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BMS153 NEUROSCIENCE > synapses and neurotransmitters > Flashcards

synapses and neurotransmitters Flashcards

1
Q

synapse

A

a specialised gap between 2 apposing cell membranes across which signals can pass

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2
Q

otto loewin discovered synapse

A 
2 isolated frog hearts
donor and recipient
ensured vagus nerve was still attached
at released from VN (parasympathetic nervous system)
1. stimulated vagus nerve of donor heart
2.heart rate slowed 
3. transferred sulotion (vagusstoff-german) from donor to recipient (now known as Ach)
4. heart rate slowed in recipient heart
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3
Q

common feature of chemical synapses

A 
presynaptic cell (usually axon terminal)
mitochondria- help clear calcium from presynaptic terminals

secretorry granules- contain peptide neurotransmitters
synaptic vesicles contain amine?

both released at active zone (membrane differentiation)

post synaptic membrane (usually dendrite)
receptors
synaptic cleft (20-50 nm wide)
contains a matrix of fibrous extracellular protein

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4
Q

types of synapses

A
  1. neuron to non neuronal
    most common= motor neurone to skeletal muscle, the neuromuscular junction
    autonomic neurons to glands, smooth muscle, heart (otto leowie)
2. neuron to neuron
within CNS (and between pre and post ganglionic neurons)
v. varied
different neurotransmitters
different sizes and morphologies
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5
Q

why synapses

A

excitatory =more positive

inhibitory= more negative

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6
Q

convergence of input

A

one cell influenced by many others

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7
Q

convergence of output

A

one cell influences many others

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8
Q

neuromuscular junction

A

fast and reliable synapse
motor neurone action potentials always causes muscle cell action potentials
uses Ach
one of the largest synapses in the body

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9
Q

specialisations of the neuromuscular junction

A

presynaptic: large number of active zones

post synaptic (motor end plate)
contains junctional folds, densely filled with neurotransmitter receptors (more of them due to larger surface areas)

at can bounce around in folds before getting degraded

precise alignment of active zones and junctional folds

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10
Q

CNS synpases

A

around 86 billion neutrons in the human brain so TOO MANY SYNAPSES TO COUNT

arrangement:

a) axodendritic (axon to dendrite)
b) axosomatic (axon to soma)
c) axaonic (axon to axon)
d) dendodendritic (dendrite to dendrite) could be inhibitory ? presynaptic

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11
Q

end bulb of held- auditory system

A

reliable type of synapse

hearing = very important e.g. danger

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12
Q

plasticity

A

synapses can grow /shrink /change in size

larger synapses usually have more active zones

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13
Q

variability of CNS synapses

A

Asymmetrical membrane differentiation= excitatory

symmetrical membrane differentiation = inhibitory

USUALLY

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14
Q

brief cascade of events of depolarisation

A

more postivie
voltage gated ca2+ open (around -40mv- -10mv)
rise in ca2+ triggers fusion of vesicles to pre synaptic membrane
diffusion of ca2+
release of neurotransmitters
diffusion across cleft
not every nt will come into contact with a receptor
the smaller the gap the more likely they are to bind

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15
Q

types of NT

A

amino acids (synaptic vesicles)
amines( ‘’)
peptides (dense core secretory vesicles)

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16
Q

amino acids

A

Glu, GABA, Gly

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17
Q

amines

A

ACh, NE

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18
Q

peptides

A

Arg, Pro, Lys, Gln,

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19
Q

synaptic vesciles

A

amino ancid and amine NT
40-50 nm diameter

synthesies in soma
filled at presynatpci terminal requires ATP to load neurotranmitter into vesicles

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20
Q

dense core secretory vesicles

A 
peptide NT
100-200 nm diameter
senthesied in ER often as precursors
bud from the golgi apparatus in soma 
transported along microtubules

Peptide neurotransmitters are formed in the rough ER. Sometimes formed as longer precursor proteins that are cleaved and processed through the Golgi apparatus. Vesicles are transported by fast axonal transport using the microtubule system.

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21
Q

where are vesicles made

A

All vesicles are made in the cell body but synaptic vesicles are transported empty.

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22
Q

abundant nt

A
  • The Amino acid neurotransmitters glutamate and glycine are abundant in all cells as they are used as the building blocks of proteins.
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23
Q

GABA and amines

A

GABA and the amines are made only in the neurons that release them. The neurons need special enzymes that enable them to synthesise the neurotransmitters from various metabolic precursors. These enzymes are found in the presynaptic terminals to allow rapid and local neurotransmitter synthesis. Specialised transporters take the neurotransmitters up into synaptic vesicles.

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24
Q

docking of vesicles

A

some vesicles are already docked at active zones within the presynaptic neuronal membrane

vesicles are held in place with snare proteins ready to be released

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25
Q

arrival of action potential

A

opens voltage gated ca2+ channels
depolarisation!
ca2+ moves into the presynaptic terminal as Eca2+ is about 123 mV
triggers vescles fusion and release (exocytosis)

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26
Q

SNARE proteins

A

some present of pre s membane and some present on vesicles

synaptotagmin binds calcium and changes the configuration and moves the vesicle closer to the pre s membrane

botulinum (BOTOX) from the black widow spider is an enzyme that selectively destroys some SNAREs and block the neurotransmission

synapses between the nerves and the muscles are disrupted by the toxin

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27
Q

diffusion

A

the synaptic cleft has a very small volume so nt conc can rise to the mM (millimolar) range

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28
Q

NT action

A

specific receptors are embedded in the post s density

some nt will bind to the receptors

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29
Q

2 types of nt receptors

A

ligand-gated ion channels (ionotropic)

G protein coupled receptors (metabotropic)

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30
Q

Fate of NT

A

nt must be cleared rapidly from the cleft
3 ways:

  1. simple diffusion out the cleft to the side (either before or after activation at receptor)
  2. reuptake into pre s membrane or glia by specific transporter for recycling (sometimes)
  3. enzymatic destruction within the cleft e.g. ach enzyme (acetylcholinesterase)
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31
Q

what happens to the vesicle

A

when it fuses it adds to the terminal membrane and becomes larger
(can measure this - compasitence measurement)
then has to recognised by molecules to be endocytose back into membrane
vesicles can be recycled and filled with new nt

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32
Q

quantal release

A

each synaptic vesicles contains about 35-50 nM and can cause mini response at the post synaptic cell

the effect of one vesicles being release is the quantal size

quantal content is the number of quanta (or vesicles) released

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33
Q

receptor dependent action

A

ligand gated ion channel permeable to Na+ e.g. at skeletal muscles contraction
immediate effect

G protein coupled receptor
slower and more complicated
activating K+ channel (parasympathetic) e.g. heart slows down

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34
Q

transmitter release at a fast excitatory chemical synapse generate an excitatory post synaptic potential (EPSP) e.g. nicotinic ACh receptors

A

EPSP propogate to soma
cause membrane to reach threshold

enough EPSP at one time you get a summation

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35
Q

IPSP

A

transmitter release at a fast inhibitory chemical synapse generate an inhibitory post synaptic potential
e.g. GABA a receptor (ionitropic chlride channel)
opening of pore and chloride moves into cell
cell more negative
hyperpolarised
takes potential further away from the threshold for AP firing

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36
Q

G protein coupled receptors

A

metabotropic
transmission is slower
and more complex than transmission via ligand gated ion channels
signal amplification occurs
1 NT and 1 receptor can activate multiple g proteins
multiple channels may be affected

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37
Q

criteria for NT

A

present in pre s terminals
released in response to stimulation
able to interact with post s receptors
rapidly removed from the synapse (timing of signal lost otherwise)

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38
Q

NT needs mechanisms

A

for syntheis and storage
for release
for transmitter action (i.e. receptors) and removal

39
Q

types of transmitters

A

achetlcholine

amino acids (GABA, Glycine, Glutamic acid, asperatic acid)

biogenic amines (catecholamines: epinephrine, norepinephrine, dopamine// serotonin, histamine)

neuropeptides: 
enkephalin
substance P
cholecystokinin
B- endorphin
40
Q

the amino acids and amine nts are

A

small molecules
stored and released from synaptic vesicles
capable of biding to and activating both
- ligand gated channel receptors
- g protein coupled receptors

short term and long term signalling

41
Q

the peptide nts are

A 
large
stored in secretory grnaules
made in soma 
only activate G protein coupled receptors (don't activate ligand gated ion channels)
slower/modulatory nts
42
Q

Dale’s principle

A

famous 1940s scientist
‘a neuron has only one nt’
classifed neutrons into mutually exclusive groups by the nt they released

BUT
many peptide containing neurones ave both peptide and aa or amine MT as well (or co transmitters e.g. ATP)

soe neurons also possess two types of aa NT e.g. GABA and glycine (co released)

therefore Dale’s principle is violated in these cases

43
Q

glutamate

A

most common excitatory nt in CNS
aa therefore found in all neurons (aa used to build proteins)

(because glutamate is everywhere, to know whether a neutron is glutamenergic, the molecule that loads it into vesicle is the marker)
3 glutamate receptor subtypes based on the drugs which act as selective agonists:
AMPA, NMDA and Kainate

action is terminated by selective uptake into presynaptic terminals and glia

44
Q

glutamate at receptor lelvel

A

AMPA receptors mediate fast excitatory transmission
permeable to cations
let more sodium in than potassium moves out
glutamate binding to AMPA receptors triggers NA and K currents resulting in an EPSP

45
Q

NMDA receptors

A

permeable to calcium and sodium
often co exist with AMPA receptors

NMDA receptors have a voltage dependent MG2+ block
so NMDA receptors need to be indirectly activated by another transmitter

NMDA recpetors are percale to ca2+ as well as na and k
therefore their activation can have more widespread, lasting changes in postsynaptic cell

really important for plastic memory strengthening synapses

46
Q

GABA

A

major inhibitory
CNS
not an aa used to build proteins
transformed from glutamate by GAD (glutamic acid decarboxylase)
GAD used to know whether a neurone is GABAergic
action is terminated by selective uptake into presynaptic terminals and glia

47
Q

action of GABA

A

produces IPSPs via GABA gated chloride channels (hyperpolarisation)
found throughout the CNS especially in cortex and striatum

the right amount of inhibition via GABA is critical:
too much=coma / loss of consciousness
too little = seizures

48
Q

why is GABA excitatory in development but inhibitory in adults ??!!

A

chloride conc can be changed - in cells in development we have different cl transporters which make sure more chloride inside cell at rest than in adult

because more chloride is increased inside cell -
negative outside
more postive =depolarised

49
Q

presynaptic inhibition GABA

A

one neutron suppresses the action of another

or auto inhibition - gabaergic neutron can inhibit itself
keeps a specific timing of a signal

50
Q

disinhibition

A

inhibiting inhibition

51
Q

modulation of GABAa receptors

A

1) ethanol has behavioural effects, addictive (because exaggeration gaba a = more inhibition)
2) benzodiazapine e.g. diazepam used to treat anxiety (enhances gabaergic response, increases inhibition)
3) barbiturates are sedatives and anti-convulsants
4) neurosteroids are metabolites of steroid hormones e.g. progesterone which can effect gaba receptors
when females have mood changes over mentrual cycle
PMT is real!

52
Q

GABA a receptors

A

PET scan from patient with panic attack
can label with benzodiazepine e.g. diazepam
shows loss of GABAa receptors

53
Q

Opioids derived from

A

opiod poppy

e.g. heroine and morphine

54
Q

opiods can be natural and synthetic

A

e,g, endorphins- nautrally occcuring small proteins or peptides including endorphin, enkephalin and dynorphin

or drugs (synthetic)

55
Q

how and when were opiod receptors discovered

A

1973 using radioactively labelled opiate compounds

56
Q

when were endorphins discovered?

A

1975

57
Q

because opioids are peptides where are they synthesised

A

formed in the rough ER and packaged into secretory granules by Golgi

58
Q

distribution of opioid receptors

A

widely distributed in CNS but concentrated in nociceptive areas

have at least 3 main types Include mu (µ), kappa, sigma

59
Q

spinal opiate receptors

A

block pain signal (analgesia)

60
Q

periaqueductal grey

A

regulates sensation of pain

61
Q

amygdala

A

regulates emotional compenent

62
Q

frontal cortex

A

cognitive aspects

63
Q

brain stem (medulla)

A

depress respiration and cough reflex (may induce vomiting) if overstimulate receptors here then get v low breathing rate

64
Q

opiate receptors act as modulators, decreasing the excitability of the cell, how?

A

can prevent voltage gated calcium channels opening or increase opening of the potassium channels, both hyperpolarise the cell

receprors coupled to inhibitory G proteins

65
Q

therapeutic uses of opiates

A

Analgesia: reduces perception of and emotional response to pain

intestinal disorders:
reduces diarrhoea, decreases dehydration

Antitussive:
cough supressant (codeine)
66
Q

problems with therapeutic use of opiates

A

serious side effects:
respiratory depression
sedation
constipation

tolerance developed- rescued cancel effect

dependence developed - withdrawal symptoms

releive dull visceral pain better than sharp pain

67
Q

catecholamines

A

dopmamine and noradrenaline

68
Q

synthesis of Ach

A

Acetyl CoA + Choline—–(choline actyltransferase ChAT)—-> Ach +CoA

69
Q

degradation of Ach

A

Ach—–actylcholinesterase—-> acetic acid + Choline

70
Q

ChAT

A

choline acetyltransferase

a good marker for cholinergic neurones

71
Q

Acetyl CoA

A

produced by cellular res in mito

72
Q

chemicals that prevent release of Ach

A

botulinum toxin (produced by bacteria)

black wider spider venom (latrotoxin) first increases ACh release at NMJ then eliminates it. Seems to work by allowing a big calcium influx.

73
Q

AChE inhibitotrs

A

nerve gas
insecticides
Alzheimers treatments

74
Q

Chemicals that block Ach Receptors

A

nicotinic
- curare
- alpha bungarotoxin
Alpha bungarotoxin from snake venom binds to nAChRs and takes days to unbind.

Muscarinic
-atropine

75
Q

ACh 2 cholinergic complexes

A

1) basal forebrain complex
amongst first neurones to die in alzehiers disease
regulate brain excitability during sleep/wake cycles + arousal
possible role in learning and memory

2)Pontomesencephalotegmental complex (brainstem)

76
Q

synthesis of catecholamines

A

1) tyrosine= amino acid

–tyrosine hydroxylase->

2) L-Dihydroxyphenylalanine (dopa)

—dopa decarboxylase—>

3) Dopamine
- Dopamine B-hydroxylse–>
4) Noradenaline

—phentolamine N-methlyltransferase(PNMT)–>

5) Adrenaline

Tyrosine hydroxylase
present in all catecholaminergic neurons
rate limiting factor

Dopamine β-hydroxylase
found in synaptic vesicles

PNMT
found in the cytosol

77
Q

MAO-A (monoamine oxidase)

A

on outer mito membrane

metabolises noradrenaline and 5HT mainly

78
Q

MAO-B

A

mainly metabolises dopamine

79
Q

catechol-O- methyltransferease (COMT)-

A

degrades catecholamines in cytoplasm

80
Q

nigrostriatal pathway

A

Neurons found in the substantia nigra of the midbrain
Axons project to the striatum
Pathway facilitates the initiation of voluntary movements

Degeneration of this pathway leads to Parkinson’s disease
Characterised by motor dysfunction e.g. tremor, rigidity

81
Q

treating parkinsons with addition of L dopa

A

removes the rate limiting step of tyrosine hydroxylase, so increases dopamine levels

82
Q

MAO-B inhibitors

A

reduce the breakdown of dopamine, increasing levels of it

83
Q

mesocorticolimbic pathway

A

Neurons found in the ventral tegmental area of the midbrain
Axons project to the frontal cortex and limbic system
Assigned many functions
Involved in a ‘reward’ system i.e. pleasure

We are motivated to perform behaviours that stimulate dopamine release
Behaviours associated with the delivery of drugs which result in dopamine release are reinforced = addiction

84
Q

noradrenergic system

A

arises form locus coeruleus
around 25,000 neurones

innervates nearly all of the brain

1 neutron can make 250,000 synapses

involved in regulating attention, aroudal, sleep-wake cycles, learning and memory, anxiety and pain, mood

most strongly activated by new unexpected non painful sensory stimuli

85
Q

serotonergic system

A

arises from Raphe nuceli

each nucleus projects to a different area

similar sighs innervation of brain to noradrenergic system

modualted pain-ralted sensory signals, sleep/wake cycles, mood and emotions
most strongly activated during wakefulness

example caudal icily innervate spinal cord

86
Q

5-HT life cycle

A

1) tryptophan: (from diet)

—tryptophan hydroxylase->

2) 5-Hydroxytrytophan

— 5HTP decarboxylase–>

3) 5-Hydroxytryptamine (serotonin, 5-HT)

87
Q

tryptohan in 5HT life cycle

A

starting molecule

Obtained from our diet e.g. grains, meat, dairy, chocolate
Moves from gut to blood to extracellular fluid
Rate limiting factor in synthesis

88
Q

treatment of affective disorders

A

tricyclic compounds- block uptake of 5HT and noradrenaline

  • SSRIs selectively prevent 5HT uptake
    e. g. prozac (fluxetine)

MAO-A inhibitors - reduce enzymatix degradation of 5HT and noradrenaline

89
Q

the cheese effect

A

tyramine is an amine found in high quantities in cheese

it has a sympathomimetic effect by increasing noradrenaline release
MAO normal breaks down tyramine
MAO-A inhibitors leads to a hypertensive crisis

90
Q

ATP

A

often packed into vesicles as a co-transmiter

binds to purinergic receptors
P2X= ligand gated ion channels
P2Y- g protein coupled receptors

91
Q

Endocannabinoids

A

endogenous forms of cannabis

small lipid molecules that do not require synaptic vesicles

binds to cannabinoid receptors that are G protein coupled

92
Q

Nitric oxide

A

Gasotransmitter that is small and membrane permeable

rapidly broken down

93
Q

catecholamines

A

dopamine, noradrenaline and adrenaline

and are produced in a a series of enzymatic conversions

BMS153 NEUROSCIENCE (24 decks)

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