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Medicine Year 1 Semester 1 - Part 2 > Synapse 1 & 2 > Flashcards

Synapse 1 & 2 Flashcards

1
Q

Features of neuronal cells

A

Dendrites
Cell body (SOMA)
Axon
Myelin sheath
Node of Ranvier

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2
Q

Function of dendrites

A

Information arrives at the cell body via the dendrites where it is assimilated and processed.

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3
Q

Describe the movement of information through a neuron

A

Information arrives at the cell body via the dendrites where it is assimilated and processed.

Processed information isn then digitised and transmitted along the axon.

At the end of the axon, the information is passed to the target (muscle or neuron) via the nerve terminal.

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4
Q

What is a synapse ?

A

A junction between 2 cells, where electrical changes in one cell cause a signal to be passed to another usually via chemical neurotransmitter.

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5
Q

What is the most common type of synapse ?

A

The majority of synapses are chemical synapses, but some are electrical.

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6
Q

Location of synapses

A

Synapses primarily occur between neurones but also at the neuro-muscular junction (NMJ).

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7
Q

Function of synapses

A

Chemical synapses transmit neuronal action potentials in one direction between cells.

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8
Q

Describe the synaptic cleft

A

The gap between 2 cells (the synaptic cleft) is approximately 20nm (20 x 10^-9)

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9
Q

Describe modulation of activity at synapses

A

Activity at synapses can be modulated (neuromodulation)

This is a slower timescale than normal transmission, and affects the excitability of the pre- and post-synaptic cell using modulation of endogenous system.

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10
Q

What is modulation of endogenous system ?

A

Receptor density
NT production
Re-uptake ability

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11
Q

What is a bouton ?

A

The terminal of the presynaptic cell forms a swelling called a bouton or nerve terminal.

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12
Q

What do vesicles in the neuron contain ?

A

Molecules of neurotransmitter

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13
Q

Size of the synaptic gap

A

20nm

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14
Q

What have very careful electrophysiological experiments shown ?

A

That the release of neurotransmitters is quantal (meaning the amount of neurotransmitter found in each vesicle is the same).

And those quanta relate to the contents of single vesicles found at presynaptic membrane.

The more vesicles released, the stronger the signal at the post synaptic membrane.

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15
Q

State the 3 categories that synaptic activity can be divided into

A

Presynaptic activity - signalling
Postsynaptic activity - listening
Neurotransmitter inactivation

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16
Q

Describe small molecule transmitters

A

Synthesis of enzymes in the cell body

Slow axonal transport of enzymes

Synthesis and packaging of neurotransmitter

Release and diffusion of neurotransmitter

Transport of precursors into terminal

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17
Q

Describe larger peptide transmitters

A

Synthesis of neurotransmitter precursors and enzymes

Transport of enzymes and pre-peptide precursors down microtubule tracks.

Enzymes modify pre-peptides to produce peptide neurotransmitters.

Neurotransmitter diffuses away and is degraded by proteolytic enzymes.

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18
Q

Small molecule transmitters VS Peptide transmitters

A

SMT - Vesicles are recycled
PT - Diffusion ad Degradation

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19
Q

Describe vesicle recycling

A

Budding from a larger molecule

Storage of vesicles
Docking of vesicles
Priming of vesicles

Ca2+ entry
Fusion/Exocitosis

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20
Q

Where are peptide neurotransmitters made ?

A

In the RER and Golgi then transported.

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21
Q

What is packaged in the bouton ?

A

Amine / Amino Acid NT’s are made and packaged in the bouton

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22
Q

When is neurotransmitter released ?

A

NT release takes about 0.2ms from calcium entry

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23
Q

Describe the release of neurotransmitters

A

SNARE proteins in the vesicle and cell membrane bind.

These then form a helical structure which brings the 2 membranes close.

Entering Ca2+ binds to synaptotagmin.

Ca2+ bound synaptotagmin catalyses membrane fusion.

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24
Q

Name some SNARE proteins

A

Synaptotagmin
Syntaxin
SNAP-25
Synaptobrevin

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25
Q

What happens at the post-synaptic membrane ?

A
26
Q

Describe membrane spanning proteins

A

Embedded in the postsynaptic membrane are membrane spanning proteins called receptors.

They all belong to either the G protein coupled receptor group, or to the ligand gated ion channel group.

27
Q

Metabotropic receptors

A

G protein coupled receptor group

28
Q

Ionotropic receptors

A

Ligand gated ion channel group

29
Q

Describe ionotropic receptors

A

When the ligand binds to its binding site, it induces a conformational change in the receptor such that a pore from the inside to the outside of the cell is formed.

The pore is characteristic of the receptor type in both size and charge, which means each receptor can be specific to a single or varied number of ions.

The passage of ions into and out of the cell changes the voltage of the cell, either to depolarise (net positive charge) the cell or hyperpolarise (net negative charge) the cell.

30
Q

PSP

A

Post-synaptic potentials

31
Q

What causes PSP’s ?

A

Post synaptic potentials or PSPs are caused by the passage of ions through ion channels which have been opened following receptor/neurotransmitter interactions

32
Q

What are excitatory PSP’s ?

A

A net flow of positive ions (Na+ or Ca2+) into the cell depolarises the membrane (brings it closer to the threshold) and is thus termed EXCITATORY (EPSP).

Single EPSPs rarely result in an action potential.

33
Q

What happens after inhibitory and excitatory PSP’s ?

A

The amplitude of signals decreases with distance from the synapse and time.

An influx of negative ions or efflux of positive ions hyper polarise the cell.

34
Q

Name the 3 types of summation

A

Single EPSP
Spatial Summation
Temporal Summation

35
Q

Single EPSP

A

One action potential

36
Q

Spatial Summation

A

Multiple action potentials from different neurons

37
Q

Temporal Summation

A

Multiple action potentials from the same neuron

38
Q

Steps leading to an action potential

A

Neurotransmitter release
Receptor binding
Ion channels open
Conductance change causes current flow
Postsynaptic potential changes
Postsynaptic cells excited or inhibited

Summation determines whether or not an action potential occurs.

39
Q

Differences between EPSP’s and action potentials

A

EPSPs do not actively propagate along the axon.

No voltage gated current in EPSPs, they are caused by direct (ionotropic) or indirect (metabotropic) ligand gating.

EPSPs have no refractory period thus a series of EPSPs can summate

40
Q

What does generation of an action potential depend on ?

A

The inherent excitability of the neurone.

The frequency or amount of incoming excitatory impulses (from one or many synaptic connections)

The frequency or amount of incoming inhibitory impulses (from one or many synaptic connections)

41
Q

Inhibitory post synaptic potential function

A

Prevents the cell from firing an action potential

42
Q

What causes excitation in our spinal cord ?

A

Glutamate (via AMPA channels mainly)

43
Q

What causes inhibition in our spinal cord ?

A

Glycine (via Cl-channels mainly)

44
Q

Function of chemical synapses

A

Computation
Rectification
Plasticity

45
Q

Computation

A

As summation of multiple PSPs is required to achieve threshold, integration acts as a decision making process based on EPSP and IPSP input.

46
Q

Rectification

A

As chemical synapses transmit impulses in one direction only, this rectification serves to channel information.

47
Q

Plasticity

A

Controlled changes in the amount of transmitter released, the number of receptors present and the efficiency of the inactivation process provide a mechanism for adaptive plasticity (LTP and LTD)

Also involved in learning and memory.

48
Q

Function of small peptide molecules

A

Modulate the transmission of pain at the level of the spinal cord.

49
Q

LTP

A

Long Term Plasticity

50
Q

LTP in memory and learning

A

Stronger synaptic connections means easier/better synaptic transmission.

Stronger synaptic connections come from more vesicles, greater excitability, more receptors, more parallel synapses.

51
Q

What is LTP achieved through ?

A

Increased neurotransmitter release through increased vesicle numbers.

Formation of new synapses or synaptic zones and dendritic spines.

Increased post-synaptic receptor density and mitochondria.

52
Q

LTD in a model of addiction

A

Overstimulation of a pleasure pathway (eg uncontrolled opiate use)

Body responds by turning down transmission (reduced vesicles) or by turning down reception (reduced receptors)

Normal dose insufficient so more taken to overcome reduced transmission

Body further attenuates transmission

New increased dose insufficient so more taken to compensate

53
Q

Function of the synaptic cleft

A

At chemical synapses the gap or cleft between the two neurones is sufficiently large (20nm) that a neurotransmitter is required, but small enough for rapid diffusion across the gap.

54
Q

Where are neurotransmitter molecules stored in vesicles ?

A

Molecules of the neurotransmitter are stored presynaptically in vesicles.

These fuse with the membrane to release neurotransmitter by exocytosis. The vesicle membrane is then recycled.

55
Q

What does an increase in dendrites result in ?

A

The more dendrites a neuron has, the higher the degree of convergence.

56
Q

Neuronal divergence in a circuit

A

Information from a single neuron is passed to a number of other neurons simultaneously and without a loss of signal strength.

57
Q

Forms of divergent neurons

A

Spatially focused
Widely divergent

58
Q

Examples of neuronal divergence

A

Knee jerk reflex
Golgi tendon organ reflex

59
Q

Describe knee jerk reflex

A

The reflex stimulates in the spinal cord, the motor neurons to the extensor muscle and inhibits the motor neurons to the flexor muscle.

60
Q

Describe Golgi tendon organ reflex

A

The reflex inhibits in the spinal cord, the motor neurons to the extensor muscle and stimulates the motor neurons to the flexor muscle.

61
Q

Local neuron feedback

A

As N1 is excited more, this information is passed to N2

If N2 crosses threshold it fires and so inhibits its target, but also feeds back inhibition to N1

Therefore N1 is moderated by negative feedback from N2.

62
Q

Truncal ataxia

A

Cerebellar hypoplasia (predominantly of the vermis)

Medicine Year 1 Semester 1 - Part 2 (37 decks)

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