Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

(OMS1) Neuro exam 2 > Neurotransmitter Systems (Karius) > Flashcards

Neurotransmitter Systems (Karius) Flashcards

1
Q

What controls the ionic gradient?

A

Membrane permeability to certain ions (ions and large proteins do not freely cross)
Na/K+ ATPase (3 Na out/2 K in, results in chemical gradient with high Na outside cell and high K inside cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Action potentials

A

Exciting “excitable” tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens to membrane potential during an action potential?

A

Increases, decreases then returns to RMP

depolarization, repolarization, hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the events of synaptic transmission:

A

AP arrives at presynaptic terminal > Ca+ channels open causing vesicles with NT release > NT binds to postsynaptic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ionotropic vs Metabotropic/Serpentine NT receptors:

A

Ligand gated vs. Second messenger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q 
Metabotropic receptors: 
Second messengers
Gs
Gi
Gq
A
  • stimulation of adenylate cyclase
  • inhibition of adenylate cyclase
  • productoin of DAG and IP3 (aka release of intracellular Ca2+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

EPSP (Excitatory Post-synaptic potential)

A

Binding to receptor opens a cationic channel (either Na+ or Ca2+ > influx of the cation > depolarization
Reach closer to a threshold to generate AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IPSP (Inhibitory Post-synaptic potential)

A

Binding to receptor opens an anionic channel (Cl-) > influx of chloride > hyperpolarization
Go further from threshold means less likely to generate AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Origin of the neurotransmitter:

A

Area of the brain that makes the NT is where the cell bodies are. Axons may travel really far from the cell body to get to the target

Example: Seratonergic neurons are found in the raphe nuclei = the cell bodies that make the serotonin are found in the raphei nuclei
Post synaptic receptors for serotonin (synapse 1) may be found really far away from this location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a tract?

A

Bundle of axons traveling to the same location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the monoamines?

A 
Epinephrine 
Norepinephrine 
Dopamine 
Serotonin
Histamine

(created from modifying single amino acids)

END Seton Hall (for rejecting me haha)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where do you find norepinephrine?

Function?

A

Locus ceruleus
Other pontine/medullary areas
Wakefulness/alertness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where do you find epinephrine?

A

Medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Synthesis of epinephrine and norepinephrine:

A

Tyrosine > ( via tyrosine hydroxylase = rate limiting step) > dopamine > vesicles > norepinephrine > released into synaptic terminal > (via PNMT/phenolethanolamine-N-methyltransferase) > epinephrine > epi moved back into vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are epinephrine and norepinephrine transported into vesicles?
Inhibitor?

A

VMAT and VMAT2

Reserpine (leads to synaptic failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are the actions of Epi and Norepi limited?

A

Reuptake

Enzyme degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which enzymes degrade epi and norepi?

A

Monoamine oxidase/MAO (metabolites released into ECF)

Catechol-O-methyltransferase/COMT (at glial cells/postsynaptic membrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What type of receptors do epi and norepi bind to?

What type of receptors are these?

A

A-adrenergic
B-adrenergic

-both are serpentine/second messenger type receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where can you find dopamine?

A 
Basal ganglia (motor control)
Hypothalamus & limbic system (endocrine and emotional control) 
Cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Synthesis of dopamine:

A

Tyrosine > ( via tyrosine hydroxylase = rate limiting step) > dopamine
(then to norepi and epi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is dopamine action limited?

A

Reuptake

Catabolism by MAO and COMT (same as norepi and epi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What receptors does dopamine bind to?

A

D1 and D5: increase cAMP
D2: decrease cAMP > increases gK causing potassium efflux
D3 and D4: decrease cAMP (aka like D2)

All metabotropic/serpentine receptors that are connected to G proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where is serotonin (5HT) found?

A

Raphe nuclei in the brainstem (modifies motor activity)
Cerebellum (modifies motor activity)
Hypothalamus and limbic system (mood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Synthesis of serotonin:

A

Tryptophan > (via Tryptophan hydroxylase) > Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you limit the action of serotonin?

A

Reuptake

Catabolism of MAO and COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Receptors for Serotonin:
Serpentine receptors:
Ionotropic receptor:

A
  • 5HT1,2,4,5 and 6

- 5HT3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q 
*Roles of these receptors: 
5HT2c
5HT3
5HT6
5HT7
A
  • knock out mice are obese and seizure prone
  • area postrema (vomiting)
  • anti-depressant effect
  • limbic system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Where is Histamine located?

A

Tuberomammillary nucleus of the hypothalamus (wakefulness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Synthesis of Histamine:

A

Histidine > (via histidine decarboxylase) > Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do you limit the action of histamine?

A

Reuptake

Catabolism by diamine oxidase and COMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

*What are the receptors for Histamine?

What type of receptors?

A

H1: PLC (phospholipase c) activation
H2: increase cAMP (associated with gastric acid release)
H3: presynaptic, decrease histamine release

All serpentine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Acetylcholine found in?

A

Striatum of the basal ganglia

Midbrain and pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Major functions of acetylcholine:

A

Voluntary motion control (via striatum)
Baseline excitation to cortex (brain arousal/wakefulness)
REM sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Synthesis of acetylcholine:

A

Choline + acetate > vAChT (vesicular Ach transporter protein) moves it into vesicles > Acetylcholinesterase removes it from synaptic trough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

*Ach receptors:

Muscarinic

A

M1 (neuronal) - increase IP3/DAG (Gq)> intracellular Ca+ release
M2 (cardiac) - decrease cAMP via Gi > K+ efflux
M3 (endothelium of vasculature) - increase IP3/DAG (Gq) > intracellular Ca+ release
M4 (presynaptic autoreceptor, striatum of basal ganglia) - decrease cAMP (Gi)
M5 (cerebrovasculature, dopaminergenic neurons of basal ganglia) - increase IP3/DAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Ach receptors:

Nicotinic

A

Located at the NMJ (somatic) and synapse 1 (autonomic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the inhibitory neurotransmitters?

A

GABA

Glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

GABA:

A

Major inhibitory amino acid NT
Widely distributed throughout higher levels of the CNS
Spinal cord has least amount of GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Roles of GABA:

A

Consciousness
Motor control
Vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Synthesis of GABA:

A

Glutamate > (via glutamate decarboxylase/GAD) > transport into vesicles via VGAT/vesicular GABA transporter protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Reuptake of GABA:

A

GAT (GABA transporter) removes it from synapse

GAT 1 is at the presynaptic terminal while GAT 2 is on glial cells surrounding the synapse

42
Q

If GABA is taken up by GAT1…
If GABA is taken up by GAT2…

-

A

Repackaged into vesicles as is

-GABA is converted to glutamine > released to the ECF > taken up at presynaptic terminal and recycled to GABA

43
Q

GABA-A receptors:

Ionotropic (Cl conductance)

A

Activation produces IPSP in adult neurons

Binding sites also receive Benzo, ethanol and steroids and cause an action potential

44
Q

GABA-A receptors (outside of synapse terminals)

A

Large number of such receptors

Site of action for anesthetics like propofol

45
Q

GABA-B receptors:

Metabotropic

A

Gi/Go coupled

  • activate the GIRK (K+ channel) and inhibit a Ca channel
  • Presynaptic receptors regulate NT release while postsynaptic receptors inhibit the post-synaptic cell
46
Q

Glycine found in?
Function?
Synthesis?

A

-Spinal cord (mostly), brainstem (particularly in the medulla)
Not much in higher CNS
-spinal inhibitions
-Amino acid is unmodified

47
Q

Removal of Glycine from synapse:

A 
GAT proteins (same as GAB)
Recycling
48
Q

Glycine receptors:

A

Ionotropic (responds to chloride) > influx of Cl- leads to IPSP

49
Q

What other substances bind to glycine receptors?

A

Ethanol and general anesthetics. Both cause action potential
Stychnine blocks it

50
Q

What are the purines?

A

ATP, ADP and Adenosine

51
Q

ATP and purines:

A

Synaptic vesicles for Purines all contain ATP. Debate on whether ATP is required for metabolic function

52
Q

Synthesis of Purines:

A

ATP by MT > stored in vesicles by VNUT > released > (ATP > ADP > Adenosine) conversion occurs in synaptic trough

53
Q

Purines are found…

A

Virtually everywhere in CNS particularly cortex, cerebellum, hippocampus, basal ganglia

54
Q

Purine receptors :

P1 (A receptors)

A

Binds adenosine
Role in sleep induction, inhibition of neural function (post synaptic locations)
Role in NT release (presynaptic locations)

55
Q

Purine receptors:

P2X receptors

A

Ionotropic

Binds ATP

56
Q

Purine receptors:

P2Y receptors

A

Metabotropic
Binds ATP, ADP, UTP and UDP
Gi/Gq coupled

57
Q

Functions of P2 purine receptors

A

Learning and memory (co-release with EAA)

Modification of locomotor pathways

58
Q

Opioid transmitters are what type of transmitters?

A

Peptide transmitters

59
Q

Opioids include…

A

Endorphins
Ekephalins
Dynorphins
Nociceptin

60
Q

Opioids are found ….

A

Basal ganglia
Hypothalamus
Multiple pontine and Medullary sites

61
Q

General functions of opioids:

A

Modification of nociceptive inputs (cutaneous)

Mood/affect (neurophysiology of emotion/drug addiction)

62
Q

Precursors for proopiomelanocortinin (POMC, precursor to ACTH):

A

B-endorphins

63
Q

Precursors for proenkephalin:

A

Tyr-gly-gly-phe-X
Met-enkephalin
Leu-enkephalin

64
Q

Precursors for pro-dynorphin:

A

3 molecules of Leu-enkephalin

dynorphin

65
Q

Precursors for Orphanin FQ

A

nociceptin

66
Q

Synthesis of Opioids:

Removal in cleft:

A
  • Standard protein synthesis

- reuptake and destruction by enkephalinase and aminopeptidase

67
Q

Opioid receptors general concepts:

A

Are all serpentine and activate second messenger systems (Gi/Gq) after ligand binding

68
Q

Opioid receptors:

U-receptors (Mu)

A

Metabotropic
Activation causes: analgesia, respiratory depression, euphoria, constipation, sedation
-leads to K+ efflux and hyperpolarization

69
Q

Opioid receptors:

Kappa (K) receptors

A

Serpentine
Activation causes: Analgesia, dysphoria, diuresis, miosis
-decrease Calcium influx

70
Q

Opioid receptors:

Delta receptor

A

Serpentine receptor
Activation causes: Analgesia
-decrease calcium influx

71
Q

Endocannabinoids are found …

A 
Basal ganglia (affects mood and motor performance)
Spinal cord (modulates nociception) 
Cortex (neuroprotection) 
Hippocampus (memory formation) 
Hypothalamus (energy control/hunger)
72
Q

Synthesis of Endocannabinoids:

A

Derived from membrane lipids (arachidonic acid)

Occurs in the presynaptic terminal

73
Q

Difference in synthesis pathways for Anandamide and 2-AG:

A

Anandamide - derived from NAPE (N-arachidonoyl phosphatidyl ethanol
2-AG: derived from arachidonoyl-containing phosphatidylinositol bisphosphate (PIP2)

74
Q

2AG

A

Major source for arachidonic acid

Manipulation of 2AG has effects beyond the endocannabinoid system

75
Q

Cannabinoid Receptor 1 (CB1)

A

Activation = psychoactive responses to cannabinoids
472 AA peptide on chromosome 6
Polymorphisms linked to obesity, ADHD, schizo and Parkinson’s depression
Forms heterodimer with other NT receptors like dopamine and orexin

76
Q

CB1 distribution:

A

CNS neurons
Uniform distribution in striatum, thalamus, hypothalamus, cerebellum and lower brain stem
Non-uniform distribution in cortex, amygdala and hippocampus (aka found in only certain neuron types)

77
Q

Where are cannabinoid receptors usually found?

Binds which molecules with great affinity?

A

-Presynaptic neurons away from the active zone where the vesicles are
Greater density in inhibitory synapses
-AEA and 2AG

78
Q

Significance of CB1:

A

Found on presynaptic terminals of EAA and GABA releasing synapses and reduces EAA and GABA release via a Gi coupled protein
-Anandamide and 2-AG are equally effective in doing this

79
Q

CB2

A

Found primarily on macrophages (microglia)
Also found in neurons and usually associated with nerve injury. Inducible in response to injury or inflammation
Binds 2-AG better than AEA

80
Q

Degradation of Endocannabinoids at the synapse

A

Hydrolysis

Oxidation via cyclooxygenase and lipoxygenase pathway (both AEA and 2-AG)

81
Q

Hydrolysis of AEA:

Hydrolysis of 2-AG:

A

Via Fatty Acid Amide Hydrolase (FAAH)

Via Mono-acyl glycerol lipase (MAGL)

82
Q

What are the excitatory amino acids:

A

Glutamate and Aspartate

83
Q

Locations of EAA

A

Widely distributed throughout the CNS Most important excitatory NT in the brain. Wide functions

84
Q

EAA receptors:

Ionotropic

A

NMDA (N-methyl-D-aspartate receptor)

Activated by Glu, Asp and NMDA (exogenous) and allows influx of calcium

85
Q

Glycine binding site of the NMDA:

A

Glycine is required as a co-agonist, but cannot open the channel alone (needs EAA to bind with it)

86
Q

Mg binding site of the NMDA:

A

Blocks channel at RMP and prevents CA+ influx

Makes the NMDA receptor both ligand and voltage gated

87
Q

PCP binding site of NMDA:

A

Blocks channel

Uses as horse tranquilizer

88
Q

Non NMDA receptors

A

Also ionotropic but causes Na influx

2 types: AMPA and Kalnate

89
Q

AMPA receptors:

A

-Activated by Glutamate, aspartate and AMPA (exogenous)
Allows Na influx when open
-Benzo binds to this receptor and reduces amount of Na that enters

90
Q

Kainate receptors:

A

EAA binds, Na influx with some Ca2+

91
Q

Activation of the NMDA receptors produce ….

Activation of the non-NMDA receptors produce …

A
  • long latency EPSP with long duration

- EPSP with short duration

92
Q

Explain the binding of EAA receptors at the postsynaptic terminal?

A
  • Co-localized at the postsynaptic terminal.
  • EAA binds to both types of receptors >Na flows into non-NMDA while Ca cannot flow into NMDA because of the Magnesium
  • Non-NMDA receptor has a short duration EPSP which causes enough depolarization to make Mg leave the NMDA channel
  • with Mg gone, Ca can now enter the NMDA channel and produce the longer lasting EPSP
93
Q

Functions of the Non-NMDA receptors:

A

Primary sensory afferents

Upper motor neurons

94
Q

Functions of NMDA receptors:

A

Short and long-term memory formation

Synaptic plasticity

95
Q

EAA Metabotropic receptors
Group 1
Group 2 and 3

A
  • Gq coupled (glu 1 and 5)

- Gi coupled (glu 2-8)

96
Q

Presynaptic Metabotropic receptors

Post synaptic Metabotropic receptors

A
  • NT release control

- learning, memory, motor systems

97
Q

How is the action of the EAA limited?

A

EAA released into synapse > Glial cell uptakes and converts EAA to glutamine > glutamine reuptake by presynaptic neuron > converted back to glutamate (EAA) > released again

98
Q

Nitric oxide and NMDA receptors

A

NMDA activation can lead to production of NO.
How? NMDA binds and triggers Ca2+ influx > Ca2+ activates calcineurin which activates NOS (Nitric oxide synthase) > cleaves Arg to produce NO

99
Q

Properties of NO:

A

Lipid soluble. Diffuses back to presynaptic neuron and affects it

100
Q

Neural functions of NO:

A

Long term potentation of memory in hippocampus & cerebellum
Cardiovascular and respiratory control in pons and medulla

101
Q

Non-neural functions of NO:

A

Immunological: released by macrophages to poison pathogens
Cardiovascular: vasodilation of smooth muscle

102
Q

Downside of NO:

A

Unstable (half life is 5 seconds)

Leads to production of free radicals and toxic to neurons in high concentrations

(OMS1) Neuro exam 2 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions