Block 1 - Synapses Flashcards

(27 cards)

1
Q

What are the 3 factors that determine the electrical activity of a cell?

A
  1. How well ions move across cell membrane - Permeable to K but no Na
  2. Why ions move across the cell membrane - Electrochemical gradient
  3. When ions move - When the cell becomes depolarised ( becomes less negative and more postive)- sodium channels open - happens at threshold ( -50mv), then +40mv, the sodium voltage gated sodium gated ion channels close, voltage gated potassium open
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2
Q

When the mv go over 0, what is this called?

A

Overshoot

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3
Q

Define depolarisation and depolarisation?

A

Depolarised = when the cell is made less negative and more positive ( which is when the voltage gated sodium chanels open)

Repolarisation = is making them different again

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4
Q

What are the different refractory periods?

A

Absolute refactory period - Where no more action potentials can take place while the action potential is happening on the part of the neuron (depolarisation)

Relative refractory period- If you have enough stimulation, you might be able to get that part od the neuron to fire an action potential (repoalirsation and hyperpolarisation)

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5
Q

Overall, what is a quick summary of what happens at the synapse?

A

-The action potential comes down the axon, reaches the terminal ( the terminal bouton) and will utimatley result in a chemical neurotransmistter being dumped out - and that neurotramsitter have have an inhibitory or excitatory effect in the postnsynaptic cell

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6
Q

2 different types of synapses

A

-Neuronal synapse -Forms between two neurons
-Neuro-muscular junction - synapse that forms between muscles and neurons

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7
Q

Describe the neuromuscular junction

A
  • Axons synapse onto a muscle fibre
  • These cause muscles to contract and allow us to move
  • At all neuromuscular junction we have the same neurotransmiter - acetylcholine
  • Calcium is a really important part of the neuromuscular system, because your muscles cannot relax without calcium
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8
Q

Describe where neurotramsitters are kept

A

Neurotransmitters live in little vesicles in the axon terminal - they are made in the cell body - packaged into vesicles and transported along the axon to the presynaptic terminal - remain dormant until an action potential arrives

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9
Q

What is the significance of calcium?

A

Calcium is really important in many things

eg. Calcium Is really important in how we habituate things

Such as habituating people not to blink when puffs of air into the eye

Habituation - happens due to reduction in influx of calcium, meaning you have less neurotransmitter release, so signal isn’t passed on

-We can see this through experiments on sea snails

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10
Q

What is the process of the electrical signal turning into chemical, passing across into the next neuron

A
  • The axon potential comes down the axon, and reaches the terminal ( terminal Button)
  • This cause an influx of calcium channels to open (Ca2+)
  • The calcium binds with the vesicles ( little sacks filled with neurotransmitters)
  • This causes them to move to the pre-synaptic membrane and release their contents into the synaptic cleft
  • Neurotransmitters float over to the post synaptic membrane - within this are receptors
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11
Q

What are the two different types of postsynaptic receptors?

A

-Iontropropic receptors

-Metabotropic receptors

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12
Q

Describe ionotropic receptors

A
  • Proteins sitting in the membrane ( ligand gated ion channels ) of the dendrite

-The linand/ key is the neurontramittes

-These have a sight where the neurotramsitter can bind ( known as the binding sight), and once a neurotransmitter binds here, it causes a channel to open in the receptor, and then ions are permitted to flow into the neuron. This can then change the membrane potential of that neuron

-The ion channel with either let in positive ions or negative ions

-Postive ions - excitatory
-Negative ions - inhibitory

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13
Q

Describe metabotropic neurotransmitter receptors, what is the process for this?

A

-These influence ion channels indirectly

-There are a number of steps in order for the ion Chanel to be accessed

Process:

-Neurotransmitter also binds to these receptors, but instead of immediately opening an ion Channel, the step after binding is the activation of an intermediate protein known as the G protein

-This G protein can then influence the opening of ion channels, but it can also effect enzymes and activate intracellular signalling molecules ( known as second messengers)- iniating signalling cascades

-Metabortopic ion channels tend to have a slower action, but more wide spread effects, take longer to switch off- can have more lasting effects

-One system that only has metabotrpic receptors - Sense of smell

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14
Q

What are the two types of synapses?

A

Neurotransmitters can either be excitatory or inhibitory

Excitatory neurotransmitters are released at type 1 synapse, and bind to receptors that cause an influx of postive ions eg sodium

Inhibitory neurotransmitters are released at type 2 synapses and cause the influx of negative ions eg chloride

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15
Q

What are the two ways the EPSPs and the IPSPs can be added together in the axon hillock?

A
  • Spacial integration
  • Temporal intergration
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16
Q

Describe intergration and the two types

A

Integration - adding together of EPSPs and IPSPs

Problem is that EPSPs and IPSPs are graded potentials - some of them are big and some of them are small - and we have to add them all together

However, the degrade over space as well, as they don’t self propagate like action potentials across the neuronal membrane, they decay over space

eg if you had an EPSP of +5mv at the top of the cell body, by the time it reached the axon hillock, likely have decayed, charge won’t have traversed the membrane very well - Degrading over space

But that also degrade over time aswell-eg if you have two EPSP happening within a millisecond of each other, they will add together and be a more powerful EPSP as oposed to ones that happen 5 seconds apart

So we add them together both across space and time

17
Q

Why is is really important there is no neurotramsitters remaining in the synapse after activation?

A

-Really important that we don’t leave our neurotamsitter sitting in the synapse, as it will overstimulate or keep stimulating the next neuron

-The nervous system needs to be ON/OFF

-So we need to remove the neurotransmitter from the synapse - needs to be taken back into the presynaptic cell

18
Q

What are the 3 ways that neurotransmitters can be removed from then synapse?

A
  • Some of it happens through simple diffusion eg floating out of the synaptic cleft
  • Another method is though enzymes - enzymes can inactivate and break down neurotransmitters (enzymatic degregation)- these products can then be taken back up into the neuron
  • Most common method is called reuptake - in which a protein ( called a transport protein) which sits embedded in the menramne of pre synaptic neuron, takes the excess neurotransmitter back up- cam then be repackaged into vesicles
19
Q

What happens if Acheyocholine is left at the neuromuscular junction?

A

if we keep acetylcholine in the neuromuscular junction, will become paralysed as the muscles are overstimulated

20
Q

What are some different examples of neurotransmitters and what they do?

A

Glutamate: the brain’s major excitatory neurotransmitter, vital in forming links between neurons that are the basis of learning and memory.

  • GABA: the brain’s main inhibitory neurotransmitter.
  • Dopamine: involved in movement control and in reward circuits.
  • Serotonin: has become known as the feel-good chemical. It has a profound effect on
    mood and anxiety.
  • Acetylcholine is the neurotransmitter usedat the neuro-muscular junction.
21
Q

When things go wrong with neurotramsitters and their process - Parkinsons disease

A

Parkinson’s disease results from a loss of dopaminergic neurons in the brain stem (Substantia Nigra) causing rigidity and trembling movements.

  • The drug levo-dopa mimics the actions of dopamine (an agonist) and can relieve

the symptoms of Parkinsonian patients, but only temporarily.

  • (Progress into Parkinson’s disease was made by the discovery of MPTP. This

neurotoxin was discovered in the heroin taken by addicts who had suddenly developed Parkinson’s disease.)

  • A side effect of L-Dopa is schizophrenic symptoms. Schizophenia is therefore thought to be caused in part by overactivity of the dopaminergic pathways
22
Q

When things go wrong with neurotramsitters and their process -Examples of Toxins that poison ion channels

A

A number of venoms have been developed that target and deactivate specific ion channels.

  • Tetrodotoxin (puffer fish)produces a potent inactivation ofNa+ channels, paralyzing animalsunfortunate to eat it
  • Scorpions use a mixture of toxinsthat activate Na+ channels by lowering the threshold at which open, thus scrambling the information flow in the soon to de devoured victim.
  • K+ channels are inactivated by toxins from wasps and bees.
23
Q

When things go wrong with neurotramsitters and their process -
Toxins that affect neurotransmitter release:

A
  • atrotoxin is released by the blackwidow spider. It causes a massive release of neurotransmitter at th enerve-muscular junction that results inparalysis
  • Botulism works by stopping the release of excitatory neurotransmitters at the neuro-muscular junction. This prevents the contraction of the affected muscles
  • The tetanus toxin works by preventing inhibitory neurotransmitters to be released in the spinal cord. This causes hyperactivity of the muscles.
24
Q

When things go wrong with neurotramsitters and their process -Toxins that affect neurotransmitter receptors:

A

Poisonous plants and venomous animals are widespread in nature

.* Many of these toxins bind to neurotransmitter receptors.

For example, Bungarotoxin which is found in the venom of the branded krait blocks neurotransmitter receptors on the nerve-muscle junction. This prevents the victim from making an escape!

25
When things go wrong with neurotramsitters and their process -Psychoactive drugs
Psychoactive drugs mimic the effectof neurotransmitters by bindingdirectly to neurotransmitterreceptors. - LSD and psilocybe (mushrooms) mimic the effect of serotonin. These drugsare known as agonists. - Alcohol stimulates GABA receptors(acting as an agonist) increasing the effect of this inhibitory neurotransmitter leading to asedative like effect. However, it also acts as an antagonist as it blocks glutamate receptors.
26
When things go wrong with neurotramsitters and their process -Drugs that affect uptake
-Cocaine effects the reuptake of dopamine - prolongs the effects of dopamine leading to arousal -Prozac works by affecting the repute of seratonin ( SSRIS)
27
Why do people become addicted to drugs?
Many theories suggest an association between drug taking and reward circuits in the brain. The reward system is used to give pleasurable feelings when we do things that keep us alive (i.e. eating). - The release of the neurotransmitter dopamine is thought to be important in reward circuits. - Many highly addictive drugs (cocaine, heroin, nicotine) activate this system in the brain.