Final review Flashcards
1
Q
What is acetylcholine
A
Critical NTs involved in both central/peripheral N.S
2
Q
What is Ach synthesized from
A
Choline+Acetate
3
Q
What is acetate also known as
A
Acetyl-CoA
4
Q
What enzyme allow for the synthesis of Ach
A
ChAT
5
Q
What enzyme packages Ach into the vessicles
A
VAchT
6
Q
What enzyme terminates Ach
A
Ache
7
Q
When broken down what part of Ach is kept to be reuptaken by transporters
A
Choline
8
Q
What is Ach primarily involved in
A
1) All voluntary muscle movement
2) Sleep (REM)
9
Q
What are the 2 types of Ach receptors
A
1) Nicotinic
2) Muscarinic
10
Q
Are the nicotinic receptors ionotropic or metabotropic
A
Ionotropic
11
Q
What is the most common AA in the body and most abundant NT
A
Glutamate
12
Q
Glutamate is synthesized from
A
Glutamine
13
Q
What enzyme allows for the synthesis of glutamune
A
Glutaminase
14
Q
What are the 2 groups of glutamate transporter proteins
A
1) VGlut
2) EAATs
15
Q
Which of the 2 glutamate transporters are used to identify glutamatergic neurons
A
VGlut
16
Q
Which glutamate transporter will remove glutamate at synapse
A
EAAT
17
Q
What are the 4 different glutamate receptors
A
1) AMPA
2) NMDA
3) Kainite
4)mGlurs
18
Q
Which of the glutamate receptors is the most common
A
AMPA
19
Q
Which of the glutamate receptors act as a coincidence detector
A
NMDA
20
Q
What does a coincidence detector mean
A
It requires BOTH
1) Glutamate AND 2) depolorization to remove Mg2+ block of receptors.
21
Q
What is NMDA and coincidence detector important for
A
Long-term Potentiation (LTP)
22
Q
What does LTP happen
A
When one is learning
23
Q
What is LTP
A
Key to form memories. Need NMDA activation and more AMPA activation.
24
Q
Where does LTP happen
A
Hippocampus
25
Which of the glutamate receptors is involved in synaptic plasticity
mGLURs
26
Which of the 4 glutamate receptors is metabotropic
mGLURs
27
What is glutamate used for
1) Learning/memory
2) Seizures
3) Excitotoxicity
28
What is excitotoxicity
Too much glutamate, Ca2+ channels open, cell swell and burst. Cell dies
29
What does GABA stand for
Gamma Amino-Butryric Acid
30
What is GABA most commonly known for
Being the most common inhibitor NT in brain
31
What is GABA synthesized from
Glutamate
32
Which enzyme synthesizes glutamate to GABA
GAD
33
What is the primary role of GABA
Calming effects in the brain
34
Can GABA be broken down at synapse like all the other NT
Nope
35
What is the transporter that removes GABA at synapse
GAT
36
Where does GAT remove GABA from
1) Neurons
2) Glial cells
37
In which of the two cells (neuron, glial) can GABA be converted back to glutamine
Glial
38
What are the 2 receptors for GABA
1) gabba-A
2) GABBA-B
39
Which of the GABA receptors are ionotropic
A
40
What are Opioids and Opiates
Substances sthat bind to opioid receptors to produce pain relief, euphoria or sedation
41
What is the main difference between opioids and opiates
All opiates are opioids but not all opioids are opiates
42
What are opioids
Any substance, natural or not that will bind to opioid receptor and produce morphine-like effects
43
What are opiates
Natural compound derived from the Opium Poppy plant
44
What are examples of opioids
Heroine, fentanyl
45
What are examples of opiates
Morphine, codeine
46
Which between opioids and opiates are endogenous drugs
Opioids
47
Which between opioids and opiates are exogenous drugs
Opiate
48
What are endogenous drugs
Made by the body
49
What are exogenous drugs
Not made by the body have to be taken.
50
What are the 3 types of opioids receptors
1) Mu
2) Delta
3) Kappa
51
Are opioid receptors metabotropic or ionotropic
All metabotropic
52
What is buprenorphine
Partial agonist for opid receptors. Has high affinity but low efficacy so it blocks other opioids but doesn't produce withdrawals and euphoria.
53
Naloxone/Narcan has
High affinity but zero efficacy.
Fast-acting opioid antagonist
54
What is tolerance due to
1) receptor downregulation
2) cAMP upregulation
55
What is the opponent process
Withdrawal, body tries to maintain homeostasis so once drug is removed= withdrawals.
56
What are the 3 key models to study opiates
1) Self-adminstration model
2) Conditioned place preference
3) Lowered brain stimulation
57
What does the Self-administration model prove
The high abuse potential of drugs due to their rewarding properties
58
What does the conditioned place preference model show
Shows the context and environment that opiate are taken are associated with drug pleasurable effects
59
What is conditioned compensatory response also known as
Contextual dependance tolerance
60
What is conditioned compensatory response
When drugs are taken repeatedly in the same environment your body learns to anticipate it, based on smell, time of day, room. Your body pre-activates process to counteract drug effect. This reduces the drugs impact
61
Why are people that are using in new environment more likely to accidentally overdose
The usual environmental cues were not present, so the body couldn't prepare, and the drug had a stronger effect than expected.
62
What did the lowered brain stimulation model show
That opiates enhance the brain's dopaminergic activity and affects reward system.
63
What are the 3 endigenous opioid peptides
1) Endorphins
2) Enkephalins
3) Dynorphins
64
Fentanyl is....
Extremely potent
High overdose risk because it has high efficacy and lipid solubility
65
Where are non-peptides (GABA, glutamate) synthesized
Locally at axon terminal
66
Where are neuropeptides (opioids) synthesized
Cell body
67
What is the major difference between neuropeptides (opioids) and monaminergic NT (ex: glutamate)
Opioids cannot be recycled after release, they need to be newly synthesized every time. As opposed to non-peptides that can rapidly replenish
68
How/when can the NMDA receptor be activated
When both pre-synaptic and post-synaptic cells activate at the SAME time
69
What are benzodiazepines
Psychoactive drug that enhances GABA.
70
What are benzodiazepines prescribed for
Anxiety, panic attacks
71
What is an example of benzos
Diazepam
72
Benzos are ab agonist for which GABA receptor
A
73
What is the natural painkiller in the body
Endorphins
74
What can happen when you take benzos and opioids together
Depress breathing
75
Excessive glutamate overactivates which glutamate receptor causing excitotoxicity
NMDA
76
What do allosteric modulators do
Change receptors response to GABA
77
Example of a allosteric modulator
Alcohol/Benzos since tget enhance inhibition without activating the receptor directly
78
What does scopolamine do
Muscarinic receptor antagonist, affects CNS (cognition).
79
Example of scopolamine
Devil's breath
80
What does the Black Widow Spider Venom di
Causes massive release of Ach, which causes the vessicles to fuse it causes spasms.
81
What does botulinium toxin do
Block Ach release
82
What does Curare do
Block Ach nicotinic receptors at NMJ causing muscle paralysis
83
What is myasthenia Gravis
Autoimmune process that destroys acetylcholine receptors
84
How can we tell if neurons are acetylcholine neurons
there will be the presence of choline acetyltransferase
85
What drug is used to induce seizures in lab animals
Picrotoxin
86
How does GABA relate to anxiety
Activation of local GABA receptors in amygdala can lower anxiety
87
Inhibition of GABA-A receptors can
Provoke anxiety
88
What GABA receptor would you want to target as an anxiety treatment
GABA-A
89
Which between benzos and barbiturates are safer
Benzos b/c they are highly safe. Barb. have a low safety margin and have strong withdrawals
90
What does too little GABA in the brain do
Seizures, insomnia, anxiety
91
GABA-A RECEPTORS
Ionotropic, fast, Open Cl-= hyperpolarization
Calming effect
92
GABA-B RECEPTOR
Metabotropic, slow, Open K+ channels, block Ca2+
Pain modulation and motor control
