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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
Q

What kind of receptor is P2Y? What are its ligands?

A

Metabotropic (Gs/Gq coupled)

ATP/ADP/UTP/UDP

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26
Q

What functions do purine NTs carry out?

A

Learning and memory

Modification of locomotor pathways

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27
Q

Where are opioid NTs generally found?

A

Basal Ganglia

Hypothalamus

Pons/Medulla

28
Q

What does proopiomelanocortinin give rise to?

A

B-endorphins

29
Q

What are the precursor molecules of opioid NTs? What do they give rise to?

A

Proopiomelanocortinin (PCOM) -> B-endorphin

Pro-enkephalin ->Met/Leu-enkephalin

Pro-dynorphin -> Leu-enkephalin, dynorphin

Orphanin FQ -> Nociceptin

30
Q

What opioid molecule is different in that it enhances pain perception rather than decreases it?

A

Nociceptin (from Orphanin FQ)

31
Q

What is the action of aminopeptidase? What NTs are affected?

A

Cleave the N-Terminus of ptns or peptides

Opioids

32
Q

Activation of what receptor will result in analgesia, respiratory depression, euphoria, constipation, and/or sedation? What type of receptor is it?

A

Mu receptor of opioids

Metabotropic

33
Q

Activation of what receptor produces analgesia, dysphoria, diuresis, and miosis? What type of receptor is it?

A

Kappa

Metabotropic (serpentine)

34
Q

What does the delta receptor produce when activated?

A

Analgesia

35
Q

What G-proteins bind to Opioid receptors?

A

Gi/Go

36
Q

What receptor leads to an increase in K+ efflux and hyperpolarization?

A

Mu receptor

37
Q

What receptors lead to calcium influx?

A

Delta and Kappa receptors

38
Q

What are the endogenous cannabinoids? What are they derived from?

A

Anandamide, 2-arachidonylglycerol

Arachidonic acid

39
Q

What effect do the endocannabinoids have throughout the CNS? (Basal ganglia, spinal cord, cortex, hippocampus, hypothalamus)

A

Basal ganglia - mood, motor performance

Spinal cord - modulation of nociception

Cortex - neuroprotection

Hippocampus - memory formation

Hypothalamus - control of body energy/hunger

40
Q

In what terminal does endocannabinoid synthesis occur? Usually what receptor?

A

Presynaptic

CB1

41
Q

What is the effect of endocannabinoids on EAA and GABA release?

A

Reduces release via Gi coupled ptn

42
Q

Where are CB2 receptors generally located?

A

Microglia in the brain

Gut

Immune system

(Anti-inflammatory)

43
Q

Activation of CB2 receptors in the brain can increase removal of what?

A

B-amyloid plaques

(Clinically significant for Alzheimer’s)

44
Q

What are the endogenous excitatory AAs?

A

Glutamate

Aspartate

45
Q

Activation of the NMDA receptor allows influx of what ion?

A

Ca++

46
Q

What molecule is a necessary co-transmitter with EAAs in opening the NMDA channel?

A

Glycine

47
Q

What ion blocks the NMDA receptor? When?

A

Mg++

At resting membrane potential (even if both EAA and Glycine are present)

48
Q

What exogenous molecule blocks the NMDA receptor? What symptoms does it cause?

A

PCP

Hallucinations

49
Q

Activation of non-NMDA receptors causes an influx of what ion?

A

Na+

50
Q

What are the exogenous EAAs?

A

NMDA

AMPA

Kainate

51
Q

What exogenous agent causes decrease of sodium influx through the AMPA receptors?

A

Benzodiazepines

52
Q

What type of EPSP do the NMDA receptors produce? Why?

A

Long latency EPSP

Mg++ must be removed to depolarize the membrane, lasts longer because of Ca++ influx

53
Q

What type of EPSP do the non-NMDA receptors produce?

A

Short EPSP

54
Q

What receptors are critical for short and long-term memory formation?

A

NMDA receptors (very plastic)

55
Q

What G-Ptns do EAA metabotrophic receptors bind?

A

Gq (Group 1)

Gi (Groups 2 and 3)

56
Q

What happens during EAA reuptake into glial cells?

A

EAA => Glutamine => Release back to Pre-synaptic neuron => Repackaged into EAA

(Similar to GABA)

57
Q

Nitric oxide synthase results from the binding of what?

A

Ca++ to Calcineurin

58
Q

Blockage of what NT from the pons can cause apneusis (ineffective relaxation of diaphragm)

A

NO

59
Q

What immune cells produce NO?

A

Macrophages

(No Can produce free radicals and is toxic in high concentrations)

60
Q

Excitotoxicity proposes overstimulation of what system after an ischemic event in the brain?

A

EAA system (Domoic acid in shellfish poisoning)

61
Q

In an ischemic event, what molecules fail to be reuptaken? Why?

A

EAA

Secondary active transport of Na+ has shut down

62
Q

What is phospholipase A released in response to?

A

High intracellular Ca++

63
Q

What are the consequences of increased PLA activity?

A

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
Q

Activation of mu-calpain causes what?

A

Proteolysis of structural proteins, disrupted protein synthesis, impariment of neuron metabolism and structure

65
Q

High intracellular Ca2+ leads to activation of apoptotic pathway, releasing what substances?

A

Cytochrome C and Caspase 9 => Caspase 3

66
Q

Why might reperfusion with O2 be unhelpful after an ischemic event?

A

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
Q

Why might a patient be placed in a medically induced coma after an ischemic event?

A

Hope to disrupt snowball effect of damaging biochemical pathways

NS Exam 2 (12 decks)

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