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SMP - Neurophysio Exam 1 > Lectures 3 & 4 - Neurotransmitter Lifecycle and Neuropharmacology > Flashcards

Lectures 3 & 4 - Neurotransmitter Lifecycle and Neuropharmacology Flashcards

1
Q

What are agonists?

A

Molecules that can bind to receptors and activate them = produce the same biological response as the endogenous ligand

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2
Q

What are antagonists? Eg?

A

Molecules that bind the receptor and are inherently inert except that they may block the functionality of an agonist

Eg: Magnesium at the NMDA receptor

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3
Q

What are the 6 ways in which a drug can act as an agonist in the NT lifecyle?

A
  1. Serve as a precursor for an NT
  2. Stimulate the release of NT vesicles
  3. Stimulate postsynaptic receptors
  4. Block autoreceptors to increase the synthesis/release of NTs
  5. Block NT reuptake
  6. Inactivate enzyme breaking down NTs
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4
Q

What are the 5 ways in which a drug can act as an antagonist in the NT lifecyle?

A
  1. Prevent storage of NTs in vesicles
  2. Inhibit the release of NT vesicles
  3. Block postsynaptic receptors
  4. Inactivate the enzyme responsible for synthesizing the NT
  5. Stimulate autoreceptors to inhibit the synthesis/release of NTs
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5
Q

What is an example of a drug serving as a precursor for an NT?

A

Drug given to Parkinson’s disease patients is L-dopa, which serves as a precursor to dopamine

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6
Q

What is an example of a drug stimulating the release of NT vesicles?

A

The black widow spider venom stimulates the release of ACh

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7
Q

What is an example of 2 drugs stimulating postsynaptic receptors?

A

Nicotine and muscarine stimulate ACh receptors

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8
Q

What is an example of a drug blocking autoreceptors to increase the synthesis/release of NTs?

A

Clonidine increases the synthesis/release of norepi

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9
Q

What is an example of a drug blocking NT reuptake?

A

Cocaine blocking dopamine reuptake by blocking DAT

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10
Q

What is an example of a drug inactivating the enzyme breaking down NTs?

A

Physostigmine inactivates acetylcholinesterase

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11
Q

What is an example of a drug preventing the storage of NTs in vesicles?

A

Reserpine inhibits the storage of monoamines in vesicles by blocking VMAT

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12
Q

What is an example of 2 drugs blocking postsynaptic receptors?

A

Curare and atropine block ACh receptors

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13
Q

What is an example of a drug inactivating the enzyme responsible for synthesizing the NT?

A

PCPA inactivating the enzyme that synthesizes serotonin

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14
Q

What is an example of a drug stimulating autoreceptors to inhibit the synthesis/release of NTs?

A

Apomorphine to inhibit the synthesis/release of dopamine

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15
Q

Describe NT secretory vesicles.

A

Very specialized organelles with lipid bilayers

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16
Q

What is an example of a drug inhibiting the release of NT vesicles? Purpose?

A

Botulinum toxin (botox) inhibiting ACh release to prevent wrinkling

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17
Q

What are the 2 types of ACh postsynaptic receptors?

A
  1. Nicotinic

2. Muscarinic

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18
Q

Why is it very important to respect drug dosages?

A

Because all drugs are poisonous and can have serious side effects including death

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19
Q

What are NT autoreceptors? Eg?

A

Receptors that bind the NT in the presynaptic nerve terminal serving as part of a negative feedback loop in signal transduction

eg: Muscarinic ACh receptors in presynaptic terminal

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20
Q

What ion does NT reuptake depend on?

A

Na+

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21
Q

What do anti-depressants do? What are they called?

A

Block the reuptake of serotonin by blocking SERT

SSRIs = selective serotonin reuptake inhibitors

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22
Q

What are the 3 criteria for defining a molecule as a neurotransmitter? Example for 1 and 3? Do you need all 3 to be an NT?

A
  1. The substance must be produced and stored by the presynaptic neuron (eg: glutamate and glycine are non-essential AAs so are found in all cells, but in some neurons they are NTs)
  2. The substance must be released in an activity (Ca2+) dependent manner
  3. Specific receptors for the substance must be present on the postsynaptic cell (eg: application of exogenous NT mimics the postsynaptic effect of presynaptic stimulation)

YES, NEED ALL 3

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23
Q

What is also packaged in vesicles on top of NTs? Eg?

A

Co-transmitters that can have multiple effects upon release

Eg: ATP

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24
Q

How to classify NTs by size? List them and provide examples.

A
  1. Small: AAs, monoamines, and ACh

2. Large: peptides, derived from larger precursor proteins (eg: enkephalin, substance P)

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25
Q

What is the difference between how small and large NTs are synthesized? Which is faster? Why?

A
  1. Small: enzymes synthesized in cell body slowly travel down the axon and synthesize NTs from NT precursors that have been transported from the synaptic cleft to the axon terminal. Packaging of NTs in vesicles then happens at the axon terminal. => FASTER because recycling of previously released NTs
  2. Large: enzymes and NT precursors are synthesized in the cell body are transported in vesicles down microtubule tracks in the axon. Once they get to the axon terminal the enzymes modify the precursors inside the vesicles
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26
Q

What are neuromodulators?

A

Molecules which may not fit all of the 3 criteria to be NTs, but influence the electrical activity of postsynaptic neurons

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27
Q

What kind of NTs are opioid analgesics?

A

Peptides

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28
Q

What are 3 endogenous opioids?

A
  1. Endorphins
  2. Enkephalins
  3. Dynorphins
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29
Q

To what receptors do opioids bind?

A

Mu-opioid GPCR (MORs)

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30
Q

What are opioids degraded by?

A

Extracellular peptidases

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31
Q

What are 4 exogenous opioids? What is another name for these?

A
  1. Morphine
  2. Codeine
  3. Oxycodone
  4. Heroin

= Analgesics

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32
Q

What NTs are released after exercise?

A

Opioids

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33
Q

What is a common and dangerous side-effect of exogenous opioids? What does this lead do?

A

Euphoria leading to abuse leading to the disinhibition of the ventral tegmental area of the brain releasing dopamine into the forebrain

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34
Q

How do opioids control pain?

A

Opioid releasing neurons inhibit C-fibers (type of nociceptors) which synapse onto neurons ascending to the dorsal horn of the spinal cord, thereby inhibiting our central perception of pain

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35
Q

What are C-fibers?

A

Fibers within our CNS that represent our ability to detect pain

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36
Q

What are 3 other side-effects of exogenous opiates? Explain each.

A
  1. Itching due to a generalized release of histamines by mast cells
  2. Slowed breathing due to a decreased sensitivity of medullary chemoreceptive neurons to CO2
  3. Nausea, vomiting, and constipation due to the activation of gut MORs
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37
Q

Where are AA NTs most prevalent?

A

CNS

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38
Q

What is the precursor to the NT GABA? What is the enzyme?

A

Glutamic acid decarboxylase (GAD): glutamate => GABA + CO2

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39
Q

What are the 2 AA NTs?

A
  1. Glutamate

2. Glycine

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40
Q

Is glutamate excitatory or inhibitory?

A

Excitatory

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41
Q

How is glutamate removed from the synaptic cleft?

A

Excitatory AA transporter (EAAT) on:

  1. Pre/Post-synaptic membranes
  2. Astrocytes
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42
Q

How is glutamate degraded intracellularly? In what cells?

A

Glutamine synthase: glutamate + ATP => glutamine + ADP + Pi

In astrocytes and neurons

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43
Q

How is glutamine transported to the presynaptic terminal?

A

SNAT7

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44
Q

What enzyme synthesizes glutamate?

A

Glutaminase

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45
Q

What transporter repackages Glu in vesicles in the presynaptic terminal?

A

Vesicular glutamate transporter (VGLUT)

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46
Q

Describe the speed of the Glu lifecycle.

A

Really fast

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47
Q

What are the 2 main types of Glu receptors? List the subtypes for each.

A
  1. Ionotropic receptors: AMPA, NMDA, kainate

2. Metabotropic GPCRs: mGluR1-8

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48
Q

Describe ionotropic and metabotropic NT receptors. What is the mechanism for each called? Which is faster?

A
  1. Ionotropic receptors form an ion channel pore = direct gating (FASTER)
  2. Metabotropic receptors are indirectly linked with ion channels on the plasma membrane of the cell through signal transduction mechanisms, often G proteins = indirect gating
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49
Q

What does AMPA stand for?

A

Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor

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50
Q

What do all of the ionotropic glutamate receptors have in common?

A

Non-selective cation channels

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51
Q

What can block the NMDA receptor?

A

Mg++

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52
Q

What ions are permeable in the AMPA receptors?

A

Na+/K+

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53
Q

What ions are permeable in the NMDA receptors?

A

Na+, K+, and Ca++

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54
Q

What ions are permeable in the Kainate receptors?

A

Cations

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55
Q

What does NMDA stand for?

A

N-methyl-D-aspartate

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56
Q

What are the metabotropic glutamate receptors very critical for?

A

Synaptic plasticity, learning and memory, and information storage

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57
Q

What 4 things can synaptic plasticity refer to?

A
  1. Synapse formation
  2. Synapse refinement
  3. Activity dependent plasticity
  4. Synaptic competition = selection of particular spines to activate
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58
Q

Describe the mechanism of activity dependent plasticity? What does it arise from? What is this important for?

A

The more you activate a postsynaptic membrane, the more you will have a flux of AMPA/NMDA receptors that are contributing to the size and shape of dendritic spines and upon binding of glutamate within specific patterns (slow/fast activation) we can change the synaptic gain of the synapse. These will also stay longer.

Arises from the use of cognitive functions and personal experience so it is the biological basis for learning and the formation of new memories

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59
Q

Is GABA excitatory or inhibitory?

A

Inhibitory

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60
Q

Describe the synthesis of GABA.

A

GAD: glutamate => GABA

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61
Q

By what is GABA packaged into vesicles in the presynaptic terminal?

A

Vesicular GABA transporter (VGAT)

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62
Q

By what is GABA removed from the synaptic cleft?

A

Presynaptic/astrocyte GABA transporter (GAT)

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63
Q

What are the 2 types of GABA receptors? List them.

A
  1. Ionotropic: GABAa, GABAc

2. GPCRs: GABAb

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64
Q

What are GABA a and c receptors permeable to? Direction of flux?

A

Cl-

Inward

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65
Q

Where are GABAc receptors found?

A

Retina

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66
Q

Which GABA receptors are more prevalent: a or c?

A

a

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67
Q

Where are postsynaptic densities (PSDs) found? What are they made of?

A

Glutamatergic synapses

Electron dense regions filled with glutamate receptors and other proteins

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68
Q

What is CaMKII? Where is it found? Role?

A

Enzyme that can detect Ca++ flow at a synapse found in PSDs

Contributes to LTP by phosphorylating substrates

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69
Q

How have researchers tried to understand how info is stored in our CNS?

A

Used an animal model of an acute brain slice preparation (hippocampus) and record the long-term potentiation of excitatory postsynaptic potential (EPSP) with extracellular field electrodes to axon stimulation at variable frequencies => the EPSP is amplified after the tetanus for long periods of time

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70
Q

What is a tetanus?

A

High frequency stimulation

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71
Q

Describe the long-term potentiation induction with glutamate.

A

Glutamate binds to its receptors at resting potential: only the AMPA receptor is activated because NMDA is blocked by Mg++ and once depolarization of postsynaptic membrane is reached, the NMDA receptors are also activated so Ca++ influx starts

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72
Q

Which receptor is called the coincidence detector?

A

NMDA receptor

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73
Q

What 2 things are required for plasticity/LTP?

A
  1. Depolarization of postsynaptic membrane = glutamate

2. Ca++ entry = depolarization

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74
Q

What is the opposite of LTP? What does it do?

A

Long Term Depression (LTD)

Depresses EPSP for long periods of time

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75
Q

When does LTD occur?

A

Sleep

76
Q

LTP stimulation frequency?

A

Brief, high frequency

77
Q

LTD stimulation frequency?

A

Low-frequency for 10-15 min

78
Q

Are NMDARs activated in both LTP and LTD?

A

YUP

79
Q

LTP Ca++ rise?

A

Large

80
Q

LTD Ca++ rise?

A

Small

81
Q

LTP: AMPARs inserted or removed?

A

Inserted

82
Q

LTD: AMPARs inserted or removed?

A

Removed

83
Q

What 2 drugs blocks NMDARs?

A
  1. Ketamine

2. PCP

84
Q

What enzymes are involved in LTP?

A

Kinases

85
Q

What enzymes are involved in LTD?

A

Phosphatases

86
Q

What are GABAb receptors a drug target for?

A

Autism

87
Q

Where are GABAb receptors located?

A

Both the pre and post synaptic cells

88
Q

How does ambient GABA affect the presynaptic terminal? What is this called?

A

It binds to GABAb receptors (GABA autoreceptors) and beta and gamma subunits of the receptor inhibit further GABA release by inhibiting VG CA++ channels

89
Q

What are the 3 subunits of GPCRs? What do we call them?

A

Heterotrimer: alpha, beta, and gamma subunits

90
Q

Describe GABA binding to GABAb receptors on postsynaptic cell.

A

It binds to GABAb receptors and beta and gamma subunits of the receptor activate G-protein inwardly rectifying K+ channels (GIRK)

91
Q

What are the 2 ways in which GABA hyperpolarizes the post synaptic cell?

A
  1. Binds GABAa receptors to let Cl- in

2. Binds GABAb receptors to let K+ out

92
Q

What is spillover GABA? How would it affect a glutamate neuron? What is this called?

A

When there are many APs flowing down a GABAnergic neuron, a lot of GABA will be released and some of it, spillover GABA, can affect a glutamate neuron by binding GABAb heteroreceptors on the presynaptic terminal to inhibit the Ca++ channels to decrease the release of glutamate

93
Q

Where are NT receptors located on a neuron?

A

Dendritic spines and shafts

94
Q

What do sedatives do generally?

A

They decrease arousal

95
Q

What are the 3 kinds of sedatives?

A
  1. Barbiturates
  2. Benzodiazepine
  3. Ethanol
96
Q

What are 2 barbituate drugs? What receptor do they target?

A
  1. Sleeping pills
  2. Anti-epileptics

GABAa receptor agonists

97
Q

What is the mechanism of action of benzodiazepine and barbituate?

A

Allosteric modulators and potentiators of the GABAa receptor to alter the effects of GABA binding = increase the flux of Cl- through the ion channel

98
Q

What are the 4 mechanisms of action of ethanol?

A
  1. NMDA receptor allosteric inhibitor
  2. GABAa receptor agonist
  3. 5-HT3 receptor allosteric activator
  4. Blocks VG-Ca++ channels
99
Q

Why is ethanol dangerous in terms of overdoses and withdrawal?

A

Because of its widespread effects

100
Q

Can ethanol cross the BBB?

A

Yes

101
Q

Why does alcohol cause memory loss (aka blackouts)?

A

Because its an NMDA receptors antagonist (allosteric inhibition) and will inhibit the formation of synaptic plasticity

102
Q

Which act faster the AA NTs or the monoamines?

A

AA

103
Q

What are the 5 monoamine NTs?

A
  1. Dopamine
  2. Norepi
  3. Epi
  4. Serotonin
  5. Histamine
104
Q

What is the shorthand for serotonin?

A

5-HT

105
Q

Is serotonin a catecholamine?

A

NOPE

106
Q

What is another name for epinephrine?

A

Adrenaline

107
Q

What are the 3 catecholamines? Why are they called like this?

A
  1. DA
  2. NE
  3. EPI

Because they contain a catechol group: aromatic ring with 2 OH groups next to one another and 1C away from ring attachment

108
Q

Describe the structure of dopamine.

A

Catechol-CH2-CH2-NH2

109
Q

Describe the structure of norepi.

A

Catechol-CH-(OH)-CH2-NH2

110
Q

Describe the structure of epi.

A

Catechol-CH-(OH)-CH2-NH-CH3

111
Q

What are the 2 main types of neurons in our CNS?

A

GABAnergic and glutamatergic neurons

112
Q

What is the role of monoamine NTs in the CNS?

A

Diffuse modulatory role

113
Q

What is the role of monoamine NTs in the PNS?

A

NTs of the sympathetic NS

114
Q

Describe the synthesis of catecholamines (4 steps). Which is the rate limiting step?

A
  1. Tyrosine hydroxylase: tyrosine = L-dopa (OH added on aromatic ring) - RATE LIMITING
  2. Dopa decarboxylase: L-dopa = dopamine (remove COOH)
  3. Dopamine beta-hydroxylase: dopamine = NE (OH added on C1 of side chain)
  4. Phentolamine N-methyltransferase(PNMT): NE = EPI (CH3 added on N)
115
Q

What does dopa stand for?

A

Dihydroxyphenylalanine

116
Q

What is dopamine critical for? 3 things

A
  1. Reward
  2. Evaluating the saliency of our day to day lives
  3. Learning mechanisms
117
Q

Where are dopamine neurons found?

A
  1. Ventral tegmental area
  2. Substantia negra
  3. Other structures deep within our midbrain
118
Q

What NT is addiction to alcohol and opiates associated with? Describe it.

A

Dopamine system: aberrant learning of substance abuse that you know is bad for you

119
Q

What is the other name of serotonin?

A

5-hydroxytryptamine

120
Q

Describe the synthesis of serotonin (2 steps)

A
  1. Tryptophan hydroxylase: trypotophan = 5-hydroxytryptophan (OH added on aromatic ring)
  2. 5-HTP decarboxylase: 5-hydroxytryptophan = 5-hydroxytryptamine (COOH removed)
121
Q

How are all monoamine NTs transported into vesicles?

A

Vesicular monoamine transporter (VMAT)

122
Q

Describe the dopamine CNS system.

A

Dopamine neurons in the substantia negra and ventral tegmental area send within ascending dopaminergic fibers into areas of the brain that are responsible for detection of reward: basal ganglia, frontal lobe, striatum

123
Q

What do all monoamine NTs stimulate?

A

Arousal

124
Q

What area of the brain is degenerative in Parkinson’s disease?

A

Substantia negra

125
Q

What is serotonin important for?

A

Mood

126
Q

Describe the serotonin CNS system.

A

Rafi nuclei secrete serotonin and there is a very diffuse innervation across the CNS: cerebellum, hypo, temporal lobe, thalamus, neocortex, basal ganglia

127
Q

Describe the norepi CNS system.

A

Locus coeruleus spontaneously secretes norepi to cerebellum, thalamus, neocortex, hypo, temporal lobe

128
Q

Describe the epi CNS system.

A

Medullary neurons secrete epi into lower brain structures: medulla, hypo, cerebellum, corpus callosum, thalamus, hypo, pons, cerebral cortex

129
Q

Rank the prevalence of nerves of the monoamines.

A
  1. Serotonin
  2. Dopamine
  3. Norepi
  4. Epi
130
Q

How are the actions of monoamine NT stopped? 2 ways

A
  1. Removal by specific transporters (reuptake): DAT, NET (NE and EPI), and SERT
  2. Degraded in presynaptic terminal by monoamine oxidase or catecholamine-O-methyltransferase (COMT)
131
Q

What are 2 examples of SSRIs?

A
  1. Paxil

2. Flouxetine

132
Q

How do tricyclic antidepressants work?

A

Block the reuptake of ALL monoamine NTs

133
Q

What is the biological issue of people who are chronically depressed?

A

They do not have enough monoamines in their CNS synapses in particular areas of the brain

134
Q

What are the 3 classes of antidepressants? Which is the most prevalently used and efficacious?

A
  1. Tricyclic
  2. SSRIs***
  3. MAOIs
135
Q

How do MAOI antidepressants work?

A

They inhibit monoamine oxidase to inhibit the degradation of monoamines at the synapse

136
Q

What enzyme synthesizes ACh? Describe the reaction.

A

Choline acetyltransferase (ChAT): choline + acetyl CoA = ACh

137
Q

How is ACh transported into vesicles?

A

Vesicular transporter AChT

138
Q

How is ACh broken down?

A

Acetylcholinesterase (AChE) in the basal lamina of the postsynaptic cell

139
Q

What are the 2 postsynaptic ACh receptors? Describe each

A
  1. Nicotinic = ionotropic non-selective cation channel

2. Muscarinic = GPCR activating K+ channels

140
Q

How is choline transported into the presynaptic cleft for ACh synthesis?

A

Na+/Choline symporter

141
Q

What is special about acetylcholinesterase?

A

One of the fastest enzymes known

142
Q

What kind of drugs are AChE inhibitors? 3 kinds

A
  1. Organophosphate sarin nerve gas and pesticides
  2. Myasthenia gravis to promote contraction at the NMJ
  3. Dementia in Alzheimer’s and Parkinson’s patients (small pop of patients)
143
Q

How can organophosphate pesticides be absorbed?

A

ALL routes: inhalation, ingestion, and dermal absorption

144
Q

Describe sarin nerve gas.

A

Oderless and colorless

145
Q

What are the initial symptoms of sarin nerve gas absorption? What do these mimic?

A

Mimic parasympathetic activation:

  1. Pupillary constriction
  2. Glandular hypersecretion
  3. Cognitive and mood effects
  4. Increased salivation and drooling
  5. Bladder and bowel emptying
146
Q

What is the ultimate symptom of sarin nerve gas?

A

Death due to suffocation from lung muscle paralysis because the muscle will be depolarized for an extended period of time which will cause constriction of the lung muscles

147
Q

What is the role of ACh in the PNS?

A

NT of the parasympathetic NS

148
Q

What are 2 sarin nerve gas antidotes? Explain how each works.

A
  1. Atropine: muscarinic receptor antagonist (called duodote)

2. Pralidoxime: regenerates AChE (only if given within 5 hrs because can prevent covalent bonding of gas with AChE)

149
Q

Describe the disease myasthenia gravis. Symptoms?

A

Autoimmune disorder caused by antibodies (IgG) binding and blocking nicotinic receptors at the NMJ

Impaired facial expressions and speech and swallowing

150
Q

What is another name for myasthenia gravis?

A

Grave muscle weakness

151
Q

How are AChE inhibitors adminstered to MG patients?

A

Orally

152
Q

Describe how the NMJ is affected in MG patients. 5 steps

A
  1. Antibodies bind to nicotinic receptors and cross-link
  2. Signals are sent to speed up the decomposition of the receptors by phagocytosis
  3. Lysosomes help with the decomposition
  4. This results in the smoothing and simplifying of the post-synaptic terminal
  5. Chances of ACh binding to one of the nicotinic receptors decreases
153
Q

Describe the ACh CNS system.

A

Pontomesencephalotegmental complex secretes ACh to medial septel nuclei, basal nucleus of Meynert, neocortex and thalamus

154
Q

What is the main effect of ACh in the CNS?

A

Arousal

155
Q

Which part of the brain are affected in dementia of Alzheimer’s and Parkinson’s disease patients

A

Neocortex

156
Q

What types of NTs are co-transmitters?

A

AAs and monoamines

157
Q

Do all vesicles in one axon terminal contain the same NT(s)?

A

NOPE

158
Q

Can peptide NTs be co-released? With what NTs?

A

Yes with small NTs but not packaged in same NT vesicles

159
Q

How many different NTs can be packaged in the same vesicle?

A

2 or more

160
Q

Which requires more AP firing/more [Ca++]: release of vesicles with small NTs or vesicles with peptides?

A

Vesicles with peptides

161
Q

What do stimulants do generally?

A

Promote arousal

162
Q

What are the 3 types of stimulants?

A
  1. Amphetamines and cocaine
  2. Caffeine
  3. Nicotine
163
Q

How do amphetamines and cocaine work in the CNS?

A

DAT and NET antagonists

164
Q

How does adderall work?

A

DAT antagonist

165
Q

How does caffeine work in the CNS?

A

Adenosine receptor antagonist

166
Q

What is the role of adenosine in the CNS?

A

Ubiquitous neuromodulator

167
Q

How does nicotine work in the CNS?

A

Nicotinic receptor agonist

168
Q

Are the nicotinic receptors at the NMJ affected by normal doses of nicotine?

A

NOPE

169
Q

What are the receptors to weed? What part of the brain are they found in? How do they worK?

A

CB1 = cannabinoid 1 receptor = presynaptic GPCR that blocks Ca++ channels and therefore NT release

Cortex, hypo, brain stem, hippocampus, cerebellum, amygdala

170
Q

What are the highest expressed GPCRs in our brains?

A

CB1 receptors

171
Q

Why does weed cause munchies?

A

Because the hypo has CB1 receptors

172
Q

How does weed affect the brain stem? 7 ways.

A
  1. Nausea relief
  2. Rapid heart rate
  3. Reduced BP
  4. Drowsiness
  5. Pain reduction
  6. Reduced spasticity (muscle contraction)
  7. Reduced tremor
173
Q

How does weed affect the hippocampus?

A

Impaired memory

174
Q

How does weed affect the cerebellum? 2

A

Reduced spasticity and impaired coordination

175
Q

How does weed affect the amygdala? 3

A

Reduced anxiety and blocking of traumatic memories, reduced hostility

176
Q

What is the active ingredient of weed?

A

Tetrahydrocannabidol (THC)

177
Q

What does THC mimic?

A

The effects of endogenous cannabinoids: 2-AG

178
Q

What is the endogenous cannabinoid?

A

2-arachidonoylglycerol (2-AG)

179
Q

Describe the signaling mechanism of 2-AG.

A

Retrograde signaling: postsynaptic release of 2-AG due to influx of Ca++ acts at presynaptic CB1 receptor

180
Q

Is 2-AG lipid or water soluble? What problem does this cause?

A

Lipid, so we do not know how it crosses the synapse

181
Q

What kind of NT is CRH?

A

Peptide NT

182
Q

Are all NTs agonists?

A

YUP

183
Q

What is synaptic plasticity?

A

The ability of chemical synapses to change their strength

184
Q

What are the 3 types of GABAb receptors? Where is each located? How does each work?

A
  1. On presynaptic neuron: GABAb autoreceptor inhibiting calcium VG channels
  2. On postsynaptic neuron: GABAb receptor activates GIRK channels
  3. On neighbor glutamate neuron: GABAb heteroreceptor inhibiting calcium VG channels
185
Q

What other NT (other than opioids) can inhibit C-fibers?

A

GABA

186
Q

What is a mu-receptor antagonist? What can it block?

A

Naloxone

Blocks placebo effect on pain reduction

187
Q

What are Schaffer collaterals?

A

Axon collaterals given off by pyramidal neurons in the hippocampus and are an integral part of memory formation

SMP - Neurophysio Exam 1 (13 decks)

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