neurones and synapses Flashcards

(71 cards)

1
Q

what is space constant?

A

how far electrical signals can propagate along the axon

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2
Q

how do you calculate space constant?

A

square root (membrane resistance/internal resistance)

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3
Q

what is membrane resistance proportional to?

A

it is inversely proportional to the surface area of the membrane and circumference of the axon

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4
Q

what is internal resistance proportional to?

A

it is inversely proportional to the cross-sectional area of the axon and the diameter of the axon

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5
Q

how do you calculate time constant?

A

membrane resistance - membrane capacitance

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6
Q

what is membrane capacitance?

A

how stretchy the axon’s walls are

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7
Q

what happens to individuals with demyelinating diseases?

A

signals won’t travel correctly because extra charge will leak out
this can lead to ectopic spikes because the neuron fires spontaneous action potentials

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8
Q

what is multiple sclerosis?

A

an auto-immune disease where the immune system attacks myelin

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9
Q

what are the symptoms of multiple sclerosis?

A

vision problems
numbness/tingling
muscle spasms/weakness

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10
Q

why do symptoms of multiple sclerosis get worse during stress and high temperatures?

A

sodium channels inactivate faster

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11
Q

what is guillain-barre syndrome and can patients recover?

A

an autoimmune disease affecting PNS myelin
patients usually recover because PNS myelin can regenerate

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12
Q

what are the symptoms of guillain-barre syndrome?

A

numbness/tingling
muscle weakness

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13
Q

how are neurons myelinated?

A

oligodendrocytes (in the CNS) or schwann cells (in the PNS) wrap around the axon surrounding it with layer of membrane

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14
Q

what does myelination do to axons?

A

increases membrane resistance and decreases membrane capacitance
increases space constant but doesn’t affect time constant
increases the distance between the extracellular and intracellular fluids

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15
Q

why does myelination decrease membrane capacitance?

A

the current can spread further and faster along the axon

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16
Q

how does myelination save space?

A

speeds up conduction without increasing the diameter of the axon

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17
Q

what are nodes of ranvier?

A

gaps between myelination where sodium channels are open and action potentials are generated

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18
Q

what is saltatory conduction?

A

sodium channels open at the nodes when the action potential reaches it to regenerate the depolarisation

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19
Q

how does saltatory conduction save energy?

A

there is less work for sodium-potassium pumps to restore the sodium ion gradient so it saves energy

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20
Q

what is a synapse?

A

a junction between two neurones that allows signals to pass between them by synaptic transmission

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21
Q

what are electrical synapses?

A

small gaps between neurones formed from gap junctions that act as pores for ions to travel through

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22
Q

why are electrical synapses important?

A

they allow for fast communication and synchronisation between neurones

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23
Q

what are chemical synapses?

A

release neurotransmitters from the presynaptic neuron that act on postsynaptic neurones

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24
Q

how are the postsynaptic terminals of chemical synapses adapted?

A

lots of mitochondria for energy-dependent processes
contains vesicles and secretory granules to store neurotransmitter

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25
what is the active zone in chemical synapses?
an area of electron density where neurotransmitter is released
26
what is the synaptic cleft?
the gap between neurones that contains lots of receptors for neurotransmitter to bind to
27
what are the steps in chemical synaptic transmission?
1. neurotransmitters are packaged into vesicles at the presynaptic terminal 2. an action potential arrives and causes calcium ion channels to open 3. an influx of calcium ions causes vesicles to fuse with the membrane and release neurotransmitters 4. neurotransmitter diffuse across the synaptic cleft and activate receptors on the postsynaptic cleft 5. neurotransmitters are removed from the cell
28
what is the difference between chemical and electrical synapses?
chemical synapses can invert signals if they are inhibitory but electrical synapses cannot
29
what are the two types of synaptic vesicle?
synaptic vesicles which carry small neurotransmitters, they can be reused and are packaged by transporter proteins dense core granules which carry peptide neurotransmitters and are filled at the golgi secretory apparatus, they can't be reused
30
what are the 2 types of SNARE protein?
t-SNAREs are expressed on the postsynaptic membrane v-SNAREs expressed on the vesicle membrane
31
what is synaptotagmi protein?
a protein that binds to calcium ions causing a shape change that causes SNARE proteins to zip together and fuse the vesicle with the membrane
32
how do toxins affect SNARE proteins?
they cut them up and prevent synaptic transmission
33
what are the 3 ways that neurotransmitters are removed?
diffuse away passively taken up by transporters using glia or the presynaptic neuron destroyed in the synaptic cleft by enzymes
34
what are the similarities between electrical and chemical synapses?
they can both modify signals they both allow summation
35
what are the differences between electrical and chemical synapses?
electrical pass signals in both directions, chemical pass in one electrical pass signals directly, chemical transform the signal electrical are fast and chemical are slower
36
what are neuromuscular junctions?
specialised synapses formed from a motor neurone connected to skeletal muscle
37
how are neuromuscular junctions fast and reliable?
action potentials in a motor neuron always cause an action potential in muscle cells
38
what are the adaptations of neuromuscular junctions?
have lots of large action zones to release more neurotransmitter have junction folds containing receptors that are lined up with active zones for binding
39
what is the criteria for neurotransmitters?
must be present in presynaptic terminals, released in response to stimulation and act on a postsynaptic neuron blocking it should prevent synaptic transmission
40
how can you determine if a molecule is a neurotransmitter?
You can collect fluid found around neurones after stimulating them and see if neurotransmitter is in the fluid you can also take fluid and put it onto postsynaptic cell to see if it mimics the effects of stimulation You can block the neurotransmitter to see if communication between neurones stops by deleting genes that encode enzymes or receptors
41
what are the 3 types of neurotransmitter?
peptides, amino acids and amines
42
how are amino acid and amine neurotransmitters and peptide transmitters different?
amino acid and amines are small, stored in vesicles and can bind to ionotropic or metabotropic receptors peptides are large, stored in granules and only bind to metabotropic receptors
43
what is divergence?
one neurotransmitter can activate multiple different receptors or subtypes of the same receptor, each receptor subtype can activate multiple different downstream effectors
44
what is convergence?
different neurotransmitters activate multiple different receptors to activate the same downstream effector to increase chance of the effect happening
45
what is glutamate?
an amino acid excitatory neurotransmitter
46
what happens when glutamate binds to AMPA receptors?
sodium and calcium ion channels open and they move into the cell potassium ions move out generates an EPSP
47
what are NMDA receptors?
ionotropic glutamate receptors found on the same membrane as AMPA receptors
48
how are NMDA receptors activated?
when AMPA receptors are activated and the membrane is depolarised the magnesium ion block is removed from NMDA receptors
49
what happens when NMDA receptors are activated?
sodium and calcium ions move into the cell potassium ions move out of the cell calcium ions cause downstream signalling
50
why are NMDA receptors used in learning and memory?
they are only activated when the membrane is already depolarised
51
what are mGluR receptors?
metabotropic glutamate receptors that trigger downstream signalling cascades to inhibit or excite other neurons
52
what is GABA and how is it synthesised?
an inhibitory amino acid neurotransmitter synthesised form glutamate using the enzyme glutamic acid decarboxylate
53
why does GABA activity have to be balanced?
too much causes comas too little causes seizures
54
what happens when GABA binds to GABA-a receptors?
chloride gated ion channels open, chloride ions can only move into the membrane when it is depolarised because the negative charge will repel negative ions
55
what happens if other chemicals (e.g. ethanol) binds to GABA-a receptors?
enhance the activity of chloride ion channels to increase hyperpolarisation causes inhibition of areas in decision making and balance
56
what happens when GABA binds to GABA-b receptors?
potassium ion channels open and calcium ion channels open second messengers are triggered such as cAMP
57
what are the 2 roles of glycine?
inhibit neurones via glycine-gated chloride ion channels bind to glutamate NMDA receptors to increase excitation
58
what is spatial summation?
lots of signals from different places are added up to reach the threshold and generate an action potential
59
what is temporal summation?
lots of EPSPs are generated in a short time, the membrane is depolarised more each time to meet the threshold and generate an action potential
60
why should inhibitory synapses be placed after excitatory?
so current doesn't leak out causing the EPSP to stop so depolarisation isn't transferred
61
how does GABA inhibit neurons?
causes calcium ion channels to close reducing the amount of calcium ions that can enter when an action potential arrives so it reduces the chance of EPSP because less neurotransmitter is released and more neurones need to be activated for an action potential to be generated
62
if neuron A's axon is 2x wider than neuron B's axon how will A's space constant be different?
A's space constant is sqrt(2) times longer than B's
63
why would neuronal conduction speed decrease if leaky potassium ion channels were inserted into the membrane?
membrane resistance decreases so space constant is smaller
64
how does botulinum toxin cause muscle paralysis?
destroys SNARE proteins so vesicles don't fuse with the presynaptic membrane and acetylcholine isn't released into the synaptic cleft
65
how would blocking endocytosis affect small molecule and peptide neurotransmitters?
small molecule neurotransmitters wouldn't be released and recycled peptide neurotransmitters wouldn't be affected because they are not recycled
66
if glutamate AMPA receptors are permeable to both potassium and sodium ions how are they depolarised?
at rest the membrane is only permeable to potassium ions so when it is activated sodium ions enter and there are more sodium ions than at rest
67
where would chloride ions move if a GABA-a receptor was activated and the membrane potential was lower than chloride's nernst potential?
chloride ion move out of the neuron because the negative potential pushing chloride out overwhelms the concentration gradient pushing chloride in
68
how does atropine treat nerve gas poisoning?
nerve gas increases acetylcholine levels in the synaptic cleft by inhibiting acetylcholinesterase atropine blocks the muscarinic receptors to prevent Ach binding
69
why is an excitatory synapse in the soma more effective at generating an action potential than a synapse on the tip of a dendrite?
the ESPS decays as it propagates from the tip of the dendrite to the soma as the current leaks out so less current is lost and the ESPS is stronger
70
how can you use immunostaining to check if a neurotransmitter is present?
Immunostaining for an enzyme or protein used to synthesise or store a neurotransmitter will show if it is in the presynaptic neuron
71
how can you use in situ hybridisation to check if a neurotransmitter is present?
In situ hybridisation can be used which is looking at RNA that codes for proteins that store neurotransmitters