains elevated in sensitizing pain?

A

increased Calcium in secondary nociceptor leads to kinase activation, leading to long term potentiation of noc. synapses

156
Q

How does kinase mediated sensitization of pain work?

A

calcium activation of PKC leads to phosphorylation of AMPA and NMDA receptors leading to increased activity and increased response of secondary nociceptors to glutamate

157
Q

How do microglia come in to play with injured neurons? What do they do?

A

injured neurons release cytokines and ATP that attract and activate microglia in DH

microglia will release BDNF

158
Q

What does BDNF do in increasing pain sensitization?

A

exacerbates secondary nociceptors by inhibiting GABAa mediated inhibition – hyperalgesia

continued release induces axonal sprouting, creating a low threshold for MA receptors and does some direct rewiring to secondary nociceptors - allodynia

159
Q

What receptors use A beta fibers?

A

Merkel cell touch receptors

160
Q

What are the origins of a descending pain pathway that modulates pain signals?

A

Anterior cingulate cortex and HT

161
Q

From the ACC and the HT, how does the rest of the descending pain pathway go?

A

both go down to synapse in PAG and then continue down to the RVM (rostral ventromedial medulla).

RVM sends its axon to the dorsal horn of the spinal cord

162
Q

What is the pain enhancement pathway?

A

amygdala to PAG to RVM to activate ‘on cells’ in RVM

this will increase activity in response to noxious stimuli - hyperalgesia

163
Q

What is the pain inhibition pathway?

A

HT and ACC to PAG to activate ‘off-cells’ in RVM

this increases activity of inhibition of pain transmission in the dorsal horn

164
Q

How are off-cells of the RVM activated?

A

endogenous opioid NT and then off-cells release endogenous opioid NT onto primary nociceptor afferents and secondary nociceptors to inhibit pain in dorsal horn

165
Q

What is the target for all opioid analgesic drugs?

A

mu (MOR)

166
Q

How does MOR work?

A
  • pre-synaptic - inhibits Cav to inhibit NT release, inhibiting GABA, to release off-cells from tonic inhibition
  • post-synaptically - activation of GIRK (inhibits on-cells)
167
Q

What are two endogenous agents that are endocannabinoids? Which one is in greater concentration in the body?

A

anandamide

2-AG (greater concentration)

168
Q

endocannabinoids are synthesized in neurons and immune cells for what purpose?

A

negative FB systems for inflammation and pain

169
Q

What are the cannabinoid receptors activated by?

A

CB1 - both anandamide and 2-AG

CB2 - only 2-AG

170
Q

Which cannabinoid receptor is expressed by periph and central neurons and immune cells like macrophages and microglia?

A

CB2

171
Q

Which cannabinoid receptor is probably a better target for analgesic effects?

A

CB2

172
Q

Which receptor is responsible for the psychobehavioral effects of THC?

A

CB1

173
Q

Where are CB receptors located?

A

pre-synaptic side of primary nociceptors and cell bodies of secondary nociceptors with MOR and alpha2-adrenergic receptors

174
Q

How do CB receptors work pre and post synaptically?

A
  • pre-synaptically - GPCR > inhibits Ca > inhibits NT release (glutamate)
  • post-synaptically - GIRK> hyperpolarizes membrane potential of secondary nociceptor and inhibits AP
175
Q

Activation of CB receptors and MOR will inhibit generation of pain by blocking what receptor pathways?

A

TRPV1

ASIC

TRPA1

176
Q

What will block the placebo effect?

A

blocking MOR with naloxone

177
Q

secondary nociceptors have their cell bodies in the

A

dorsal horn of spinal cord

178
Q

What NT is released by secondary nociceptors to produce excitatory post-synaptic potentionals in tertiary nociceptors?

A

glutamate

179
Q

A clinically important ion channel subunit is…

A

Nav Beta subunit

180
Q

Silent nociceptors are termed silent because they…

A

are not activated by noxious stimuli, but still produce pain

181
Q

Which channel type is activated during both nociceptive and inflammatory pain?

A

ASIC channels

182
Q

In neuropathic pain, the levels of which ion channel type or subunit type is reduced to increase nociceptor activity?

A

Kv channels

183
Q

Increased ion channel activity in peripheral neuropathic pain results from changes in

A

gene transcription

184
Q

Sunburn produces allodynia by activation of

A

Protein Kinase A

185
Q

A noxious stimulus that produces the same level of pain both before and after a sunburn is an example of

A

nociceptive pain

186
Q

In gate-control of pain, which NT is released by Abeta fibers to cause the inhibition of secondary nociceptors?

A

glutamate

187
Q

What ion channel provides calcium needed to produce Windup in secondary nociceptors?

A

NMDA receptor/channels

188
Q

The primary activator of kinases to induce kinase-based sensitization is…

A

calcium

189
Q

Which NT activates microglia to release BDNF?

A

ATP

190
Q

What induces the block of GABAa receptor-induced inhibition of secondary nociceptors to generate central sensitization?

A

BDNF

191
Q

Irreversible allodynia results from…

A

axonal-sprouting of non-nociceptors

192
Q

The on-cells of the RVM are directly activated by excitatory input from neurons located in the…

A

PAG

193
Q

The NT used to activate on-cells is…

A

glutamate

194
Q

The mechanism that activates ‘off-cells’ involves disinhibition. The NT that induces disinhibition is/are…

A

opioid peptides

195
Q

Morphine blocks pain signaling in the dorsal horn by…

A

hyperpolarizing the membrane potential of secondary nociceptors

196
Q

Disinhibition of Off-cells is achieved by the…

A

inhibition of presynaptic calcium channels to block the release of GABA

197
Q

THC is an agonist of…

A

CB1

198
Q

Analgesia induced from activation of CB1 by anandamide results from…

A

inhibition of GABA release in RVM

199
Q

We know that placebos activate endogenous analgesic pathways because …

A

blocking MOR receptors with naloxone inhibits the placebo effect

200
Q

Central hyperalgesia can be caused by activation of…

A

on-cells in the RVM

Neuro (9 decks)

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