developmental neurobiology > synapse stabilisation > Flashcards

synapse stabilisation Flashcards

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1
Q

what does the pre-synaptic cell contain?

A

mitochondria, transport vesicles, synaptic vesicles and the active zone

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2
Q

what is the active zone?

A

where the synaptic vesicles are located

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3
Q

what does the post-synaptic membrane contain?

A

neurotransmitter receptors and ion channels located within the post-synaptic density

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4
Q

what is the post-synaptic density (PSD)?

A

an area beneath the post-synaptic membrane that is rich in proteins and appears as an electron-dense area through an electron microscope

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5
Q

what morphological changes happen when a growth cone reaches its target and becomes a pre-synapse?

A

filopodia retract and tight junctions form
extracellular glycoproteins are added to the membrane
presynaptic vesicles, dense ECM, PSD and receptors accumulate in the synaptic cleft

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6
Q

how are newer born synapses different from adult synapses?

A

they have fewer and smaller vesicles, a narrower cleft between cells and a thinner post synaptic density

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7
Q

apart from growth cones, what other structures can initiate synaptogenesis?

A

axon branches can form contacts with dendrites
dendritic filopodia can make contacts with the axons of incoming presynaptic cells

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8
Q

what can cause synapses to form/not form?

A

pre-established presynaptic specialisations
random contacts from cell adhesion molecules
guidepost cells such as glia that guide axons

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9
Q

what is synaptogenesis and what are synapses?

A

the brains process of forming new synapses
synapses are connections between 2 neurons or a neuron and a muscle or gland

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10
Q

when does synaptogenesis happen?

A

as axons reach their targets
in some areas such as the spinal cord and brainstem and other regions this happens around 15 weeks after fertilisation but most cortical synapses form after birth

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11
Q

how is netrin used to form synapses in C elegans?

A

in C elegans RIA axons form a ring and are synapsed on by AIY interneurons at specific points
sheath cells locally secrete netrin that guides RIA axons towards it and affects where the synapse will form

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12
Q

how does netrin cause synaptogenesis?

A

netrin secretion causes the receptors on the incoming axons to cluster around where the AIY interneurons are to promote assembly of pre-synaptic terminals

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13
Q

what happens to synaptogenesis when netrin is lost?

A

loss of netrin causes synapses to form all along the axon showing that netrin encourages synapse formation in a specific place

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14
Q

what is synapse specification?

A

the selection of an appropriate contact to form a synapse

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15
Q

what is synapse induction?

A

the clustering of synaptic machinery

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16
Q

what are neurexins and neuroligins?

A

synapse-specific cell adhesion molecules
they are large families of molecules with lots of diversity

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17
Q

how are neurexins and neuroligins used in synaptogenesis?

A

they bind very specifically to each other causing the pre and post synaptic membranes to stick together creating specific synapses

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18
Q

what is the structure of neurexins and neuroligins and why is this important?

A

they have large intracellular domains that assemble the active zone and the post synaptic density of the synapse

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19
Q

what can happen if there is aberrant neurexin and neuroligin signalling?

A

it is associated with autism and schizophrenia

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20
Q

how do neurexins and neuroligins help form specific synapses?

A

dendrites express counter receptors that bind to specific neuroligins and neurexins
the differential expression of multiple neurexin and neuroligin families allow different pre-synaptic neurons to select different post-synaptic partners

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21
Q

how do neurexins and neuroligins allow neurons to receive excitatory and inhibitory inputs?

A

differential localisation of neuroligins on the post-synaptic cell also allows separated innervation of excitatory and inhibitory post-synaptic neurons

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22
Q

what happens to synapses over time?

A

they can rearrange

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23
Q

what are the 3 different mechanisms of synaptogenesis?

A

dendritic spines can form without input from a presynapse and dictate where synapses form
growth cones can induce synapse formation at specific places where they make contact
dendritic filopodia can stop passing axons and form synapses with them

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24
Q

what happens when an axon and a dendrite make contact?

A

there is a rapid calcium influx

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25
what mediates the contact between an axon and a dendrite?
cell adhesion molecules such as neurexins and neuroligins soluble factors released by the pre or post synaptic cell such as Wnts
26
what happens when there is signalling after an axon and dendrite make contact?
it promotes recruitment of scaffold proteins such as the protein CASK and PSD-95 that provide a framework for the formation of protein complexes that form the active zone and post-synaptic density
27
why is the neuromuscular junction highly studied?
it is accessible (because it is in the periphery) simple larger than other synapses which allows the proteins involved to be purified and identified it can organise components of the post synaptic cell
28
what happens to acetylcholine receptors on muscle fibres before innervation?
they are present at a low density
29
what happens to acetylcholine receptors on muscle fibres during innervation?
they cluster where contacts with the motor neuron are stabilised increasing their density at these nerve terminals
30
what happens to acetylcholine receptors on muscle fibres after innervation?
they will only be found under nerve terminals
31
what is agrin and what is its role?
an ECM protein secreted by motor neurons it induces Ach receptor clusters to form when myotubes and motor neurons make contact
32
what happens to motor neurons that lack agrin?
they have disrupted neuromuscular junctions and Ach receptors are scattered along muscle fibres instead of in clusters showing that agrin is important for induction
33
what happens happens before agrin is released?
Ach receptor mRNA is expressed at low levels in the myotube nuclei and Ach receptor channels are widely distributed but at a low density
34
what happens after agrin is released from the incoming motor neuron?
agrin binds to LRP4 which activates MuSK MuSK recruits scaffold protein raspyn causing AChR to cluster other factors released by the motor neuron growth cone cause expression of AChR in nearby synaptic nuclei
35
what prevents ach receptors from clustering away from the nerve terminal?
electrical activity from Ach release destabilises receptors not under nerve terminals because MuSK is not activated
36
what is the role of ach in receptor clustering?
supresses Ach receptor mRNA and causes Ach receptors to be degraded
37
what happens in mice with ach knocked out?
Ach receptor clusters grow faster and larger showing Ach release destabilises clusters away from contact points
38
what is LRP4?
an agrin-binding component
39
what happens when LRP4 and MuSK are knocked out?
it prevents Ach receptor clusters from forming and causes insensitivity to agrin showing MuSK and LRP4 are needed for neuromuscular junctions to mature
40
what happens when MuSK is overexpressed?
synapse formation happens in aberrant places showing it is a master organisers of where synapses form on muscles
41
what is the role of Rapsyn?
it interacts directly with Ach receptors to hold them in place and blocks intracellular signals that could destabilise the Ach receptor clusters
42
what happens if to rapsyn mutants?
they do not have Ach receptor clusters or neuromuscular junctions
43
what is polyinnervation?
when motor neurons innervate multiple muscle fibres and each fibre receives multiple inputs this happens during early development
44
what is monoinnervation?
when a motor neuron innervates one fibre this happens after the muscle matures
45
what happens to synapses during development?
they are eliminated this happens due to non-random competition between synapses
46
why is polyinnervation discoordinated?
any motor neuron firing leads to a fibre contraction even if the other neurons that innervate that muscle did not fire
47
what is TTX?
a small molecule drug that blocks sodium ion channels and causes muscle paralysis because it blocks activity at the neuromuscular junction
48
what happens when synaptic competition is blocked by TTX?
the muscle fibre cannot go from polyinnervation to monoinnervation there will not be elimination of synapses and more fibres will be polyinnervated this shows that this elimination is dependent on activity at the neuromuscular junction
49
what does synapse survival depend on?
coordinated electrical activity between the pre and postsynaptic cells of the neuromuscular junction
50
what happens when there is deliberate non-coordination of muscle fibres?
it increases the rate of synapse loss, this causes muscle fibres to contract even when the motor neurons are not firing
51
which neurotrophin and receptors are expressed at the neuromuscular junction?
BDNF and its receptors TrkB and p75-NTR
52
what is BDNF processing?
when pro-BDNF (unprocessed) is converted to BDNF (processed) it is done by a proteinase called MMP
53
what causes MMP expression?
coordinated activity causes MMP expression
54
what happens when MMP is expressed?
more pro-BDNF is processed into BDNF BDNF binds to TrkB this triggers synaptic potentiation (synapse strengthening) the synapse is not eliminated and survives (reward)
55
what happens when there is low MMP expression?
there is more pro-BDNF it binds to p75-NTR this supresses transmission and cause axons to retract which eliminates the axon (punishment)
56
what happens if BDNF is added to synapses in the neuromuscular junction?
synapses are not eliminated
57
what happens if TrkB is blocked in the neuromuscular junction?
more synapses are eliminated
58
what happens if MMP is added to synapses at the neuromuscular junction?
prevents synapse strengthening
59
what happens if pro-BDNF is added to synapses at the neuromuscular junction?
more synapses are eliminated
60
what happens if p75-NTR is lost?
synapses are not eliminated
61
what does the Hebbian theory state?
that coordinated activity of a presynaptic terminal and a postsynaptic neuron strengthens the synaptic connections between them
62
what are ocular dominance columns?
alternating stripes of neurons in the primary visual cortex that receive input from the LGN from either the left or right eye forming a striped pattern needed for binocular vision and depth perception
63
what experiment was done to show ocular dominance columns?
radioactively labelled amino acids were injected into the eye and traced from the LGN to the primary visual cortex
64
what was observed in the ocular dominance column experiment?
in adults inputs formed layers in the LGN and columns in the visual cortex in early development there was no organisation and the inputs were messy
65
what did the ocular dominance column experiment show?
ocular dominance column formation is dependent on visual inputs over time
66
do neurons in the visual cortex receive inputs from one or both eyes?
a lot of the cells get input from both eyes but there are some (especially in layer 4) that only receive inputs from one eye
67
what happened in the monocular deprivation experiment and what was observed?
one eye was kept shut in the developing embryo all cells in the cortex received input from the open eye and its columns expanded into the territory of the closed eye
68
what does monocular deprivation experiment show?
activity is important in establishing ocular dominance columns and the columns reflect the dominant input there is competition between eyes for territory in the cortex
69
what is long term potentiation?
when the firing rate of a neuron increases due to high frequency stimulation the synapse is strengthened
70
what is long term depression?
when the firing rate of a neuron is decreased due to low frequency stimulation the synapse is weakened
71
what receptors do hippocampal presynaptic neurons express?
glutamate AMPA and NMDA receptors
72
what happens when glutamate binds to hippocampal presynaptic neurons?
the cell is depolarised by glutamate sodium ions will flow through AMPA receptors which unblocks the NMDA receptors releasing calcium ions into the cell
73
why is NMDA described as being a coincidence detector?
it detects when the presynaptic neuron fires and the postsynaptic neuron responds
74
what are the 3 main ways that synapses are strengthened?
post-synaptic changes in numbers of AMPA receptors and responsiveness, LTP increases the number of AMPA receptor and LTD decreases it increases in synaptic size presynaptic changes in the neurotransmitter release due to retrograde signals such as BDNF and nitric oxide)
75
what happens if NMDA receptors in the visual cortex are blocked?
it prevents the effects of monocular deprivation because it cannot detect high frequency stimulation
76
what shows that TrkB signalling is needed to form ocular dominance columns?
BDNF is released in response to high frequency stimulation
77
what happens if BDNF is lost?
there is more pro-BDNF it causes long term depression
78
what determines the identity of a neuron?
the set of transcription factors expressed in the cell early on many of these remain in the differentiated neuron
79
what determines when and where neuronal maturation occurs?
axon-target interactions
80
do neuronal behaviours and characteristics stay the same?
no they change as their axons reach their targets
81
what is the monosynaptic stretch reflex?
when the kneecap is tapped it causes a muscle to contract that lifts the leg
82
what causes the monosynaptic stretch reflex?
target-derived factors between motor neurons and proprioceptive Ia sensory neurons
83
how are the triceps and pectoral muscles innervated?
monosynaptically motor neurons innervate proprioceptive neurons directly
84
how is the latissimus dorsi innervated?
polysynaptically motor neurons signal through interneurons
85
why are different muscles innervated differently?
different targets have different patterns of innervation
86
what causes polysynaptic innervation of latissimus dorsi?
latissimus dorsi secreted glial cell derived neurotrophic factor (GDNF) GDNF shapes the pattern of innervation of the nervous system
87
how does GDNF pattern innervation?
GDNF turns on the transcription factor Pea3 in motor neurons
88
what happens if pea3 is lost?
motor neurons innervate the wrong target and have a different morphology
89
what is the role of neurotrophin 3 (NT3)?
it is expressed by muscles and induces the expression of the transcription factor Er81 by Ia proprioceptors
90
what happens if Er81 is knocked out?
prevents Ia proprioceptive axons from reaching the ventral horn and forming monosynaptic connections with its correct target
91
how does NT3 allow the maturation of neurons?
it tells the neuron where to send its projections and checks the projections have reached a certain place before it can mature
92
are axon targets signal dependent or independent?
they can be either dependent, independent or inter-dependent
93
what is an example of a dependent target?
muscle spindles need sensory innervation in order to differentiate and fully mature
94
what is an example of an independent target?
Merkel cells are specialised epithelium overlying free nerve endings that form Merkel discs and they mature before sensory innervation
95
what is an example of an inter-dependent target?
mechanosensory neurons change their morphology as their target matures which can vary depending on where the target is
96
what is an example of a neuron's property changing as its target matures?
sweat gland motor input changes from noradrenergic to cholinergic as the glands mature and change function
97
what is an example of a neuron changing independent of its target?
neurotransmitters and their receptors are expressed before synaptogenesis
98
what is an example of neuronal excitability changing as neurons mature?
early action potentials are generated by calcium ions instead of sodium ions flow later on sodium flow appears because there are changes in the ion channel subunits being expressed
99
what determines neuronal phenotype?
initial patterning factors that dictate the complement of transcription factors expressed the targets and signals encountered as the circuit forms
developmental neurobiology
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