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BMS11004 > W3 Neuronal conduction > Flashcards

W3 Neuronal conduction Flashcards

1
Q

Action potential is like a moving wave

A

Action potential propagation is like a stadium wave = the Action potential moving down the axon is like the wave traveling across the stadium.
If you’re a person sitting down, and you see people next to you standing up, you stand up. That’s like the voltage-gated Na+ channels in “front’ of the action potential “seeing” the positive charge flowing in and opening because the membrane depolarised enough for them to open.
After you’ve been standing up a while, you sit down again. That’s like the voltage-gated K+ channels opening for the downstroke of the action potentials. And after you’ve stood up for the wave, you won’t stand up again.

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2
Q

Time constant

A

= how quickly does the membrane depolarise.
T = rm x Cm
rm = membrane resitance = how un-leaky is the hose wall
Cm = hwo stretchy is the hose wall

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3
Q

Space constant

A

Lenght constant = how far can current spread passively along the axon?

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4
Q

Electricity is like water

A

Electric charge = water standing still
Electric current = flowing water
Voltage = water pressure.
Resistance = what prevents water from flowing (e.g. narrow pipe). Property of the matter, what is stopping that water from flowing in a pipe.
Current = flow charges themselves.
Electricity is like water = electrical charge (positive or negative); if it is not moving it’s like water just sitting there. If it’s current, it’s like flowing water down a river.

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5
Q

An axon is like a leaky water hose

A

Outside cell = conducting fluid. Inside cell = conducting fluid. Membrane = limpids = don’t allow ions to pass through (w/ ion channels). Certain resistance inside/outside cell and across the cell. If you inject a current into the axon, it will flow through the axon but with the protein channels the current.
Current (“water”) flows down the axon (“hose”). But it also leaks out through channels in the membrane (“holes in the hose pipe”).

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6
Q

internal resistance

A

current (flowing water) spreads further if there is little resistance to it moving down the axon (hose)

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7
Q

Membrane resistance

A

Current (flowing water) spreads further if the membrane (hose wall) is less leaky.

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8
Q

Capacitor

A

two plates with a gap between them. Charge can build up on one side, creating voltage. This is like a stretchy rubber membrane in a hose pipe:

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9
Q

Myelination and membrane resistance/capacitance

A

Myelin increases membrane resistance and decreases membrane capacitance.

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10
Q

Iternal resistance

A

How hard is ti for current to pass along the axon

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11
Q

Saltatory conduction

A

Current enters through Na+ channels at a node of Ranvier. Then depolarization spreads passively down the axon (this is sped up by longer space constant) At the next node of Ranvier depolarization triggers voltage-gated Na+ channels to regenerate the action potential. => ¤ __ ¤ __ ¤ __ § (final action potential)

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12
Q

Demyelinating disease impair …

A

neuronal conduction.
The distribution of ion channels is designed with myelin in mind (voltage gated Na+ channels are only at the nodes of Ranvier), so if myelin disappears, signals will not travel correctly.

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13
Q

Demyelinating = Multiple sclerosis

A

auto-immune disorder, immune system attacks myelin.
episodic: symptoms get worse, then better, then worse, etc.
diverse neurological symptoms, e.g., vision problems, numbness/tingling, muscle spasms/weakness, many others.
symptoms might be worse when under stress or at high temperatures – neuronal conduction is “safer” at low temperatures because Na+ channels inactivate more slowly

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14
Q

Demyelinating diseases = Guillain-Barré sclerosis

A

auto-immune disorder affecting PNS myelin.
symptoms: numbness, tingling, weakness.
patients usually recover because PNS myelin can regenerate (unlike CNS myelin)

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15
Q

Synapse

A

= a junction between two neurons allowing signals to pass from one to the other. The process of signaling via synapses is synaptic transmission

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16
Q

What are electrical synapses good for?

A

Fast communication and Synchronizing neuron

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17
Q

Steps in chemical synaptic transmission

A
  1. Package neurotransmitters in vesicles, put them at the pre-synaptic terminal.
  2. Action potential arrives voltage gated Ca2+ channels open.
  3. Ca2+ influx vesicles fuse to membrane, neurotransmitters released.
  4. Neurotransmitters diffuse across the synaptic cleft, activate receptors on the postsynaptic cell  further signaling.
  5. Neurotransmitters are removed from the cleft.
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18
Q

Synaptic vesicles

A

= ‘clear’ small (40-50nm), small molecule neurotransmitter, filled by transporter proteins at the presynaptic terminal, recycled by endocytosis

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19
Q
  1. Ca2+ influx vesicles fuse to membrane, neurotransmitters released.
A

Vesicles fuse via SNAREs = When Ca2+ binds to synaptotagmin, a conformational change makes the SNAREs ‘zipper’ together, forcing the vesicle to fuse to the plasma membrane. SNAREs are targets for toxins (botulinum toxin, tetanus toxin). SNAREs are important in transporting proteins.

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20
Q
  1. Neurotransmitters diffuse across the synaptic cleft, activate receptors on the postsynaptic cell further signaling.
A

Neurotransmitters affect the postsynaptic neuron by binding to receptors:
Ligand-gated ion channels (ionotropic receptors)  directly depolarize or hyperpolarize the postsynaptic cell.
Note: the neurotransmitter itself DOES NOT enter the postsynaptic cel.
G-protein-coupled receptors (metabotropic receptors)  more complex effects.

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21
Q
  1. Neurotransmitters are removed from the cleft
A
  1. They diffuse away.
  2. They are actively taken up by transporters for recycling (into the presynaptic neuron or glia).
  3. They are destroyed in the synaptic cleft by enzymes.
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22
Q

Electrical synapses

A

Signals pass in both directions. Signals are passed directly, can only be attenuated. Fast (<0.3 ms)

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23
Q

Chemical synapse

A

Signals pass in one direction. Signals can be radically transformed (inverted, amplified, modulated…). Slower (0.3–5 ms)

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24
Q

Electrical and Chemical synpases

A

Both are = ‘plastic’ (i.e., can be modified), but chemical synapses probably more so. allow summing up inputs by the post-synaptic neuron.
Most synapses are chemical synapses.

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25
Q

Neuromuscular junctions (NMJ)

A

Fast and reliable neurotransmission.
Motor neuron action potentials always cause muscle cell action potentials.
Uses the neurotransmitter acetylcholine.

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26
Q

How does the NMJ achieve such efficient transmission?

A

One of the largest synapses in the body
- Presynaptic:
Large number of active zones
- Postsynaptic (motor end-plate):
Contains junctional folds, densely filled with neurotransmitter receptors.
Active zones and junctional folds are precisely aligned.

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27
Q

Acetylcholine

A

= created by combined acetyl and choline. Acetylcholine Destroyed in the synaptic cleft by an enzyme. Choline is recycled to make more acetylcholine.

28
Q

ChAT

A

good marker for cholinergic neurons.

29
Q

Acetylcholine acts on nicotinic (ionotropic and muscarinic (metabotropic) receptors

A

Nicotinic (nAChRs): ACh-gated Na+/Ca2+ channel, found at neuromuscular junction, CNS.
Muscarinic (mAChRs): 5 types of GPCRs, found in CNS and autonomic nervous system. Recall Loewi’s 1921 experiment on the heart: the ‘vagusstoff’ was ACh!

30
Q

Acetylcholine = pharmacology

A

1- Block release
2- Block AchE
3- Activate ACh receptors
4- Block ACh receptors

31
Q

Acetylcholine = pharmacology 1- Block release

A

= functions as paralyzing you
Botulinum toxin (produced by bacteria).
Black widow spider venom () first increases ACh release at NMJ then eliminates it. Seems to work by allowing a big calcium influx).

32
Q

Acetylcholine = pharmacology 2- Block AchE

A

Nerve gas. (the recent Russian poisoning of Yulia and Sergei Skripal in Salisbury was by one of these Ache inhibitors.)
Organophosphate pesticides (class of insecticide)
Alzheimer’s treatments.

33
Q

Acetylcholine = pharmacology 3- Activate ACh Receptors

A

Nicotine, muscarine
Neonicotinoid pesticides

34
Q

Acetylcholine = pharmacology 4- Black ACh receptors

A

Nicotinic: curare ( = used in poison arrow darts by indigenous South Americans - reversible
Alpha bungarotoxin from snake venom binds to nAChRs and takes days to unbind.
Bungarus multicinctus), α-bungarotoxin.
Muscarinic: atropine (can be an antidote for nerve gas. Also pupil dilation, increase heart rate – bc ACh used by autonomic nerves).

35
Q

Monoamines

A

Are synthesised from amino acids.
Don’t need to memorise these enzymes.
Ephinphrine ( adrenaline)

36
Q

Storage and removal of monoamines

A

Packed into vesicles by vesicular monoamine transporters (VMAT).
Removed from the synaptic cleft by re-uptake transporters (specific ones for each monoamine).
Destroyed by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT; on postsynaptic cell; only for catecholamines, not serotonin).

37
Q

Dopamine’s receptors

A

D1-like: D1,D5
D2-like: D2,D3,D4

38
Q

Epinephrine, norepinephrine’s receptors

A

Adrenergic receptors: α and β types

39
Q

Serotonin’s receptors

A

7 receptors – one is a ligand-gated Na+/K+ channel.

40
Q

Dopamine = Motor control

A

Dopaminergic neurons in the substantia nigra project to the striatum
This ‘nigrostriatal’ pathway facilitations initiation of voluntary movement
These neurons die in Parkinson’s disease  motor dysfunction (tremor, rigidity

41
Q

Parkinson’s can be treated with increasing dopamines

A

TH is rate-limiting in synthesis of dopamine, so can give L-DOPA (dopamine doesn’t cross the blood-brain barrier
The loss of the dopaminergic neurons causes the motor symptoms.

42
Q

Dopamine = reward

A

Dopaminergic neurons in the ventral tegmental area (VTA) project to the cortex and limbic system
This ‘mesolimbic’ pathway mediates ‘reward’/‘motivation’

43
Q

Noradrenergic neurons regulate arousal

A

Small number (~12,000 per hemisphere) in the locus coeruleus (the ‘blue place’) innervate the whole brain.
Sleep/wake, attention, arousal, mood, memory, anxiety, pain, etc. (complex!)
(Note: distinct from the role of norepinephrine in the autonomic nervous system

44
Q

Mainy important drugs affect monoamines

A

Cocaine, amphetamines: block reuptake of dopamine, norepinephrine
Antipsychotics: block dopamine receptors (possible side effect: Parkinson’s-like symptoms)
Antidepressants
- tricyclics: block reuptake of NE, serotonin
-selective serotonin reuptake inhibitors (SSRIs), e.g. fluoxetine (Prozac)
-MAO-A inhibitors

45
Q

Opioid peptides (endorphins) (neurotransmitter)

A

= bind to opioid receptors, regulate pain, also regulate coughing, opiod receptors are the targets of morphine, herion.

46
Q

ATP (neurotransmitter)

A

= often a co-transmitter, P2X2 = ATP-gated ion channels, P2Y2 = GPCRs

47
Q

Endocannabinoids (neurotransmitters)

A

lipid-soluble, not in vesicles
a2+ triggers synthesis, not vesicle fusion
etrograde signaling (postpre)
bind to GPCRs (the targets of the active compound in cannabis)

48
Q

Nitric oxide (neurotransmitters)

A

gas, membrane-permeable,e acts on soluble guanylate cyclase, not a membrane receptors.

49
Q

Neuron A has axon x2 wide neuron B’s. How long is neuron A’s space constant compared to Neuron B?

A

A’s space constant is square(2)° times longer than B’s space constant

50
Q

Why does botulinum toxin cause paralysis?

A

It destroys SNARE proteins, prevents vesicle exocytosis, no synaptic transmission, neurons can’t signal to muscles.
SNARE proteins helps vesicle fuse, which is needed for synaptic transmission and to pass on a signal to the muscle.

51
Q

If AMPA receptors are permeable to both Na+ and K+ why does activation cuase depolarisation?

A

The receptors reversal potential is ~ 0mv, so opening the channel moves the membrane potential closer to 0 (depolarization), at rest, membrane is only remeabl to K+ even if you increase permeability to both Na+ and K+, Na+ permeability is ‘proportionally’ higher than at rest.

52
Q

Why is atropine used to treat nerve gas poisoning?

A

= nerve gas increase acetylcholine by blocking acetylcholinesterase, atropine blocks muscarinic acetylcholine receptors.

53
Q

Criteria for neurotransmitters

A

A neurotransmitter should.
–be present in presynaptic terminals.
–be released in response to stimulation.
–act on the postsynaptic neuron.
Blocking the neurotransmitter should prevent synaptic transmission.

54
Q

Types of neurotransmitters receptors

A

Ligand-gated ion channels (ionotropic receptors) directly depolarize or hyperpolarize the postsynaptic cell.
G-protein-coupled receptors (metabotropic receptors) more complex effects.

55
Q

Convergence and Divergence allow flexibility

A

Each transmitter can activate multiple different receptors.
Each receptor can activate different downstream effectors.
Different transmitters or receptors can activate the same downstream effector.

56
Q

Glutamate

A

Most common excitatory transmitter in CNS.
Amino acids, therefore, found in all neurons.
3 ionotropic glutamate receptor subtypes based on the drugs which act as selective agonists.
Action is terminated by selective uptake into presynaptic terminals and glia.

57
Q

Glutamate = AMPA receptors

A

AMPA receptors mediate fast excitatory transmission.
Glutamate binding to AMPA receptors triggers Na+ and K+ currents resulting in an EPSP.
When you are below 0 mini volt = positive charge came in. Above 0 negative charge.  depolarization.

58
Q

Glutamate = NMDA receptors

A

NMDA receptors often co-exist with AMPA receptors.
They have a voltage-dependent Mg2+ block.
NMDA receptors only open when the neuron is already depolarized.
NMDA receptors let Ca2+ in leads to downstream signaling.
NMDA receptors function as a coincidence detector: when a neuron is activated right after it was already activated  important for learning!
 When the cell is at rest there is a magnesium ion sitting at its pore = black any sodium or ion to come through. This magnesium block only sits there at resting potential, if it gets depolarized. Negatively charge inside pulls the magnesium ion (positive) but when depolarized the charge inside is now positive and the magnesium detached

59
Q

Glutamate alse activated metabotropic glutamate receptors

A

mGluRs allow glutamate to sometimes be inhibitory (e.g., in the retina)

60
Q

GABA

A

Not an amino acid used to synthesise proteins.
Synthesised from glutamate by the enzyme glutamic acid decarboxylase.
Action is terminated by selective uptake into presynaptic terminals and glia.

61
Q

GABA is normaly inhibitory neurotransmitter

A

Most common inhibitory transmitter in the CNS
Produces IPSPs (inhibitory postsynaptic potentials) via GABA-gated chloride channels (GABAA receptors), if the membrane potential is above chloride’s Nernst potential.
The right amount of inhibition via GABA is critical:
– Too much coma or loss of consciousness
– Too little seizures

62
Q

Modulation of GABAa, receptors

A

Other chemicals can bind to the GABAA receptor and modulate the response to GABA binding.
These chemicals have no effects without GABA binding (allosteric drug)
Ethanol (alcohol) ( = makes GABA more effective )
Benzodiazepines e.g. diazepam, used to treat anxiety.
Barbiturates are sedatives and anti-convulsants.
Neurosteroids are metabolites of steroid hormones e.g. progesterone (possible natural regulators?)

63
Q

GABA also acts via metabotropic GABAB receptors.

A

Like the mGluRs, GABAB receptors are GPCRs. They act in diverse ways in different cells, but might:
– open K+ channels
– close Ca2+ channels
– trigger other second messengers like cAMP.
Often presynaptic or autoinhibitory

64
Q

Glycine

A

Inhibits neurons via glycine-gated chloride channel (glycine receptor). But it also binds to NMDA glutamate receptors.

65
Q

Matter how excitatory and inhibitory synapses are arranged spatially

A

An inhibitory synapse can block the propagation of an EPSP toward the soma.
GABAA receptors don’t always produce an IPSP, e.g. if Vm is near chloride’s Nernst potential.
In this case, they act by shunting inhibition.
Opening chloride conductance decreases the membrane resistance  current leaks out the membrane

66
Q

What is inhibition for?

A

Ihibitory neurons conrtolling excitatory neurons, just like a sheppered dog contorlling the sheep.

BMS11004 (12 decks)

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