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Psych 421 > Week 5-NT synthesis pathways > Flashcards

Week 5-NT synthesis pathways Flashcards

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1
Q

Categories of NTs

A
  1. ACh
  2. Biogenic Amines
  3. Amino Acids
  4. Neuroactive Peptides
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2
Q

Types of Biogenic Amines

A
  1. Dopamine (DA)
  2. Norepinephrine (NE)
  3. Serotonin
  4. Histamine
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3
Q

Types of Amino Acid NTs

A
  1. GABA
  2. Glutamate
  3. Glycine
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4
Q

Types of Neuroactive peptides

A
  1. POMC w/in beta-endorphin group
  2. pro-enkephalin w/in met & leu-enkephalins
  3. Pro-dynorphin in which group is dynorphin
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5
Q

4 criteria for NT

A
  1. Must be synthesized in the neuron
  2. must be released in sufficient amounts upon an AP to yield PSPs
  3. Exogenous (artificial) applications will mimic normal activity
  4. there must be some deactivating mechanisms to terminate NT-receptor interactions
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6
Q

Dale’s law

A

a mature neuron makes use of the same combination of NT substances in all of its synapses

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7
Q

coexistence

A

the use of more than 1 NT by a neuron

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8
Q

Synthesis for all NT (except neuro-active peptides) occurs in

A

pre-synaptic terminal

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9
Q

ACh synthesis pathway

A 
Acetyl CoA (from metabolism) + choline (from diet)
--->free ACh via CAT (choline acetyl transferase)
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10
Q

Deactivating mechanism for ACh

A

AChE: in synapse, next to ACh receptor

-also in pre-synaptic terminal

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11
Q

AChE in synapse by receptor

A

breaks ACh as soon as it unbinds

  • leaves choline + acetate
  • ->Acetate diffuses
  • ->choline recycled via transmembrane protein
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12
Q

AChE in pre-synaptic terminal

A

breaks up any ACh not bound or in a vesicle

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13
Q

3 critical issues in NT systems

A
  1. vesicles are “safety zone” to protect NT from enzymes
  2. vesicles not saturated (not filled to capacity)
  3. how do NT molecules get into the vesicle

*filling vesicles important in synaptic plasticity

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14
Q

Vesicle membrane mechanisms

A
  1. transmitter transporters (uses energy from H+ flowing down gradient outside the cell, in exchange for NT coming into cell)
  2. proton pumper-energy source for transmitter transporter (uses ATP to pump H+ against gradient)

vesicle exchanges 2H+/1NT brought in

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15
Q

Vesicle NT uptake mechanism (Vesicular NT transporter)

A
  1. H+ binds inside–>conformational change–>expose NT binding site
  2. NT binds on outside
  3. 2nd H+ binds inside–>another conformational change
  4. NT released inside vesicle, 2 H+ released into cytoplasm
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16
Q

4 transmitter transporters

A
  1. one for ACh
  2. one for biogenic amines (VMAT)
  3. one for glutamate
  4. one for GABA
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17
Q

Catecholamines

A
  1. DA
  2. NE
    (similar synthesis pathway)
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18
Q

Indoleamines

A

Serotonin

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19
Q

Catecholamine synthesis

A

Tyrosine

  • ->L-Dopa via tyrosine hydroxylase
  • ->free dopamine via dopa decarboxylase
  • ->DA within vesicle becomes NE via Dopamine Beta hydroxylase
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20
Q

Tyrosine hydroxylase cofactor mechanism

A

*must have pteridine cofactor to become active

pteridine H4 cofactor gives 2 H+ to tyrosine hydroxylase

  • ->becomes pteridine H2 cofactor
  • ->pteridine reductase adds 2 H+ back to pteridine H2 cofactor
  • ->back to pteridine H4 cofactor
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21
Q

Synthesis of NE

A

same as DA except neurons that use NE have additional enzyme (Dopamine beta-hydroxylase) to convert DA to NE within vesicle

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22
Q

Deactivating mechanism for catecholamines

A

reuptake

-membrane transporters have high affinity for NT to draw NT back into terminal

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23
Q

types of membrane transporters

A
  1. one for glutamate itself

2. others for GABA, glycine, NE, DA, Serotonin, and choline

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24
Q

NET

A

NE membrane transporter

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25
DAT
DA membrane transporter
26
SERT
Serotonin membrane transporter
27
membrane transporter similarities
1. both driven by Na+ concentration gradient | 2. both co-transport another ion
28
membrane transporters differences
1. GluT is smaller (span 6-8x) others are larger (span 12x) 2. GluT cotransports K+ along with Na+ others cotransport Cl- along with Na+
29
2 enzymes needed to break down catecholamines
1. MAO 2. COMT * both exist on pre AND post synaptic sides - breakdown FREE NT
30
Reuptake of NT into terminal
NTs must be taken up into vesicles immediately otherwise MAO/COMT will destroy them *Vesicles dump close to membrane transporters for efficient reuptake
31
2 short term feedback systems on rate limiting enzyme (tyrosine hydroxylase) for synthesis of catecholamines
1. end product inhibition | 2. Ca++ feedback
32
End product inhibition
Short term negative feedback - accumulation of DA in pre-synaptic terminal will DECREASE activity of tyrosine hydroxylase - presence of NT decreases enzyme activity accumulation of NT in pre-synaptic terminal will shut down activity of tyrosine hydroxylase by converting pteridine H4 to pteridine H2 (limits cofactor)
33
Tyrosine hydroxylase structure
site for Tyrosine site for pteridine cofactor site for NT
34
Ca++ feedback
short term positive feedback accumulation of pre-synaptic Ca++ indicates high synaptic activity -->Ca++ can directly & indirectly accelerate activity of tyrosine hydroxylase
35
Long term feedback system for tyrosine hydroxylase (general)
continued firing of neuron may cause nucleus to produce MORE tyrosine hydroxylase induction & CREB (transcriptional activator protein)
36
Long term feedback system MECHANISM
(induction) autoreceptors on terminal (G-protein system) prolonged release of NT - ->prolonged pre-synaptic cAMP stimulation - ->activation of CREB (transcriptional activator protein) - ->activates transcription to produce more tyrosine hydroxylase
37
CREB
transcriptional activator protein
38
synthesis of serotonin
Tryptophan - ->5-HTP via tryptophan hydroxylase (rate limiter) - ->5-HT via 5-HTP decarboxylase
39
Deactivation of serotonin
broken down by MAO
40
Histamine synthesis pathway
Histidine | -->histamine via aromatic amino acid decarboxylase
41
Histamine differences from other mono-amines
1. no reuptake | 2. glial cells act as deactivators
42
Glutamate sources
1. product of Krebs cycle (free glutamate) | 2. neighboring glial cells supply neuron with glutamate
43
Glutamate synthesis pathway
Glutamine | -->Glutamate via glutaminase
44
Glutamate deactivation and synthesis sycle
deactivated glutamate -->reuptake into glial cells AND post-synapse via membrane transporters while in glial cells glutamate-->glutamine-->released to pre-synaptic terminal-->glutamate
45
GABA synthesis pathway
same as glutamate with extra enzyme (GAD) that converts glutamate-->GABA *Glial cells also convert GABA-->glutamate-->glutamine
46
Neuroactive peptides synthesis
synthesis occurs in SOMA of neuron in polyribosomes of ER, then transported to terminal along way to terminal, long peptides are cleaved to make specific NT
47
Neuroactive peptides vs small NT differences
1. site of synthesis 2. type of vesicles that store them 3. how they're released
48
Dense-cores
where neuroacive peptides are stored - do not have herding proteins to active zone - do not have proteins for recycling *one use only = no fast/sustained release of NT
49
Dense-core vesicles characteristics
- can release anywhere along membrane | - requires Ca++, but Ca++ must be HIGH to release NT since they are not localized in the active zone
50
Neuroactive peptides characteristics
1. synthesized in the soma 2. stores in dense cores 3. require prolonged/intense stimulation to be released
51
Nitrites
dilate blood vessels
52
Nitric oxide
rapidly dilate vessels *modifies metabolism & release from pre-synaptic side
53
Nitric oxide gas synthesis
L-arganine -->nitric oxide via nitric oxide synthase Glutamate-NMDA receptor-->release of NO -->increase cGMP in neurons
54
Nitric oxide weird characteristics
- not stored in vesicles - not released via Ca++ - no deactivation process because its so fast - freely diffuses across membrane - can increase NT release
55
Endogenous cannabinoids types found in brain tissue
1. anandamide | 2. 2DG
56
Endogenous cannabinoids synthesis
Not stored like regular NTs | -rapidly synthesized by neurons in response to depolarization and Ca++ influx
57
CB1
Receptor for cannabinoids Most abundant in brain Especially hippocampus, cortex, cerebellum -located on pre-synaptic terminal
58
Major function of hippocampal endocannabinoids
Regulate GABA release via Depolarization-induced suppression inhibition (DSI)
59
DSI
1. Initiated by depolarization-opening of V-Ca++ channels - ->release of endocannabinoids by Ca++ dependent process - ->endocannabinoids diffuse from post-synaptic membrane to bind to CB1 receptors on pre-synaptic terminal - ->inhibit release of GABA
60
NE nuclei cluster
A6-locus coeruleus Projects to other nuclei via: 1. Dorsal bundle 2 central bundle * contribute to Medial Forebrain Bundle (MFB) - -important in positive reinforcement (pleasure)
61
Dopamine nuclei cluster
A9-substantial nigra -projects to: corpus striatum in basal ganglia (Nigra-striatal pathway) *vital for motor control A10-VTA - projects to nucleus accumbens and frontal cortex * important in reinforcement
62
A6
Locus coeruleus - NE nuclei - projects yo MFB Important in positive reinforcement/pleasure
63
A9
Substantial nigra -projects to corpus striatum in basal ganglia *major DA nuclei Vital for motor control
64
A10
VTA Projects to nucleus accumbens & frontal cortex *major Dopamine nuclei Important in reinforcement
65
Serotonin nuclei cluster
B7-B9: raphe nuclei Projects to MFB *involved in limbic system (emotions)
66
B7-B9
Raphe nuclei -projects to MFB * serotonin nuclei - involved in limbic system
67
3 important ACh pathways
1. Interneurons in basal ganglia 2. Septo-hippocampal pathway: septal area-->hippocampus 3. Habenulo-interpedencular pathway: Habenula-->VTA(A10), substantial nigra, and raphe nucleus (modulates serotonin & dopamine)
68
Important glutamate pathway
Hippocampus-->septal area
69
Important GABA pathway
Basal ganglia-->substantia nigra
70
Histamine pathway
Originates in hypothalamus | *important in wakefulness for cognitive functioning

Psych 421 (8 decks)

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