014 + 015 an introduction to neurons and action potentials Flashcards

1
Q

what are the 4 main structures of neurons?

A
  • soma
  • axon
  • dendrite
  • pre-synaptic terminals
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2
Q

what is the soma of a neuron?

A
  • the cell body
  • contains nucleus and other organelles involved in metabolism and making proteins
  • also receives some signals
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3
Q

what is the dendrite of a neuron?

A

-receives input from many synapses
- tend to taper and covered with spines
- on the soma

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4
Q

what is the axon of a neuron?

A
  • transmits signals from the soma/body to the presynaptic terminals
  • usually uniform in diameter and can be myelinated or unmyelinated
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5
Q

what are the presynaptic terminals of a neuron?

A
  • little terminals louded with synaptic vesicles at the end of an axon
  • gives the output of a neuron = release a neurotransmitter to a receptor or another neuron
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6
Q

what are the 4 main types of neurons?

A
  • bipolar/interneuron
  • unipolar/sensory neuron
  • multipolar/motorneuron
  • pyramidal cell
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7
Q

what transmitters do excitatory/projection neurons use?

A
  • glutamate, acetylcholine, noradrenaline…
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8
Q

what transmitters do inhibitory neurons use?

A
  • GABA, serotonin, peptides…
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9
Q

what is the neuron pathway in a reflex?

A

sensory neuron –> interneuron –> motor neuron
or sometimes sensory neuron –> motor neuron

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10
Q

what are the differences in action potentials within a neuron vs between neurons?

A
  • within neuron = all or nothing action potential
  • between cells = synapse potential varies due to variations in size of terminals
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11
Q

what is the resting membrane potential of a neuron?

A

-70mV

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12
Q

what maintains the resting potential of a neuron?

A
  • Na/K ion ATPase pump
  • 3 Na out for 2 K in
  • so more positive leaving cell so inside cell stays negative
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13
Q

describe the cell membrane of a neuron

A
  • phospholipid bilayer
  • has ion channels that allows ions to flow down their electrochemical gradienr
  • ion pumps that control the resting potential of the cell (Na/K ATPase pump)
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14
Q

what are the 2 ion forces opposing each other in a neuron membrane?

A
  • concentration of ions gradient
  • membrane potential (electrical charges, + to -) gradient
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15
Q

what is the Nernst equation used for?

A

use the temperature, charges of ions, concentration of ions and constants to work out the membrane potential of a cell

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16
Q

what is the Nernst equation?

A

E =RT/zF . ln Co/Ci

E = membrane potential
R= gas constant
T = temperature (Kelvin)
z = charge of ion
F = Faraday’s constant
ln = natural log
Co = concentration of ion outside cell
Ci = concentration of ion inside cell

17
Q

if you are at 37 degrees, what does the Nernst equation simplify to?

A

E = 62/z . LogCo/Ci

so for Na, if Co = 100 and Ci = 10

E = 62/1 . 1
= +62mV

18
Q

what is the equilibrium potential and resting concentrations for Cl- in a neuron?

A

-70mV
(7mM in, 120mM out = channels shut, some leak in)

19
Q

what is the equilibrium potential and resting concentration for K+ in a neuron?

A

-90mV
(135mM in, 2mM out = channels open, flow out of cell)

20
Q

what is the equilibrium potential and resting concentration for Na+ in a neuron?

A

+60mV
(18mM in, 150mM out = channels shut)

21
Q

what is the equilibrium potential and resting concentration for Ca2+ in a neuron?

A

+130mV
(0.1mM in, 120mM out, channels shut)

22
Q

what causes an action potential in a neuron?

A
  • depolarisation from the axon hillock (the connection between soma and axon)
  • if the threshold if greater than -50mV then it causes Na+ channels to open so Na moves into the cell, causing further depolarisation as it is positive, producing an action potential
23
Q

what are the 5 phases of an action potential?

A

1 = resting potential at -70mV with Na/K ATPase pump maintaining the balance (3 Na out, 2 K in), some K leaking out and some Na leaking in
2 = stimulus increases potential to -50mV, depolarisation near axon hillock due to neurotransmitter binding
3 = threshold is reached causing Na channels to open causing more depolarisation up to +40mV producing an action potential
4 = the potential of Na becomes greater than K, so the Na channels shut and the K channels open causing repolarisation down to -70mV
5 = hyperpolarisation of K channels still open letting K out of the cell down to -90mV
then back to 1 when the Na/K ATPase pump reactivate during the refractory period and balance to resting potential at -70mV

24
Q

what can mutations of sodium channels in neurons cause?

A
  • decreased Na channels in interneurons decrease inhibition which can cause severe epilepsy (Dravet syndrome)
  • increased Na channels in excitatory neurons can lead to too much excitation = also cause epilepsy
25
Q

what can mutations in potassium channels of neurons cause?

A
  • some can lead to hyper excitable motor neurons and thus over active muscles (myotonia)
  • mutations in the CNS can cause neurons to be too excitable and lead to epilepsy
26
Q

describe the phases of an action potential in the heart ventricle

A

phase 4 = resting membrane potential, K channels are open so K is leaking out so resting potential at about -90mV
phase 0 = stimulus causing depolarisation cause Na channels to open causing increase in depolarisation, the Na channels inactivate almost as soon as they open, up to +50mV
phase 1 = notch, partial repolarisation as Na channels inactivate, K channels rapidly open allowing efflux of K out
phase 2 = plateau, K channels remain open, L type Ca channels now open, allowing influx of Ca, causing a plateau of positive in and out of cell (at around +40mV)
phase 3 = repolarisation, Ca channels shut and K remain open continuing efflux of K down to -90mV

27
Q

describe the phases of an action potential in the heart SA node

A

phase 4 = unstable slow depolarisation due to opening of HCN (Hyperpolarised-activated cyclic nucleotide-gated channels) channels (If = funny current) allowing Na influx, T type Ca channels open towards end of phase allowing Ca influx ( from -60mV to -40mV)
phase 0 = reach threshold of about -40mV and L type Ca channels open causing depolarisation up to +10mV (HCN channels shut)
phase 3 = repolarisation due to inactivation of Ca channels and opening of K channels causing K efflux down to -60mV

28
Q

what current/channel controls heart rate via the SA node?

A

If = funny current
HCN (hyperpolarised-acivated cyclic nucleotide-gated) channel - Na channel = activated by hyperpolarisation (-60mV)

29
Q

why are heart action potentials slower than neuron action potentials?

A
  • heart action potentials rely on Ca channels which are much slower release than Na channels in neurons
30
Q

why does an action potential in a neuron only travel in 1 direction?

A
  • Na channels open locally in response to stimulus/depolarisation
  • this causes Na to move into the cell causing further depolarisation which causes neighbouring Na channels to open
  • upstream channels inactivate after they have opened and K channels open and it repolarises upstream as the depolarisation continues downstream
31
Q

what does the rate of propagation of action potentials depend on?

A

diameter of axon ( the larger the faster / less resistance)
myelination

32
Q

how does myelination increase the speed of propagation of action potentials down an axon?

A
  • Schwann cells wrap around the axon leaving gaps in between called nodes of Ranvier
  • the depolarisation jumps between the nodes of Ranvier which is faster than going through the whole axon
  • ion channels are also not open where it is myelinated, only at the node of Ranvier so less ATP and time is wasted opening and closing channels
33
Q

what happens to the action potential at the end of the axon?

A
  • the depolarisation is converted to chemical signals/release of neurotransmitters at the pre-synaptic terminals across the synapse to another neuron or a target tissue
34
Q

describe the steps of action potential causing neurotransmitter release at the synapse

A
  1. action potential causes depolarisation at the presynaptic terminals
  2. this causes voltage-gated Ca channels to open
  3. Ca enters the presynaptic terminal which triggers a conformational change in the docking and SNARE proteins causing the vesicles containing neurotransmitters to fuse to the plasma membrane and release the neurotransmitter into the synapse
35
Q

describe the recycling process of vesicles in the presynaptic terminal

A
  1. vesicle fuses with plasma membrane and exocytose neurotransmitters
  2. vesicle endocytoses back into the terminal
  3. vesicle translocates, and fuses into an endosome
  4. budding off the endosome forms individual vesicles
  5. vesicle uptakes neurotransmitter
  6. vesicle moves to plasma membrane and docks
  7. vesicle fuses with the plasma membrane…
36
Q

what happens if you block K channels in a neuron?

A
  • keeps K stuck in the cell, causing depolarisation, cannot repolarise
37
Q

what diseases are associated with the presynaptic terminal?

A

-congenital myasthenic syndromes cause impaired endocytosis of vesicles
- LEMS (Lambert-Eaton myasthenic syndrome) attacks presynaptic Ca channels (autoantibodies)
- Botulinum and tetanus toxins affect SNARE proteins involved in vesicle fusion