Chapter 53 Flashcards
broadly classify neurons into two types
excitatory and inhibitory
spiny exitatory neurons
glutamatergic neurons
projection neurons
pyramidal neurons
non-spiny inhibitory interneurons
GABAergic neurons
all neurons have how many layers
six
name the developing layers of the cortex from ventricle side to sub-arachnoid space
ventricular layer subventricular layer intermediate zone cortical plate marginal layer
giving rise to two stem cells resulting in amplification of the stem cell pool
symmetric divisions
when one stem cell gives rise to another stem cell and a differentiated cell maintains stem cell populations
asymmetric division
when one stem cell gives rise to two differentiated cell resulting in exhaustion of the stem cell pool
symmetric terminal division
what is the order of making cells in the nervous system during development
all neurons are made first then switch to astrocytes and glial cells
what type of cells are around the ventricular zone during development
neruoprogenetor cells
what is the formal term for cells bouncing up and down
inter kinetic nuclear migration
vertical planes cause what type of division
symmetric
horizontal planes cause what type of division
asymmetric
neuroblasts have an affinity for this which they move along to migrate in the cortex
radial fiber
all of the cells that are born along one radial fiber are
ontonogenetically related
this is a receptor for the integral membrane protein- delta
notch
what happens when detla and notch come together
notch undergoes cleavage by protease and translocate to the nucleus to form a transcriptional complex
two things notch signaling in the glial progenitor results in
- differentiation as astrocytes and inhibits differentation as oligodentrocytes
- inhibits progenitor cells from differentiating into neurons
how to neurons climb the radial fiber
have a leading edge with microtubules and a lagging edge
first microtubules that neuroblasts will turn on
DCX
regulates migration of neurons in the cortex during development
reelin
under normal circumstances how does the cortex develop
from the inside out
what happens when reelin protein is mutated
cortical plate is severely disrupted and partially inverted
neurons generated in the medial ganglionic eminence migrate..
tangentially and settle in the neocortex
medial ganglionic eminence gives rise to what interneurons
cajal-retzius neurons
neurons generated in the lateral ganglionic eminence migrate
rostrally to the olfactory bulb
neural crest cells that migrate just beneath the ectoderm become
melanocytes
neural crest cells tat migrate deeper through the somites becomes
dorsal root sensory ganglia
neural cells that migrate between the neural tube and somites become
sympathetic ganglia and adrenal medulla
neurons that innervate muscles generate which neurotransmitter
norepinephrine
sympathetic neurons that innervate sweat glands are induced to generate which neurotransmitter
acetylcholine
the default of most neurons is to live or die after development
die
what signal saves a neuron from undergoing apoptosis
neurotrophin
when neurotrophin attaches to receptors on the axonal terminal how do they get to the nucleus
retrograde movement along the axon
the three main neurotrophins interact with what type of receptor
tyrosine kinase receptor
when this receptor is present it can actually induce cell death
P75
when growth factor binds to receptor what happens
homodimyrization of receptor activating protein kinase AKT to promote survival
when death pathway is induced what proteolytic enzymes are activated
caspases
what induces the death pathway
Cytochrome C leaking out of the mitochondria activates caspases
or activation of death receptors on the cell membrane
which cell in the nervous system is very active during the time of development when apoptosis is happening
microglia
three hallmarks of apoptosis
membrane blebbing
cell shrinkage
DNA fragmentation
protooncogene that prevents the creation of pores on the mitochondria surface
Bcl2
inhibits Bcl2 which allows pores to form in mitochondria
bad
neurotrophin cascade causes
AKT to be activated which phosphorylates the bad protein inactivating it
happens when caspase9 is knocked out causing additional folding of the cerebral cortex
cobblestone complex
