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NEURO 523 > Synaptogenesis > Flashcards

Synaptogenesis Flashcards

1
Q

Pre- and Post-synaptic specializations form at sites of active contact

Synapse formation in the CNS

A
  • Dendritic filopodium contacts axon
  • Synaptic vesicles and active zone proteins recruited to presynaptic membrane
  • Receptors accumulate at postsynaptic membrane
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2
Q

What we know about synapse formation comes from the NMJ

Neuromuscular junction formation

Axon terminal, muscle, and basal lamina in between

A
  1. Motor neuron axon secretes a protein called
    agrin into the basal lamina
  2. Agrin receptor on muscle receives Agrin signal
    * MuSK – muscle specific kinase
  3. MuSK activates Rapsyn
  4. MuSK and Rapsyn together cluster Acetylcholine receptors into plaques
    * Reciprocal signaling is necessary for synapse
    formation
    * Not just axon to muscle!
    * Basal lamina can trigger calcium influx into axon terminal
    * This causes release of more neurotransmitter
    * Positive feedback

Size of receptor cluster dictated by neuregulin secreted by axon

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3
Q

Cell Adhesion Molecules

Not just for axon guidance

A
  • Cell adhesion molecules can regulate synapse
    formation and stabilization
  • Best characterized synaptic cell adhesion
    molecules: Neurexin and Neuroligin
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4
Q

Neurexin

A

3 Neurexin genes and multiple isoforms in the brain

Typically pre-synaptic

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5
Q

Neuroligin

A

4 Neuroligin genes and multiple isoforms in the brain

Typically post-synaptic

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6
Q

Deletion of all Neurexins causes:

A
  • Decreased pre-synaptic calcium influx
  • Decreased synaptic release probability
  • Decreased synapse number (only in some brain regions)
  • Differences maybe due to only partial redundancy between Neurexins
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7
Q

Neuroligins are targeted to distinct post synaptic types

A
  • Neuroligin 1 – excitatory synapses
  • Neuroligin 2 – inhibitory, dopaminergic, and cholinergic synapses
  • Neuroligin 3 – excitatory and inhibitory synapses
  • Neuroligin 4 - glycinergic synapses
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8
Q

Neuroligin functions at the synapse

A
  • Increasing Neuroligin protein levels can increase synapse density and synaptic transmission
  • Loss of Neuroligin function causes decreased synaptic transmission but no change in synapse number

Have diverse functions at the synapse important for synaptic activity

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9
Q

Neuropsychiatric disorders are linked to Neurexin mutations

A
  • Large genomic deletions that remove Neurexin 1 are linked to: schizophrenia, tourette syndrome, intellectual disability, epilepsy, autism
  • Mutations in Neuroligin 3 and Neuroligin 4 are linked to autism spectrum disorder
  • Expression of an autism-linked Neuroligin 3 mutant gene in mice causes synaptic and behavioral abnormalities
  • Deficits in social behavior
  • Proxy for autism-like behavior
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10
Q

Synapses change with development and activity

  • Axons leave the retina and go to the LGN (thalamus)
  • Axons leave the LGN and go to striate cortex (visual cortex)
A
  • Axon pathfinding can proceed using all of the mechanisms we have previously discussed but synaptic refinement requires synaptic pruning
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11
Q

Types of synaptic refinement

A
  1. Changes in synaptic capacity
  2. Synaptic rearrangement
  3. Synaptic segregation
  4. Programmed cell death
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12
Q

Changes in Synaptic Capacity

A

The neuromuscular junction
1. Start with an alpha motor neuron that innervates
multiple muscle fibers
2. Maturation – refines so each motor neuron innervates 1muscle fiber

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13
Q

Synaptic Loss Requires Muscle Activity

A
  • Silencing muscle = retain polyneuronal innervation
  • Activating muscle = accelerates removal of all but 1 innervating neuron
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14
Q

Temporal Aspects of Motor Neuron Capacity Refinement

A
  1. Loss of post-synaptic acetylcholine receptors on the muscle fiber
  2. Disassembly of the pre-synapse
  3. Axon retraction
    * This is due to a loss of activity at a subset of acetylcholine receptors
    * Loss of activity at all receptors causes maintained polyneuronal innervation
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15
Q

Activity Dependent Synaptic
Rearrangement

A

Change in how many synapses individual input
neurons have on receiving neuron
* Receiving neuron maintains same total number of
synapses but varies how many come from each input
* Is due to neural activity and synaptic transmission
* Final steps of address selection

Change in which neurons axon synapse on
* Due to neural activity as well
* Classic example is the visual system
* Segregation of eye-specific inputs in the cat LGN

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16
Q

Waves of activity occur across the retina during development

A
  • Retinas do this independently
  • This means that neurons from one retina fire simultaneously which strengthens their synapses on target neurons in the LGN
    Also called Hebbian synapses – First posited as a possible mechanism of synapse remodeling by Donald Hebb in the 1940s.
17
Q

Synaptic Plasticity

Strengthening or weakening synaptic connections

A

Two rules for synaptic modification
* Fire together, wire together (Hebbian modifications)
* Fire out of sync, lose their link

A single synapse has little influence on firing rate of postsynaptic neuron.
* Activity of a synapse must be correlated with activity of many other inputs converging on the same postsynaptic neuron.

18
Q

Excitatory synaptic transmission in the immature visual system

A

Receptors can be metabotropic or ionotropic

19
Q

Ionotropic glutamate receptors can be further classified as:

A
20
Q

Ionotropic glutamate receptors can be further classified as:

AMPA receptors

A

glutamate-gated ion channels

21
Q

NMDA receptors

A

Ion channels with unique properties
* Voltage gated due to Mg2+ at the channel
* At resting potential, Mg2+ block channel
* Further depolarization leads to Mg2+ is displaced allowing current to pass
* Also unique because it conducts Ca2+
* Magnitude of Ca2+ passing through the channel signals pre- and post-synaptic activity

22
Q

Long-term synaptic potentiation

A
  • It was hypothesized that NMDA receptors serve as Hebbian detectors of simultaneous pre- and postsynaptic activity
  • Ca2+ could serve to trigger downstream modulators of synaptic effectiveness
  • Experiments indicate this is true – strong NMDA
    receptor activation strengthen synapses through long-term potentiation (LTP)
23
Q

What changes downstream of Ca2+ cause strengthing?

LTP results from AMPA receptors addition

A
  • Experiments show that continued depolarization/ glutamate release causes increased AMPA receptors clustering at post-synapse
  • This leads to longer depolarization with stimulation
  • LTP
24
Q

LTD: Long-term synaptic depression

A
  • Neurons that fire out of sync lose their link
  • Rather than Ca2+ with consistent depolarization, consistent low levels of Ca2+ due to decreased synaptic activity decrease synapse effectiveness
  • Converse of LTP, consistently low Ca2+ levels lead to a reduction of AMPA receptors at the synapse
  • Leads to decreased likelihood and amplitude of firing
25
Q

LDP: the underlying reason for reduced visual responses with monocular deprivation?

A

Control – normal visual cortex showing ocular dominance columns
* Stripes correspond to input from two eyes
* Permanently close one eye, columns from that eye are reduced and those from opposite eye expanded
* Can be reversed if eye is opened
* Ability to modify columns is not infinite
* Loss of input from one retina- Critical period exists during which inputs can modify synaptic contacts/ocular dominance columns
* After 6 weeks of age in macaques the innervation pattern is cemented

26
Q

Critical period in development

A
  • Spemann found that Spemann-Mangold organizer transplantation could induce a second axis in the host
  • But only during a certain period of development before the host cells had already been committed to a different fate
27
Q

Critical period in behavior

A
  • Konrad Lorenz found that social attachment formed within a certain period of time for graylag geese
  • Within 2 days of hatching, goslings would imprint on a moving object and treat that object as their mother
28
Q

Critical period at the synapse

Not permanently modifiable after
timepoint of development or activity?

A
  • Early in development, large scale changes of innervation patterns can change
  • This is not possible at later/adult stages
  • In the adult, plasticity is restricted to local changes in synaptic efficacy
29
Q

Hypotheses on critical period endings

A
  1. Plasticity diminishes when axon growth stops
  2. Plasticity decreases when synaptic transmission
    matures
  3. Plasticity decreases when cortical activation is
    constrained

Astrocytes can also regulate closing of the critical period

Understanding the critical period could provide some
insight into why recovery is limited after injury to the adult
brain

30
Q

programmed cell death

Apoptosis

The elimination of neurons

A
  • Occurs largely after axons have reached their
    targets
  • Noticeable decline in neuron and axon number due to programmed cell death

NEURO 523 (7 decks)

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