Neurotransmission Flashcards

(112 cards)

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
2 ways to reach threshold at inhibitory post synaptic potentials
Spatial summation Temporal summation
26
Spatial summation
simultaneous signals coming from multiple presynaptic neurons being received by a single postsynaptic neuron
27
Temporal summation
involves a single presynaptic neuron rapid-firing signals to a postsynaptic neuron
28
Symptoms of multiple sclerosis
Eye movements – uncontrolled, seeing double Speech – slurred Paralysis – partial/complete, any part of body Tremor Co-ordination – lost Weakness – tired Sensory – numbness, prickling, pain
29
Diagnosis of multiple sclerosis
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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Who is affected by multiple sclerosis
Young adults 20-40 Slightly more women than men Temperature zones Areas with high standards of sanitation
31
Chemical synapse
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
32
Size of synaptic cleft
20-30 nm
33
After binding to postsynaptic knob, what happens to the neurotransmitter
Enzyme degradation Reuptake into presynaptic knob
34
Acetylcholine
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………
35
Symptoms of novichok poisoning as for many other nerve agents (which usually also target the ACh system)
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)
36
Treatment of nerve agent poisoning
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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5 fundamental processes of synaptic transmission
Manufacture- intracellular biochemical processes Storage - vesicles Release- by action potential Interact with post-synaptic receptors- diffuse across synapse Inactivation- break down or re uptake
38
Common fast neurotransmitters- short lasting effects
Acetylcholine (ACh) Glutamate (GLU) Gamma-aminobutyric acid (GABA)
39
Common neuromodulators - slower timescale
Dopamine (DA) Noradrenalin (NA) (norepenephrine) Serotonin (5HT) (5-hydroxytryptamine)
40
Mechanism of local anaesthetics (procaine and lignocaine)
Na+ channels blockers - particularly well absorbed through mucous membranes Blocks progress of action potential
41
ACh is affected by
Cigarettes (nicotine - agonist) Poison arrows (curare - antagonist) Spider toxins (black widow - release) Nerve gas (WW-I – blocks break-down)
42
Noradrenaline is affected by
Antidepressant drugs (Imipramine – blocks re-uptake) Antidepressant drugs (MAO inhibitors – block break-down) Stimulants (Amphetamine – increases release and blocks re-uptake)
43
Where is noradrenaline commonly found
Peripheral (heart) and central nervous system
44
Where is dopamine an important transmitter
Basal ganglia
45
Dopamine transmission affected by
Antipsychotic drugs (Chlorpromazine – receptor blocker) Stimulants (Amphetamine/cocaine – increase release and block re-uptake) Anti-Parkinson drugs (L-DOPA increases manufacture
46
Serotonin transmission is affected by
Antidepressant drugs (Prozac – serotonin re-uptake inhibitor – SSRI) Hallucinogens (LSD, psilocybin –5HT receptor agonist) Ecstasy (MDMA, increase release, reduce reuptake)
47
How do hallucinogenic drugs work
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
Examples of hallucinogenic drugs
LSD Magic mushrooms Ketamine
49
Gamma-aminobutyric acid affected by
Anti-anxiety drugs (benzodiazepines - valium – inhibitory effect at GABA receptors Anticonvulsant drugs (benzodiazepines – see above) Anaesthetics (Barbiturates – potentiate the effect of GABA
50
Side effects of GABA agonists
Anti-anxiety Anti-convulsant Anaesthetic
51
Side effects of L-DOPA
Anti-parkinson Causes psychosis at high doses
52
Side effects of dopamine blockers
Anti-psychotic Causes Parkinson-symptoms at high doses
53
Problems for drug design
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
Mechanism of novichok
Disrupts normal synaptic transmission of acetylcholine
55
Local currents
Action potentials propagated along axons via local currents Flow following depolarisation and allow depolarisation of adjacent axonal membranes
56
Why does the local current only flow in one direction
Refractory period
57
Capacitance
Ability to store charge Lower capacitance = greater distance travelled
58
Resistance
Number of ion channels open Higher resistance (less channels open) = greater distance travelled
59
What decreases capacitance
Myelin
60
What is the distance an action potential travels dependent on
Capacitance and resistance
61
Greater distance travelled
Lower capacitance Higher resistance
62
Absolute refractory period
Another action cannot be generated again under any circumstances
63
Relative refractory period
Another action potential can be fired if the stimulus is strong enough
64
What is myelin stained with
Osmium - white matter turns black
65
Myelin is composed of
70 % lipid 30% protein
66
Which cells produce myelin sheath in CNS
Oligodendrocytes
67
How many axons can a single oligodendrocytes myelinate
50
68
Which cells myelinate axons in the PNS
Schwann cells
69
How long of a segment does a single Schwann cell myelinate
1.5mm
70
How is the myelin sheath formed
Concentric wrapping of cell membranes —> from 20 to 200 layers
71
When does myelinated begin
During 3rd trimester Progresses rapidly during infancy Continues through adolescence
72
Where are unmyelinated neurones commonly found
In post-ganglionic autonomic fibres and olfactory neurones and interneurones eg hypothalamus
73
Where are myelinated neurones typically found
Somatic nerves
74
How does myelination improve conduction
Increases resistance Decreases capacitance
75
Node of Ranvier
Periodic gaps along myelinated axon High density of ion channels Action potentials happen here
76
Guillain-Barré syndrome
Rapid onset of muscle weakness Caused by autoimmune damage to PNS- damages myelin sheath
77
Symptoms of Guillain-Barré syndrome
Pain and weakness Typically begins in feet and hands Spreads proximally.
78
Where are electrical synapses found
Brainstem neurons eg hypothalamus Hormone secretion
79
Electric synaptic transmission
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
Types of post-synaptic receptors
Ionotropic receptors Metabotropic receptors
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Iomotropic receptors
Ligand gated ion channels Allows ion flux, changing cell voltage
82
Speed of response in ionotropic receptors
Rapid
83
Length of response in ionotropic receptors
Short-acting
84
Metabotropic receptors
G protein coupled receptors (GPCRs) Acts through secondary messengers, causing cellular effects
85
Speed of response of Metabotropic receptors
Slow
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Length of response of Metabotropic receptors
Prolonged resposne
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Action of neuromodulators
Cause change in synaptic membrane that’s longer lasting Tend to be slower events eg learning and development
88
Examples of neuromodulators
Dopamine Noradrenaline Serotonin
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2 types of ACh receptors
Nicotinic Muscarinic
90
Nicotinic receptors respond to
ACh and nicotine
91
Nicotinic receptors are found in
Neuromuscular junctions
92
Nicotinic receptors
Contain ion channels that open in response to ACh
93
Nicotinic receptors in the brain
Important in cognitive function and behaviour
94
Muscarinic receptors are present in
Brain Where PNS innervates peripheral glands and organs eg salivary glands, Bronchoconstriction
95
Muscarinic receptors
Receptors coupled with G proteins Not ion channel- instead trigger signalling pathways in the target cell that inhibit action potentials
96
What is the main excitatory neurotransmitter
Glutamate
97
What is the main inhibitory neurotransmitter
GABA
98
How does imipramine affect noradrenaline
Blocks reuptake Antidepressant
99
How does monoamine oxidase affect noradrenaline
Increases amount of noradrenaline by inhibiting MAO (which breaks it down) Antidepressants
100
How does amphetamines affect noradrenaline
Increase release and block reuptake Stimulant
101
How does amphetamines affect dopamine
Increase release and block reuptake
102
How does L-DOPA affect dopamine
Increases manufacture Parkinson’s medication
103
How does chlorpromazine affect dopamine
Antagonist and blocks receptors Antipsychotic drugs
104
How does Prozac affect serotonin
Increases concentration of synaptic serotonin- selective serotonin reuptake inhibitor Antidepressants
105
How does ecstasy affect serotonin
Neurotoxic to serotonin neurones- destroys the terminal of axons
106
Length of refractory period
5-10ms
107
Tonic receptors
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
Phasic receptors
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
What affects conduction velocity
Myelination Diameter Membrane capacitance Membrane resistance
110
Membrane capacitance
Ability to store charge Lower capacitance = greater distance travelled before threshold no longer reacher
111
Membrane resistance
Depends on number of ion channels open Lower number channels open = greater membrane resistance = greater distance travelled before threshold no longer reached
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How does myelination speed up conduction velocity
Decreases membrane capacitance Increases membrane resistance Saltatory conduction