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NS Exam 2 > NTs and EAA > Flashcards

NTs and EAA Flashcards

1
Q

Neurotransmitter transport into vesicles relies on what type of transport?

A

ATP-dependent (against gradient)

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2
Q

What muscarinic receptors are associated with Gq?

A

M1, M3, M5 (IP3/DAG)

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3
Q

What muscarinic receptors are associated with Gi?

A

M2, M4 (decrease cAMP)

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4
Q

Where are nicotinic receptors located?

A

NMJ

Synapse b/w pre and post-ganglionic cells in autonomic ganglia

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5
Q

What are the major inhibitory AAs?

A

GABA (gamma-amino-butyric acid

Glycine

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6
Q

Where is GABA most widely distributed?

A

Higher levels of CNS (Cortex, cerebellum, basal ganglia)

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7
Q

What AA is GABA synthesized from?

A

Glutamate (via glutamate decarboxylase)

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8
Q

Where is GAT1 located? Function?

A

Presynaptic terminal

Repackages GABA into vesicles as is

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9
Q

Where is GAT2 located? Function?

A

On astrocytes

Converts GABA to Glutamine and releases into ECF => taken up by presynaptic terminal and recycled into GABA

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10
Q

What kind of receptor is the GABAaR?

A

Ionotropic

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11
Q

What kind of potential is produced by GABA Receptors?

A

IPSP (inhibitory postsynaptic potential)

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12
Q

What type of substances can bind to GABAa receptors to modulate GABA release?

A

Benzodiazepines

Ethanol

Certain steroids

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13
Q

What kind of receptor is GABA B?

A

Metabotropic

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14
Q

What channels are activated/inhibited by GABA B receptor binding to Gi/Go proteins?

A

Activate K+ channels

Inhibit Ca++ channels

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15
Q

What is the function of GABA B receptors on presynaptic cells?

A

Regulate NT release

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16
Q

What is the function of GABA B receptors on postsynaptic cells?

A

Inhibit post-synaptic cell

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17
Q

Where is glycine majorly found?

A

Spinal Cord (less distribution in higher areas of CNS)

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18
Q

Glycine receptors lead to IPSP via influx of what ion?

A

Cl-

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19
Q

What substance antagonizes glycine receptors? What is the result?

A

Strychnine - inhibitory response blocked (rat poison, convulsions)

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20
Q

What is the role of the VNUT protein?

A

Storage of ATP in vesicles

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21
Q

What is the ligand of the P1 receptor?

A

Adenosine

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22
Q

What are the functions of the post-synaptic P1 receptors?

A

Sleep induction

General inhibition of excitable tissue

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23
Q

What is the general funciton of pre-synaptic P1 receptors?

A

Inhibition of NT release

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24
Q

ATP binding to P2X receptors facilitates transports of what ions?

A

Ca++ and Na+ out

K+ in

(ionotropic receptor)

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25
What kind of receptor is P2Y? What are its ligands?
Metabotropic (Gs/Gq coupled) ATP/ADP/UTP/UDP
26
What functions do purine NTs carry out?
Learning and memory Modification of locomotor pathways
27
Where are opioid NTs generally found?
Basal Ganglia Hypothalamus Pons/Medulla
28
What does proopiomelanocortinin give rise to?
B-endorphins
29
What are the precursor molecules of opioid NTs? What do they give rise to?
Proopiomelanocortinin (PCOM) -\> B-endorphin Pro-enkephalin -\>Met/Leu-enkephalin Pro-dynorphin -\> Leu-enkephalin, dynorphin Orphanin FQ -\> Nociceptin
30
What opioid molecule is different in that it enhances pain perception rather than decreases it?
Nociceptin (from Orphanin FQ)
31
What is the action of aminopeptidase? What NTs are affected?
Cleave the N-Terminus of ptns or peptides Opioids
32
Activation of what receptor will result in analgesia, respiratory depression, euphoria, constipation, and/or sedation? What type of receptor is it?
Mu receptor of opioids Metabotropic
33
Activation of what receptor produces analgesia, dysphoria, diuresis, and miosis? What type of receptor is it?
Kappa Metabotropic (serpentine)
34
What does the delta receptor produce when activated?
Analgesia
35
What G-proteins bind to Opioid receptors?
Gi/Go
36
What receptor leads to an increase in K+ efflux and hyperpolarization?
Mu receptor
37
What receptors lead to calcium influx?
Delta and Kappa receptors
38
What are the endogenous cannabinoids? What are they derived from?
Anandamide, 2-arachidonylglycerol Arachidonic acid
39
What effect do the endocannabinoids have throughout the CNS? (Basal ganglia, spinal cord, cortex, hippocampus, hypothalamus)
Basal ganglia - mood, motor performance Spinal cord - modulation of nociception Cortex - neuroprotection Hippocampus - memory formation Hypothalamus - control of body energy/hunger
40
In what terminal does endocannabinoid synthesis occur? Usually what receptor?
Presynaptic CB1
41
What is the effect of endocannabinoids on EAA and GABA release?
Reduces release via Gi coupled ptn
42
Where are CB2 receptors generally located?
Microglia in the brain Gut Immune system (Anti-inflammatory)
43
Activation of CB2 receptors in the brain can increase removal of what?
B-amyloid plaques (Clinically significant for Alzheimer's)
44
What are the endogenous excitatory AAs?
Glutamate Aspartate
45
Activation of the NMDA receptor allows influx of what ion?
Ca++
46
What molecule is a necessary co-transmitter with EAAs in opening the NMDA channel?
Glycine
47
What ion blocks the NMDA receptor? When?
Mg++ At resting membrane potential (even if both EAA and Glycine are present)
48
What exogenous molecule blocks the NMDA receptor? What symptoms does it cause?
PCP Hallucinations
49
Activation of non-NMDA receptors causes an influx of what ion?
Na+
50
What are the exogenous EAAs?
NMDA AMPA Kainate
51
What exogenous agent causes decrease of sodium influx through the AMPA receptors?
Benzodiazepines
52
What type of EPSP do the NMDA receptors produce? Why?
Long latency EPSP Mg++ must be removed to depolarize the membrane, lasts longer because of Ca++ influx
53
What type of EPSP do the non-NMDA receptors produce?
Short EPSP
54
What receptors are critical for short and long-term memory formation?
NMDA receptors (very plastic)
55
What G-Ptns do EAA metabotrophic receptors bind?
Gq (Group 1) Gi (Groups 2 and 3)
56
What happens during EAA reuptake into glial cells?
EAA =\> Glutamine =\> Release back to Pre-synaptic neuron =\> Repackaged into EAA (Similar to GABA)
57
Nitric oxide synthase results from the binding of what?
Ca++ to Calcineurin
58
Blockage of what NT from the pons can cause apneusis (ineffective relaxation of diaphragm)
NO
59
What immune cells produce NO?
Macrophages (No Can produce free radicals and is toxic in high concentrations)
60
Excitotoxicity proposes overstimulation of what system after an ischemic event in the brain?
EAA system (Domoic acid in shellfish poisoning)
61
In an ischemic event, what molecules fail to be reuptaken? Why?
EAA Secondary active transport of Na+ has shut down
62
What is phospholipase A released in response to?
High intracellular Ca++
63
What are the consequences of increased PLA activity?
Physical damage to the membrane =\> Arachidonic acid release =\> More Ca++ release =\> Unfolded ptn response (ER stops making ptns), mito dysfunction, eIF2a-kinase activation Damage to semi-permeable membrane =\> Destroyed gradient
64
Activation of mu-calpain causes what?
Proteolysis of structural proteins, disrupted protein synthesis, impariment of neuron metabolism and structure
65
High intracellular Ca2+ leads to activation of apoptotic pathway, releasing what substances?
Cytochrome C and Caspase 9 =\> Caspase 3
66
Why might reperfusion with O2 be unhelpful after an ischemic event?
Mitos may be unable to use O2 =\> O2 becomes toxic free radicals Mitos may use O2 =\> ATP but ATP is used to P-late damaging enzymes (eIF2a kinase, caspase 3) =\> increased apoptotic signaling, decreased ptn synthesis
67
Why might a patient be placed in a medically induced coma after an ischemic event?
Hope to disrupt snowball effect of damaging biochemical pathways

NS Exam 2 (12 decks)

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