task 3 Flashcards

1
Q

synaptic transmission

A

transmission of messages from one neurone to another through synapse
> messages are carried by neurotransmitters & released by terminal buttons
> these chemicals diffuse across fluid-filled gap between terminal buttons & membranes of the neurones which form synapses

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2
Q

postsynaptic potentials

A

alterations in membrane potential of the postsynaptic neuron
-> (brief depolarisations/ hyperpolarisations)
> increase or decrease the rate of firing of the axon
> produced by neurotransmitters
> two types:
- EPSP
- IPSP

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3
Q

binding site

A

location on a receptor protein to which ligand binds

> neurotransmitters exert their effect by attaching to a binding site

> shape of binding site and shape of molecule of neurotransmitter are complementary

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4
Q

ligand

A

A chemical that attaches to a binding site.

> Neurotransmitters are natural ligands, produced and released by neurons.

> other chemicals found in nature can also act as ligands
-> for example in venom of animals: blocks binding sites and causes us to be paralyzed

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5
Q

axon terminal

A

= synaptic button

> End of an axon which forms a synapse on a neuron or other target cell (dendrites or the soma of another neuron for example)

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6
Q

axodendritic & axosomatic synapses

location / function

A

axodendritic synapses
> presynaptic membrane on axon
> postsynaptic membrane on dendrite

axosomatic synapses
> presynaptic membrane on axon
> postsynaptic membrane on soma

=> chemicals released by these synapses excite / inhibit dednrites / cell body of postsynaptic neurone
=> if sufficiently excited -> AP

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7
Q

components of synapse

A

presynaptic membrane:
> membrane of a terminal button that lies adjacent to the postsynaptic membrane
> releases neurotransmitter

postsynaptic membrane:
> cell membrane opposite the terminal button in a synapse;
> the membrane of the cell that receives the message.

synaptic cleft:
> contains extracellular fluid (serves as a glue that binds pre and postsynaptic membranes),
->through which the neurotransmitter diffuses.

synaptic vesicles:
> small, hollow, beadlike structure found in terminal buttons
> contains neurotransmitter molecules
> larger vesicles are called secretory granules

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8
Q

neurotransmitter

kinds / classes

A

A chemical that is released by a terminal button; has an excitatory or inhibitory effect on another neurone.
> Excitatory neurotransmitters – activates receptors on the postsynaptic membrane and enhances the effects of the AP (triggers depolarisation – usually by opening of Na+ channels).
> Inhibitory – reverse mechanism – triggers hyperpolarisation (usually by opening K+ channels or Cl- channels).
> Three classes of neurotransmitters:
- amino acids,
- monoamines,
- acetylcholine and peptides.

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9
Q

release zone

A

The region from which the neurotransmitter is released. Synaptic vesicles are found in greatest numbers around the part of the presynaptic membrane that faces the synaptic cleft – near the release zone.

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10
Q

receptors

A

Specialized protein molecules that detect he presence of neurotransmitters in the synaptic cleft. The presence of the receptors causes postsynaptic density.
Postsynaptic density means, that in the postsynapse (the side the receives the neurotransmitters) there is high amount of proteins accumulated (receptors).

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11
Q

postsynaptic density

A

Function 1: to anchor receptors for neurotransmitters in the postsynaptic membrane.
Function 2: Transduction. What is transduction? When receptors change neurotransmitters into a change in membrane potential – They read the message that the neurotransmitter gives and turn it into an action potential. The nature of postsynaptic response depends on the type of protein receptor that is activated by the neurotransmitter – either excitatory or inhibitory.

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12
Q

requirements for chemical synaptic transmission

A

There must be a mechanism for:
> synthesising neurotransmitters and packing it into the synaptic vesicles
> causing vesicles to spill their contents into the synaptic cleft in response to presynaptic action potential.
> producing electrical or biochemical response to neurotransmitter in postsynaptic neurone.
> removing neurotransmitters from the synaptic cleft.

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13
Q

amino acids

= slow speed of neurotransmission

A

‘building blocks of proteins’
-> protein is made up of one or more linear chains of amino acids (a.k.a. polypeptides)

> Glutamate
-> excitatory

> Gamma-aminobutyric acid (GABA)
-> inhibitory

> others:

  • Aspartate = excitatory.
  • Glycine = inhibitory.
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14
Q

monoamines

A

synthesised from a single amino acid

> Dopamine = pleasure neurotransmitter
-> can be inhibitory or excitatory

> Serotonin = mood neurotransmitter
-> inhibitory

> Adrenaline = fight or flight neurotransmitter
-> excitatory

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15
Q

acetylcholine (ACh)

A

learning neurotransmitter
-> excitatory

> activates muscle contraction in body & stimulates hormone secretion
binds to nicotine receptors or m1-m5
involved in thought / learning / memory within brain
in CNS implicated n awakening / attention / anger / aggression / sexuality / thirst
associated with Alzheimer’s disease -> 90% loss of acetylcholine in brain of ‘victims’
=> mediates fast transmission at all neuromuscular junctions

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16
Q

peptides

A

> Synthesis of peptides takes place in the soma.
Peptides are released from all parts of the terminal button – not just active zone – once released, destroyed by enzymes. No reuptake.
Endogenous opioids – peptides secreted by the brain that act as opiates. Opiates reduce pain because they have direct effects on the brain.

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17
Q
unconventional neurotransmitters 
(fourth class)
A

> Soluble gases – immediately and easily diffused through cell membrane into the extracellular fluid into nearby cells.

> Endocannabinoids – similar to THC. Tend to have most of their effects on presynaptic neurons – inhibiting synaptic transmission.

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18
Q

steps in chemical synapses

A
> synthesis 
> storage 
> release 
> binding 
> inactivation
19
Q

synthesis

A

> Neurotransmitter molecules are synthesised from precursors under the influence of enzymes.
There are two general classes of neurotransmitter:
-> Large peptides: synthesised in the cell body of the neurone and then transported to synaptic terminal through the axon.
-> Smaller amines/amino acids: synthesised at the presynaptic terminal itself.

20
Q

storage

A

Once neurotransmitters are synthesized, they need to be put into ‘small groups’ (store in vesicles) ready to be launched across the synaptic cleft.

21
Q

exocytosis = release of neurotransmitters

A

> membrane of the terminal button is depolarised by arriving action potential -> calcium channels (presynaptic membrane; release zone) open -> calcium flows into the cells by diffusion
calcium ions bind to synaptic vesicles -> allows the vesicles to fuse with fusion pores (presynaptic membrane)
Once vesicle fuses with fusion pore, it can release the neurotransmitters into the synaptic cleft.

22
Q

binding

A

> Neurotransmitter diffuses across synaptic cleft until they reach the postsynaptic neurone
raptors (postsynaptic membrane) control how a neurotransmitter is translated into an electrical signal.
neurotransmitters bind to postsynaptic receptors -> Activation of postsynaptic receptors,
-> either leads to depolarising (EPSP) or
-> hyperpolarising (IPSP)
–> which is caused by the types of ions channels that are opened: Na+ for EPSP / K+, Cl- for IPSP

23
Q

inactivation

A

Once neurotransmitter signal has been translated into an electrical signal, postsynaptic receptors need to be ‘cleared’ so that they can receive new transmitters from new signals.
> Some neurotransmitters will be degraded,
> some will be transported back to the presynaptic terminal to be recycled
> sometimes they are ‘absorbed’ by the postsynaptic terminal.

24
Q

three types of vesicles

A

> Release-ready vesicles: are docked against the inside of the presynaptic membrane, ready to release their contents when an action potential arrives.
Recycling pool vesicles: constitute 10% of the total pool of vesicles.
Reserve pool vesicles: remaining 90%.

25
Q

vesicles after release
(what happens to membrane)

> Release-ready vesicles -> kiss and run.

> Recycling pool -> merge and recycle (full fusion).

> Reserve pool –> bulk endocytosis

A

> Kiss and run = release their neurotransmitter, break away from the presynaptic membrane and are filled with a neurotransmitter.

> Merge and recycle (full fusion) = The membranes of the vesicles merge with the presynaptic membrane, and then little buds of the presynaptic membrane break off to form a new synaptic (in the process vesicle loses its identity).

> Bulk endocytosis = large pieces of the membrane of the terminal bottom fold inward, break off and enter the cytoplasm. New vesicles are formed from small buds that break off these pieces of membrane.

26
Q

neurotransmitter recovery and degradation

A

> Clearing of the synapse is an essential step in synaptic transmission
-> new signals would be unable to propagate if released neurotransmitter is not cleared.
There are two mechanism for terminating neurotransmitter action:
1. Reuptake
2. Enzymatic degradation

27
Q

reuptake

A

> Neurotransmitter can be recycled directly.
-> common to the ‘small molecule’ neurotransmitter.

> Presynaptic membrane expresses a reuptake transporter
-> a protein that pushes the neurotransmitter against its concentration gradient and brings it across the cell membrane.

> important because it controls how long signals last

28
Q

enzymatic degradation

A

> Enzymes in extracellular fluid in synaptic cleft break the neurotransmitters down into their building blocks.

> Building blocks are partially taken up again through the presynaptic membrane, where they can be recycled.

29
Q

types of postsynaptic receptors

A

> Ionotropic receptors

> Metabotropic receptors

> Auto-receptors

30
Q
ionotropic receptors 
(= ligand-gated ion channels)
A

transmembrane molecules that can ‘open’ / ‘close’ a channel that allow smaller particles to travel in / out of cell

direct gating: they open channels through which ions can flow in / out
> usually closed until neurotransmitter binds itself to specific sites on extracellular region of channel -> causes pore to open
> these receptors don’t show same degree of ion selectivity as voltage-gated channels

if open channels are permeable to positive ions:
> depolarisation
> EPSP
if open channel are permeable to negative ions:
> hyperpolarisation
> IPSP
ions that can travel through them: K+ / Na+ / Cl- / Ca2+

=> short lasting effects

31
Q

metabotropic receptors

= G-protein-coupled receptors

A

indirect gating:
1. neurotransmitter molecules bind to receptor proteins embedded in postsynaptic membrane
2. receptor activates small proteins (G-proteins) -> free to move along intracellular face of postsynaptic membrane
3. G-proteins active ‘effector proteins’:
can be either:
> G-protein-gated ion channels in membrane
> enzymes that generate second messengers that diffuse away in cytosol
–> secondary messenger = chemical whose function is to go and activate other particles:
a) it binds to & opens ion channel located somewhere in membrane
b) goes and activates other intermediate molecules inside cell

=> long-lasting effects
[> cannabinoid receptors (CB1 / CB2) ]

32
Q

auto-receptors

A

presynaptic receptors that are sensitive to neurotransmitter released by presynaptic terminal
> typical G-protein-coupled receptors that stimulate second messenger formation
main consequence:
-> inhibition of neurotransmitter release / in some cases neurotransmitter synthesis
–> allows presynaptic terminal to control itself

> Appear to function as a safety valve to reduce release when concentration of neurotransmitters around presynaptic terminal gets too high

33
Q

drugs

how they work / kinds

A

any substance or product that is used or intended to be used to modify or explore physiological systems or pathological states for the benefit of the recipient
> drugs mimic actions of neurotransmitters

agonist: drugs that facilitate the effects of a particular neurotransmitter
> e.g. nicotine: binds & activates the ACh receptors in skeletal muscle

inverse antagonist: same as agonist but it completely closes ion channels causing opposite reaction
> e.g. if instead of waking up, Red Bull made you more tired

Antagonist (=receptor blockers): drugs that inhibit effects of a particular neurotransmitter
> binds to postsynaptic receptor without activating them -> blocks the access of usual neurotransmitters

partial agonist: does activate receptor less than the normal ligand does

34
Q
different drug effects 
> Atropine 
> Botox 
> Morphine 
> Prosac
> L-dopa 
> Cocaine
A

> Atropine
- blocks effects of acetylcholine
Botox
- blocks the release of acetylcholine at neuromuscular junctions
- used in medicine to reduce tumours and wrinkles
Morphine
- binds to receptors in hypothalamus or limbic areas in brainstem
Prosac
- used against depression
- serotonin is blocked (no reuptake) so it stays in the synaptic cleft.
L-dopa
- increases production of dopamine.
- used to help Parkinson’s disease
Cocaine = agonist
- blocks reuptake and neurotransmitters stay in the synaptic cleft

35
Q

axoaxonic synapses

location / function

A

> presynaptic membrane on axon
postsynaptic membrane on axon

=> axoaxonic synapse on (or near) a terminal button can facilitates / inhibits the effects of that button (postsynaptic neurone)
-> ‘postsynaptic facilitation / inhibition’ can selectively influence one particular synapse rather than the entire postsynaptic neurone

36
Q

dendrodendritic synapses

location / function

A

> presynaptic membrane on dendrite
postsynaptic membrane on dendrite

=> capable of transmission in either direction

37
Q

neuropeptides

A

large-molecule neurotransmitters

38
Q

neuromodulator

A

naturally secreted substance
> acts like neurotransmitter but is not restricted to synaptic cleft
-> defuses through extracellular fluid

39
Q

glutamate (Glu)

A

memory transmitter

> mainly interacts with ionotropic NMDA or AMPA receptors
most common Brian neurotransmitter
produces EPSP -> excitatory
regulates development & creation of nerve pathways -> involved in learning & memory
oversupply -> overstimulation of brain -> migraines or seizures
low levels -> Alzheimer’s disease

40
Q

Gamma-AminoButyric Acid (GABA)

A

calming neurotransmitter

> binds to GABA(a) receptors because it’s partly ionotropic
binds to GABA(b) receptors because it’s partly metabotropic
produces IPSP -> inhibits neurone friring in CNS
-> high levels improve focus
-> low levels cause anxiety
very common in cortex neurones: contributes to motor control / vision / cortical functions
drugs that increase GABA levels are used to treat epilepsy / calm shakings due to Hunting’S disease

41
Q

dopamine (DA)

A

(-> catecholamine) pleasure neurotransmitter
-> inhibitory or excitatory

> binds to D1-D5 receptors
primarily responsible for feelings of pleasure
-> also involved in movement and motivation
people tend to repeat behaviours that lead to dopamine release -> addiction
abnormal low levels of secretion -> Parkinson’s disease
abnormal high levels of secretion -> schizophrenia

42
Q

serotonin (5-HT)

A

(-> indolamine) neurotransmitter that plays role in regulation of mood / eating / sleep / arousal
-> mostly inhibitory / can be excitatory

> binds to 5-HT receptors
contributes to feelings of well-being and happiness
affected by exercise / light exposure -> plays role in sleep cycle and digestive system regulation
unbalanced serotonin secretion -> depression, suicide, impulsive / aggressive behaviour

43
Q

adrenaline

A

(-> catecholamine)
fight or flight neurotransmitter
-> excitatory

> primarily a hormone released by adrenaline gland
-> some neurones release it as neurotransmitter
increases heart rate / blood flow
-> physical boost & heightened awareness
produced during stressful / exciting situations

44
Q

psychopharmacology

A

study of the effects of drug on the nervous system and on behaviour