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202 Theme 1 > Lecture 4 Chemicals in the Brain > Flashcards

Lecture 4 Chemicals in the Brain Flashcards

1
Q

what are the types of neurotransmitters

A

amino acids
monoamines
acetylcholine - fast
neuropeptides - slow

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2
Q

how are neurotransmitters stored and released

A

Synthesized locally in presynaptic terminal
Stored in synaptic vesicles
Released in response to local increase in Ca2

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3
Q

how are neuropeptides stored and released

A

Synthesized in the cell soma and transported to terminal
Stored in secretory granules
Released in response to global increase in Ca2+

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4
Q

how are fast neurotransmitters released

A

close to voltage gated ca2+ channels in terminal so released in short bursts when membrane depolarised

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5
Q

how are slow neurotransmitters released

A

stored in vesicles further from membrane so release slower as must migrate so released when ca2+ released sufficiently

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6
Q

what are amino acid transmitters

A

glutamate
GABA
Glycine

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7
Q

what are excitatory neurotransmitters

A

slightly depolarises the post synaptic cell’s membrane

glutamate (cns)

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8
Q

what are inhibitory neurotransmitters

A

slightly hyper polarises the post synaptic cell’s membranes
GABA (brain)
Glycine (spinal cord and brainstem)

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9
Q

what do diffuse modulatory systems do

A

Serotonin
Nt synthesised in small set of neurons, usually in brainstem and then acts across a large area
1 synthesising neuron can affect >100,000 neurons

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10
Q

what is the function of diffuse modulatory systems

A 
mood
sleep
pain
emotion
appetite
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11
Q

why have multiple neurotransmitters

A

release of neurotransmitters (other than GABA or Glu) tends to activate or inhibit entire circuits of neurons that are involved in particular brain functions

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12
Q

how is glutamate made

A

synthesised in presynaptic terminal from 2 sources:

1) from glucose via the Krebs cycle
2) from glutamine converted by glutaminase into Glutamate

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13
Q

how is glutamate stored

A

loaded and stored in vesicles by vesicular glutamate transporters (VGLUTs)

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14
Q

how is glutamate recycled

A

reuptake by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell and surrounding glia (convert Glu to glutamine and this is transported from the glia back to nerve terminals where it is converted back into Glu)

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15
Q

how is GABA made

A

synthesised from glu in a reaction catalysed by GAD

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16
Q

how is GABA stored

A

loaded and stored into vesicles by a
vesicular GABA transporter, GAT
(Gly uses the same transporter)

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17
Q

how is GABA recycled

A

cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
higher proportion of GABA is made de novo to refill vesicles rather than recycling to ensure enough as can be kept at Glu

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18
Q

what happens with too much Glu/too little GABA

A

hyper-excitability
epilepsy and excitotoxicity
eg cerebral ischaemia (electrochemical gradient abolished, Na+/K+ reversed, transporters release Glu in reverse, excitotoxic death (ca2+, enzymes, digestion)

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19
Q

what happens with too much GABA

A 
sedation/coma
eg GHB (date rape drug), GABA metabolite converted back to GABA
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20
Q

what are the types of monoamines

A

catecholamines and indolamines

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21
Q

examples of catecholamines

A

Dopamine
Epinephrine (adrenaline)
Norepinephrine

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22
Q

examples of indolamines

A

serotonin

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23
Q

how does dopamine synthesis occur

A

step 1 of catecholamine synthesis

tyrosine (TH) to dopa (Dopa DC) to dopamine (DA)

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24
Q

how can Parkinson’s be treated with dopamine

A

administration of
Levodopa (L-DOPA)
Dopa DC converts it to DA to inc amount

25
how is dopamine turned to epinephrine
catecholamine synthesis 2 DA (DBH) to NE (PNMT) to E DBH located in synaptic vesicles only, and NE is the only transmitter synthesised within vesicles
26
how are catecholamines stored
Loaded into vesicles by vesicular monoamine transporters (VMATs) (proton gradient like Glu and GABA transporters)
26
how are catecholamines stored
Loaded into vesicles by vesicular monoamine transporters (VMATs) (proton gradient like Glu and GABA transporters)
26
how are catecholamines stored
Loaded into vesicles by vesicular monoamine transporters (VMATs) (proton gradient like Glu and GABA transporters)
27
how are catecholamines released
released by Ca2+ - dependant exocytosis | binds and activates receptor
28
how are catecholamines recycled
signal terminated by reuptake into the presynaptic axon terminal by transporters powered by electrochemical gradient (Dopamine transporters (DATs), Norepinephrine transporters (NETs))
29
what happens to catecholamines once back in cytoplasm
reloaded back into vesicles | enzymatically degraded by Monoamine oxidases (MAOs) or inactivated by Catechol-O-methyl-transferase (COMT)
30
how do amphetamines modulate catecholamine release and reuptake
reverses transporter, so pumps out transmitter and blocks reuptake (DA & NE)
31
how does cocaine and methylphenidate modulate catecholamine release and reuptake
(eg Ritalin) block DA reuptake into terminals | More DA in synaptic cleft – extended action on postsynaptic neuron
32
how does selegiline modulate catecholamine release and reuptake
``` MAO inhibitor (in dopaminergic nerve terminals) stop breakdown of DA, more released on subsequent activations (treatment of early-stage PD, depression and dementia), and overall increasing the available amount of DA ```
33
how does entacapone modulate catecholamine release and reuptake
COMT inhibitor (treatment of PD), increases the available amount of neurotransmitter
34
how is serotonin synthesised
tryptophan to 5-HTP to Serotonin aka 5-HT
35
how is serotonin stored
vesicles
36
how is serotonin recycled
signal terminated by reuptake (Serotonin transporters (SERTs)) on presynaptic membrane destroyed by MAOs in the cytoplasm
37
how does fluoxetine affect serotonin release and reuptake
(eg Prozac) blocks reuptake of serotonin (SSRI – selective serotonin reuptake inhibitor) (treatment of depression, OCD)
38
how does fenfluramine affect serotonin release and reuptake
stimulates the release of serotonin and inhibits its reuptake (has been used as an appetite suppressant in the treatment of obesity)
39
how does MDMA affect serotonin release and reuptake
causes NE and serotonin transporters to run backwards, releasing neurotransmitter into synapse/extracellular space (therapeutic potential in PTSD?)
40
how is Ach made
``` Choline acetyltransferase (ChAT, CAT) converts choline+Acetyl CoA (coenzyme A) into acetylcholine ```
41
how is Ach stored
packaged into vesicles by vesicular acetylcholine transporter (VAChT).
42
how is Ach broken down
``` rapidly degraded in synaptic cleft by acetylcholinesterase (AChE) Choline is transported back into the presynaptic terminal and converted to acetylcholine ```
43
how does AchE modulate Ach degradation
block the breakdown of ACh, prolonging its actions in the synaptic cleft e.g. Neostigmine (treatment of myasthenia gravis, MG)
44
how are neuropeptides different from small molecule transmitters
Vary in their methods of synthesis and | release from small molecule transmitters
45
what are neuropeptides
Short polypeptide chains (3 to 36 amino acids) Over one hundred neuropeptides described e.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
46
how are small molecules transmitted
``` synthesised in cell body slow axonal enzyme transport synthesis and packaging of nt released, diffusion transport of precursors into terminal ```
46
how are small molecules transmitted
``` synthesised in cell body slow axonal enzyme transport synthesis and packaging of nt released, diffusion transport of precursors into terminal ```
47
how are peptides transmitted
synthesis of nt precursors and enzymes in cell body transport down microtubule tracks enzymes modify precursors to produce them diffuse degraded by proteolytic enzymes
48
how does neuropeptide degradation vary from small molecules
neuropeptide vesicle membrane recycled but not refilled bind to and activate receptor neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
49
how does neuropeptide release vary from small molecules
needs sustained or repeated depolarisation of Ca2+ | release is slower than small molecule release and signals may be maintained for longer
50
what are other transmitters (retrograde signalling)
soluble gases - NO and CO | Endocannabinoids
51
how is NO made
NO made in postsynaptic neuron by NO synthase (activated by the binding of Ca2+ and calmodulin)
51
how is NO stored
not stored but rapidly diffuses from its site of synthesis. Diffuses between cells (into presynaptic cell - retrograde transmitter)
52
what does NO do
Activates guanylyl cyclase which makes the second messenger cGMP
53
how is NO eliminated
in a few secs of being produced NO is converted to biologically inactive compound
54
what is NO used for
Potentially useful for coordinating activities of multiple cells in a small region (tens of micrometers)
55
what are Endocannabinoids
Small lipids which mostly cause reduced GABA release at certain inhibitory terminals (lower inhibition) cannabinoid active component in marijuana

202 Theme 1 (6 decks)

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