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Neuro > Neurotransmission > Flashcards

Neurotransmission Flashcards

1
Q

Parts of the neuron

A

Dendrites
Cell body/soma
Axon
Presynaptic terminals

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2
Q

Basic neuron types

A

Multipolar neuron
Bipolar neuron
Pseudo-unipolar neuron
Unipolar neuron

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3
Q

Axonal transmission

A

Transmission of information from location A to location B

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4
Q

Synaptic transmission

A

Integrating/processing of information and transmission between neurons

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5
Q

Neuron’s resting potential

A

-70 mV

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6
Q

Why is the neurons resting membrane potential negative

A

Potassium and calcium cross readily
Sodium crosses with difficulty
Large organic proteins (-ve charge) cannot cross

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7
Q

Electrostatic attraction/repulsion

A

Forces determining distribution of charged ions

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8
Q

Electrostatic pressure

A

Ions move according to charge

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9
Q

Where are anion proteins mostly found

A

Restricted to inside the cell

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10
Q

Where are Na+ mostly found

A

Mostly outside neuron

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11
Q

Where are K+ mostly found

A

Mostly inside neuron

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12
Q

Where are Cl- mostly found

A

Mostly outside neuron

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13
Q

Sodium-potassium pump

A

3 Na+ out for 2 K+ in
Requires ATP- primary active transport

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14
Q

Final resting potential of neuron - -70mV

A

Na+/K+ pump- results in high Na+ concentration outside but with both force of diffusion and electrostatic pressure pushing in
Membrane and pump resists Na+ inward movement
K+ and Cl- move backward and forward across membrane so reach steady state by opposing forces of diffusion and electrostatic pressure
Some Na+ leaks back in but is expelled by pump

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15
Q

Which forces determine movement of ions across membrane at resting membrane potential

A

Forces of diffusion
Electrostatic pressure

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16
Q

Events within the action potential

A

Depolarisation and threshold
Reversal of membrane potential
Repolarisation to resting potential
Refractory period

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17
Q

Synaptic transmission triggers an action potential

A

Neurotransmitters activate receptors on dendrites / soma
Receptors open ion channels
Ions cross plasma membrane, changing the membrane potential
The potential changes spread through the cell
If the potential changes felt at the axon hillock are positive (+mV), and large enough, an action potential is triggered

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18
Q

Where do neurotransmitters initiate a change in membrane permeability

A

Dendrites of neurones

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19
Q

Excitatory neurotransmitters

A

Depolarise the cell membrane
Increase probability of an action potential being elicited
Cause an excitatory post synaptic potential

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20
Q

Inhibitory neurotransmitters

A

Hyperpolarise the cell membrane
Decreases probability of an action potential being elicited
Cause an inhibitory post synaptic potential

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21
Q

The action potential at an EPSP

A

EPSPs begin to depolarise cell membrane
Threshold ~ -60mV
When reached Na+ channels open (Na+ rushes in) and polarity reverses to +30 inside
Membrane potential reverses with the inside going positive
…at which point voltage-gated Na+ channels close and K+ channels open (K+ rushes out)
…which restores resting membrane potential

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22
Q

Threshold value

A

-60 mV

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23
Q

Propagation of the action potential

A

Signal loss due to lack of insulation –could be overcome by continual opening of next ion channel
But SLOW due to time to activate each channel.
Mainly short axon interneurons

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24
Q

Saltatory conduction

A

Decremental conduction between nodes of Ranvier (but ‘re-boosted’ each time)
But very fast along axon.
Most CNS neurons.

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25
Q

2 ways to reach threshold at inhibitory post synaptic potentials

A

Spatial summation
Temporal summation

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26
Q

Spatial summation

A

simultaneous signals coming from multiple presynaptic neurons being received by a single postsynaptic neuron

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27
Q

Temporal summation

A

involves a single presynaptic neuron rapid-firing signals to a postsynaptic neuron

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28
Q

Symptoms of multiple sclerosis

A

Eye movements – uncontrolled, seeing double
Speech – slurred
Paralysis – partial/complete, any part of body
Tremor
Co-ordination – lost
Weakness – tired
Sensory – numbness, prickling, pain

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29
Q

Diagnosis of multiple sclerosis

A

Initial symptoms – slight with remission…
….becoming more numerous, frequent and severe
Difficult to diagnose:
Early symptoms slight – person doesn’t go to doctor
Other diseases have similar symptoms
No definitive test: repeated presentation of symptoms combined with MRI

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30
Q

Who is affected by multiple sclerosis

A

Young adults 20-40
Slightly more women than men
Temperature zones
Areas with high standards of sanitation

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31
Q

Chemical synapse

A
  1. Action potential arrives at presynaptic knob and depolarises membrane
  2. Voltage activated Ca2+ channels open and influx of Ca2+
  3. Causes vesicles contains neurotransmitter to fuse with membrane and release neurotransmitter by exocytosis
  4. Diffuses across synaptic cleft
  5. Neurotransmitter binds to receptors on postsynaptic membrane causing Na+ channels to open
  6. Influx of Na+ causing depolarisation of membrane
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32
Q

Size of synaptic cleft

A

20-30 nm

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33
Q

After binding to postsynaptic knob, what happens to the neurotransmitter

A

Enzyme degradation
Reuptake into presynaptic knob

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34
Q

Acetylcholine

A

key neurotransmitter at the neuromuscular junction – it activates muscles

Not just skeletal muscles (for voluntary movement), also heart, respiratory muscles, gastrointestinal tract, eye muscles, muscles around blood vessels………

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35
Q

Symptoms of novichok poisoning as for many other nerve agents (which usually also target the ACh system)

A

Excessive activation of muscles (convulsions) initially
Subsequent paralysis as muscle cannot continually contract
Failure of heart muscles (heart failure)
Failure of muscles controlling respiration (asphyxsiation/drowning)
Failure of muscles in eye (pupils constricted / paralysis)
Failure of skeletal muscles (paralysis)
Failure of muscles of digestive tract (vomiting/diarrhoea)

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36
Q

Treatment of nerve agent poisoning

A

Atropine is an ACh receptor blocker – but doses needed to be effective very high (side effects)
Drugs which can re-activate AChE may also be administered
Usually intensive life-support required (due to cardiovascular effects)
Long-term damage of neuromuscular function probable

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37
Q

5 fundamental processes of synaptic transmission

A

Manufacture- intracellular biochemical processes
Storage - vesicles
Release- by action potential
Interact with post-synaptic receptors- diffuse across synapse
Inactivation- break down or re uptake

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38
Q

Common fast neurotransmitters- short lasting effects

A

Acetylcholine (ACh)
Glutamate (GLU)
Gamma-aminobutyric acid (GABA)

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39
Q

Common neuromodulators - slower timescale

A

Dopamine (DA)
Noradrenalin (NA) (norepenephrine)
Serotonin (5HT) (5-hydroxytryptamine)

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40
Q

Mechanism of local anaesthetics (procaine and lignocaine)

A

Na+ channels blockers - particularly well absorbed through mucous membranes

Blocks progress of action potential

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41
Q

ACh is affected by

A

Cigarettes (nicotine - agonist)
Poison arrows (curare - antagonist)
Spider toxins (black widow - release)
Nerve gas (WW-I – blocks break-down)

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42
Q

Noradrenaline is affected by

A

Antidepressant drugs (Imipramine – blocks re-uptake)
Antidepressant drugs (MAO inhibitors – block break-down)
Stimulants (Amphetamine – increases release and blocks re-uptake)

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43
Q

Where is noradrenaline commonly found

A

Peripheral (heart) and central nervous system

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44
Q

Where is dopamine an important transmitter

A

Basal ganglia

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45
Q

Dopamine transmission affected by

A

Antipsychotic drugs (Chlorpromazine – receptor blocker)
Stimulants (Amphetamine/cocaine – increase release and block re-uptake)
Anti-Parkinson drugs (L-DOPA increases manufacture

46
Q

Serotonin transmission is affected by

A

Antidepressant drugs (Prozac – serotonin re-uptake inhibitor – SSRI)
Hallucinogens (LSD, psilocybin –5HT receptor agonist)
Ecstasy (MDMA, increase release, reduce reuptake)

47
Q

How do hallucinogenic drugs work

A

mimic serotonin, and can activate numerous different serotonin receptor subtypes

But the hallucinogenic effect itself appears to be specifically related to the way they target the serotonin ‘2a’ receptor (5-HT2a)

48
Q

Examples of hallucinogenic drugs

A

LSD
Magic mushrooms
Ketamine

49
Q

Gamma-aminobutyric acid affected by

A

Anti-anxiety drugs (benzodiazepines - valium – inhibitory effect at GABA receptors
Anticonvulsant drugs (benzodiazepines – see above)
Anaesthetics (Barbiturates – potentiate the effect of GABA

50
Q

Side effects of GABA agonists

A

Anti-anxiety
Anti-convulsant
Anaesthetic

51
Q

Side effects of L-DOPA

A

Anti-parkinson
Causes psychosis at high doses

52
Q

Side effects of dopamine blockers

A

Anti-psychotic
Causes Parkinson-symptoms at high doses

53
Q

Problems for drug design

A

A region of the brain engaged in a particular function uses several neurotransmission systems e.g. basal ganglia
Glutamate
GABA
Dopamine
Acetylcholine
Substance P
Enkephalin

Regions of the brain engaged in different functions use the same neurotransmission systems
Glutamate
GABA
Acetylcholine
Serotonin
Dopamine/Noradrenalin

54
Q

Mechanism of novichok

A

Disrupts normal synaptic transmission of acetylcholine

55
Q

Local currents

A

Action potentials propagated along axons via local currents
Flow following depolarisation and allow depolarisation of adjacent axonal membranes

56
Q

Why does the local current only flow in one direction

A

Refractory period

57
Q

Capacitance

A

Ability to store charge
Lower capacitance = greater distance travelled

58
Q

Resistance

A

Number of ion channels open
Higher resistance (less channels open) = greater distance travelled

59
Q

What decreases capacitance

A

Myelin

60
Q

What is the distance an action potential travels dependent on

A

Capacitance and resistance

61
Q

Greater distance travelled

A

Lower capacitance
Higher resistance

62
Q

Absolute refractory period

A

Another action cannot be generated again under any circumstances

63
Q

Relative refractory period

A

Another action potential can be fired if the stimulus is strong enough

64
Q

What is myelin stained with

A

Osmium - white matter turns black

65
Q

Myelin is composed of

A

70 % lipid
30% protein

66
Q

Which cells produce myelin sheath in CNS

A

Oligodendrocytes

67
Q

How many axons can a single oligodendrocytes myelinate

A

50

68
Q

Which cells myelinate axons in the PNS

A

Schwann cells

69
Q

How long of a segment does a single Schwann cell myelinate

A

1.5mm

70
Q

How is the myelin sheath formed

A

Concentric wrapping of cell membranes —> from 20 to 200 layers

71
Q

When does myelinated begin

A

During 3rd trimester
Progresses rapidly during infancy
Continues through adolescence

72
Q

Where are unmyelinated neurones commonly found

A

In post-ganglionic autonomic fibres and olfactory neurones and interneurones eg hypothalamus

73
Q

Where are myelinated neurones typically found

A

Somatic nerves

74
Q

How does myelination improve conduction

A

Increases resistance
Decreases capacitance

75
Q

Node of Ranvier

A

Periodic gaps along myelinated axon
High density of ion channels
Action potentials happen here

76
Q

Guillain-Barré syndrome

A

Rapid onset of muscle weakness
Caused by autoimmune damage to PNS- damages myelin sheath

77
Q

Symptoms of Guillain-Barré syndrome

A

Pain and weakness
Typically begins in feet and hands
Spreads proximally.

78
Q

Where are electrical synapses found

A

Brainstem neurons eg hypothalamus
Hormone secretion

79
Q

Electric synaptic transmission

A

Plasma membranes of pre and postsynaptic cells are joined by gap junctions
Local currents flow directly across junction through connecting channels
Depolarises membrane of 2nd neuron to threshold propagation
Very rapid communication

80
Q

Types of post-synaptic receptors

A

Ionotropic receptors
Metabotropic receptors

81
Q

Iomotropic receptors

A

Ligand gated ion channels
Allows ion flux, changing cell voltage

82
Q

Speed of response in ionotropic receptors

A

Rapid

83
Q

Length of response in ionotropic receptors

A

Short-acting

84
Q

Metabotropic receptors

A

G protein coupled receptors (GPCRs)
Acts through secondary messengers, causing cellular effects

85
Q

Speed of response of Metabotropic receptors

A

Slow

86
Q

Length of response of Metabotropic receptors

A

Prolonged resposne

87
Q

Action of neuromodulators

A

Cause change in synaptic membrane that’s longer lasting
Tend to be slower events eg learning and development

88
Q

Examples of neuromodulators

A

Dopamine
Noradrenaline
Serotonin

89
Q

2 types of ACh receptors

A

Nicotinic
Muscarinic

90
Q

Nicotinic receptors respond to

A

ACh and nicotine

91
Q

Nicotinic receptors are found in

A

Neuromuscular junctions

92
Q

Nicotinic receptors

A

Contain ion channels that open in response to ACh

93
Q

Nicotinic receptors in the brain

A

Important in cognitive function and behaviour

94
Q

Muscarinic receptors are present in

A

Brain
Where PNS innervates peripheral glands and organs eg salivary glands, Bronchoconstriction

95
Q

Muscarinic receptors

A

Receptors coupled with G proteins
Not ion channel- instead trigger signalling pathways in the target cell that inhibit action potentials

96
Q

What is the main excitatory neurotransmitter

A

Glutamate

97
Q

What is the main inhibitory neurotransmitter

A

GABA

98
Q

How does imipramine affect noradrenaline

A

Blocks reuptake
Antidepressant

99
Q

How does monoamine oxidase affect noradrenaline

A

Increases amount of noradrenaline by inhibiting MAO (which breaks it down)
Antidepressants

100
Q

How does amphetamines affect noradrenaline

A

Increase release and block reuptake
Stimulant

101
Q

How does amphetamines affect dopamine

A

Increase release and block reuptake

102
Q

How does L-DOPA affect dopamine

A

Increases manufacture
Parkinson’s medication

103
Q

How does chlorpromazine affect dopamine

A

Antagonist and blocks receptors
Antipsychotic drugs

104
Q

How does Prozac affect serotonin

A

Increases concentration of synaptic serotonin- selective serotonin reuptake inhibitor
Antidepressants

105
Q

How does ecstasy affect serotonin

A

Neurotoxic to serotonin neurones- destroys the terminal of axons

106
Q

Length of refractory period

A

5-10ms

107
Q

Tonic receptors

A

slow adapting receptors. They will respond to the stimulus as long as it persists, and produce a continuous frequency of action potentials. Hence, they convey information about the duration of the stimulus

108
Q

Phasic receptors

A

rapidly adapting receptors. They will respond quickly to stimuli but stop responding upon continuous stimulation. Therefore, action potential frequency decreases during prolonged stimulation. This class of receptor conveys information about the changes to the stimulus such as intensity.

109
Q

What affects conduction velocity

A

Myelination
Diameter
Membrane capacitance
Membrane resistance

110
Q

Membrane capacitance

A

Ability to store charge
Lower capacitance = greater distance travelled before threshold no longer reacher

111
Q

Membrane resistance

A

Depends on number of ion channels open
Lower number channels open = greater membrane resistance = greater distance travelled before threshold no longer reached

112
Q

How does myelination speed up conduction velocity

A

Decreases membrane capacitance
Increases membrane resistance
Saltatory conduction

Neuro (22 decks)

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