Neuronal Development Flashcards

1
Q

Neurogenesis

A

When progenitor cells undergo mitotic division and produce new stem cells or neuroblats they will differentiate into neurons

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2
Q

Process of neurogenesis

A

Dividing precursor cells from ventricular zone - some leave and form marginal zone and intermediate layer layer forms these neurons develop into glia and neurons

As no of cells increases cells must migrate along frail glia
When cells reach destination they begin to definterate
Process outgrowth - dendritic and axon Growth and proliferation of synapses

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3
Q

Stages of nervous system development
L

A

Neurogenesis- mitotic production of neurons from non neuronal cells
Cell migration- movement of cells to establish distinct populations
Differentiation- transformation of precusor cells to distinctive neurons or glia
Synaptogeneus- synaptic connections
Neuronal cell death- selective death of many nerve cells
Synapse rearrangement - loss or development of synapses

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4
Q

Critical period and theory

A

Between childhood and adolescence - defined as window which sensitivity to sensory stimuli is temporarily heightened and promotes changes in connectivity
Theory- explains decline in synaptic dynamics during brain development and understanding pathogensis if asd

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5
Q

Neural tube formation

A

Medial neural hinge point cells anchor to notochord and change shape
Epidermal cells move to centre
Neural gold elevated while epidermal cells continue to move to midline
Neural fold converge as Dorsolateral hinge point cells become wedge shaped
Neural folds are brought together and crest cells link the neural tube with epidermis
Crest cells disperse and tube separates (forms)

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6
Q

Where are crest cells formed

A

Along most of anterior-posterior axis of the embryo from posterior diencephalon to lunbosacral region of embryo
Grouped according to position of spinal

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7
Q

What are SHH cells

A

Morphogen secreted by the notochord which is required for development of midline structures and then for dorsoventral specification of the neural tube

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8
Q

What determines neuron type differntation

A

Conc of SHH- more is motor neuron
More BMP is sensory neuron

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9
Q

What projenitor cells are made by neurogenesis

A

Apical progenitors- mitosis near ventricle and can turn into radial glia
Basal- migration scaffold
Subapical- same as apical but can u deffo mitosis anywhere

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10
Q

When does neurogeneis begin

A

When projenitor cells switch from symmetric to asymmetrical cell division

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11
Q

What become pyramidal cells

A

Apical and basal projenitor in ventricular and subventrucular zone

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12
Q

How is neuronal growth guided

A

Growth cones at the end of axons
Spiny bodies sense environment
They avoid contact with unfavourable surfaces and remain on favourable ones
Form synapses at target cells
Must retentive enough neurotrophic factor secreted from target cell to survive

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13
Q

Sema3

A

Dorsal root ganglia are repelled by sema - when neurophorin is knocked out they loose sensitivity to sema3f but not 3a

Okay a key role in projection- acts as receptor by acting ligands and transmitting signals to expressing cells

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14
Q

What are mechanisms of synaptic connections

A

Topography-refining dendrites
Convergence- reducing two converging synapses to one
Post synaptic component - cut post synaptic to just pre

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15
Q

Synapses during development

A

Functional synapses are eliminated during development
Larger stimulation= larger post synaptic potentials in immature neurons. At end of maturation process only one axon remains connected

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16
Q

Spontaneous movements of embryo

A

Movements of embryo cause correct synaptic connections and refinement of synapses when animal opens eyes

Spontaneous activity propagates rostral my in cortex

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17
Q

How can you view pattern of innervation in eyes

A

Inject dye in one eye and can see pattern of innervation in layer 4 of cortex. Innervates in stripes I’m response to light- also seen in LGN

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18
Q

What can cause stripes not to develop

A

If the spontaneous activity in the retina that occurs before the eye opens is blocked by TTX

19
Q

How should activity occur in eye for best correlation

A

Synchronous stimulation means domain of overlap is increased in LGN in both sides but asychnorous activity there is less overlap . The correlation between two retina determine the pattern of synaptic refinement . Too correlTed means no segregation between two eyes

20
Q

How come excitatory blocking doesn’t stop episodic activity in the eye

A

There are compensatory mechanisms but they aren’t necessary because immature cells have high cl levels inside the cell so GABA causes a large cl movement out of cell that causes depolarisation
Cl is high because there’s a high expression of NKCC1 brings cl into immature cells
As the neuron matures it switched to KCC2 as the dominant transporter which moves cl out of the cell

21
Q

What happens to synaptic potentials after an episode

A

It increases before episode then decreases . The spread of waves is limited in the retina by refractories . If second wave appears it won’t propogate in the depleated /same areas
Slow negative feedback

22
Q

What determines episode duration

A

Interval time
Duration increases with interval time
Correlated with length of proceeding interval but not the following

23
Q

What amplitude do episodes return to

A

Zero

24
Q

Why are developing networks excitatory

A

Early in development GABA and glycine are functionally excitatory
That means fast feedback

25
Q

Causes of asd

A

Single gene disorders
Metabolic disorders
Unknown like nutrition, pollution etc

26
Q

Subgroups of genetic asd classification

A

Post synaptic density - synaptic function and transmission of nts
Chromatin modification and regulation
(epigenetics)- dysfunction
Neuronal signalling and cytoskeleton
Channel activity

27
Q

Mechanisms that contribute to development of guiding of growth comes

A

Contact attraction
Chemoattraction
Contact repulsion
Chemo repulsion

28
Q

Pluripotent stem cells different during asd

A

Double in number faster
Less time in growth phase
Greater proliferation correlated with brain overgrowth

29
Q

Synapses in asd

A

Change or variation in some synaptic formation genes
Synaptic elimination- reduces synaptic contacts
Maintenance of unnecessary synapses in asd - lack of synaptic pruning
Causes Overlap of firing which leads to over sensitivity to light or sound
Asd has hyper connectivity in Brain and more synapses in many regions - over excitation and imbalance between more excitation and inhibition

30
Q

Fragile x syndrome asd

A

Genetic condition
Intellectual disability
Features of asd
Physical features like long ears and face
Causes by gene repeat expansion of FMRI gene that codes for fmrp

31
Q

What is fmrp

A

RNA building protein that inhibits mRNA translation - located in dendrites abs synapses

32
Q

What happens if fmrp is lost and what treats it

A

Excessive protein synergies and altered spine morphology and synapse function - density of spines increase
Inhibition of mglur5 protein corrects fmrp knockout mice - it inhibits direct pathway to prevent over stimulation of movement

33
Q

What asd symptoms can you measure in animals

A

Social interaction
Communication
Repetitive behaviours

34
Q

Impairments in Alzheimer’s

A

Day to day memory
Concentrating, planning
Language
Visio spatial skills
Spatial orientataion

35
Q

Changes to wave bands during dementia

A

Decreased alpha frequency and increased power in theta and delta bands - seen by EEG
changes in eeg are well correlated to the degree of cog impairments

36
Q

Progression through brain of Alzheimer’s

A

Starts and hippocampus and moves to frontal areas

37
Q

What does 4 mountains task show

A

Asses spatial memory and is a good marker to show dementia pathology
Performance is correlated to degree of hippocampal atrophy

38
Q

Place and grid cells in dementia

A

Place cells have decreased spatial info in dementia
Grid cells dissapear

39
Q

What is epilepsy

A

Group of neurological disorders that exhibit periodic seizures

Occurs from an imbalance between excitation and inhibition (glu and gaba)

40
Q

What are seizures

A

Associated with high frequency discharge impluses by a group of neurons in the brain

41
Q

What are the types of seizures

A

Tonic-clonic= person jerks and May loose consciousness and control
Absence = person looks to be dreaming or blank for a few seconds and unresponsive- person is unaware
Parietal/focal= abonornal actuvity in only one area - still consciousness (simple) or not conscious (complex)

42
Q

What constrains speed and extent of seizure propagation

A

Feed-forward inhibition

43
Q

How do seizures affect gaba

A

During seizures gaba can switch to excitatory
- kcc2 takes cl out of cell making gaba inhibitory
Nkccl moves cl into cell an makes gaba excitatory. When gaba is activated it causes cl to move out leading to depolarisation
During seizures you can see increasing cl levels in cell and gaba starts depolarising cell. And inhibition of gaba leads to hyperpolarising

44
Q

What happens to cell after seizure

A

Minutes after seizure there is post translational downregulation of kcc2
Hours to weeks after - genomic downregukation if kcc2 means that it’s more likely to experience hyperexcitability in the future