Von Bartheld Development Flashcards
the CNS appears in the (blank) week of human development.
3rd week
Explain early brain development
neural plate (thickening of ectoderm) occurs due to notochord signals-> neural plate folds inward making neural groove-> neural tube-> fusion starts central of tube and moves cranial and caudally. -> neuropores created-> closure of neural tube-> spinal cord and wide cephalic portion with several dilations (brain vesicles)
failure of the neural tube to close results in….?
neural tube defects (can involve vertebrae, muscles and skin)
what do you call a neural tube defect that occurs in the spinal cord
spina bifida
What do you call a neural tube defect that occurs at the cephalic end?
anencephaly (forebrain doesnt form)
When the flow of CSF is obstructed CSF will accumuate and will result in (blank)
hydrocephalus
What do you call a neural tube defect when the meninges protrude?
meningomyelocele
What do you call a neural tube defect when the meninges protrude and the nervous system protrudes?
meningoencephalocele
During neuralation (neural tube formation) another impotant structure forms at the “crest” (upper portion) of the neural tube called the (blank)
neural crest
Cells of the neural crest subsequently migrate along distinct paths and give rise to a variety of structures in the body, including (blank) and (Blank).
sensory and sympathetic ganglia
Most nerve cells derive from what?
the nerual tube or the neural crest
Is the retina part of the PNS or CNS?
CNS
At 4-6 weeks what happens to the brain?
you get subdivision
What are the subdivisions of the brain that occur at 4-6 weeks of development?
prosencephalon (telencephalon + diencephalon)
mesencephalon (midbrain)
rhombencephalon (metencephalon and myelencephalon)
What is the mesencephalon?
the midbrain
What is the metencephalon?
pons and cerebellum
What is the myelencephalon?
medulla
The neural tube becomes patterened along the longitudinal axis into (blank) which have specific sets of (blank) that regulate the segmental development in the embryo.
neuromeres
homeobox genes
What happens if you have a mutation in a homeobox gene?
disease like aniridia and waardenburg syndrome (craniofacial defects, spina bifida and hearing loss)
The develops from (blank) compnents that make the lens and (blank) components that make the retina
placodes
neural tube
At 22 days of development what happens to the eye?
optic vesicles form and induce lens placode in ectoderm, then optic vesicle invaginates and forms optic cup
What does the inner surface of the optic vesicle form?
the choroid fissure and hyaloid artery,
Please describe inner ear development
at 22 days->otic placode (level of rhombencephalon) invaginates and forms otic vesicle (otocyst). Otic vesicle makes the membranous labyrinth.
The otic placode, together with neural crest, also give rise to the (blank) and (blank) ganglia
auditory and vestibular
What are the components of the membranous labyrinth?
saccule, cochlear duct, utricle, semicircular canals, endolymphatic duct
Rubella virus or toxoplasmmosis in the first trimester may cause severe damage to (blank)
the organ of corti
The olfactory placode gives rise to what? How often are these replaced?
olfactory receptor cellsevery 6-8 weeks
Some cells within the region of the olfactory placode migrate into (blank)
CNS and become part of the hypothalamus.
The pituitary develops from 2 different parts, what are they?
an outpocketing of the oral cavity -> rathkes pouch
and
a downward extension of the diencephalon-> infundibulum
Does rathkes pouch stay connected to the oral cavity through development?
no
What does rathkes become in the hypothalamus?
forms anterior lobe of the hypophysis or adenohypophysis.
What does the infundibulum become in the hypothalamjus?
stalk, pars nervosa (posterior lobe of hypophysis)
(blank) can rise from remnants of Rathkes pouch, causing hydrocephalus and pituitary dysfunction
craniopharyngiomas
When do spinal nerves pass through the intervertebral foramina at the level of their orign?
as an embryo
Where does the spinal cord end?
L2-3
What do nerve fibers form below L2-3?
the cauda equina
Where should you do a lumbar puncture?
below L2-L3 to avoid the spinal cord
What does neuraltion require from the notocord? Name a few please
signals :)
noggin and chordin
What does noggin and chordin do?
it inhibits BMP so that neuralation can occur
What is an agent that is well known but can interfere with neuraltion?
vitamin A (retinoic acid)
What happens if fibroblast growth factors and transforming agents are altered?
you get nervous system problems
The most sensitive periods for teratogenic agents is when?
3rd to 5th week in the first trimester
What will rubella cause?
eye and ear defects
Wht will cytomegalovirus cause?
eye defect, microcephaly
What will toxopasmosis cause?
hydrocephalus
What will X rays cause?
spina bifida
What will hyperthermia cause?
neural tube defects
What can epilepsy meds cause?
neural tube defects
What can alcohol cause?
mental retardation
What can Vit A overdose cause?
neural tube defects
What can folic acid antagonists cause?
neural tube defects
Describe the sequence of neuronal development
neural induction-> neural tube formation-> generation of neurons and glia-> axon growth from neurons-> synapses made with targets-> dendrite growth-> myelination
The about 100 billion neurons of the adult human brain are with few exceptions generated over a time course of a (blank) from a small population of precursor cells.
few months
Whre are the precurosr cells for neurons located?
in the ventricular zone of the neural tube (inner most layer)
Dividing precursor cells undergo a sterotyped pattern of cell movement during the mitotic cycle. During mitosis, the cell nucleus is at the (blank) side, but during the S-Stage, the nucleus mirates toward the (blnak) side where DNA replicates.
luminal
pial (outer) surface
Postmitotic cells leave the ventricular zone and migrate to their final destinations in the (blank)
brain
WHere are the newest replicated cell found?
most superficially
(blank) can indefnitely self-renew, and can give rise to ALL tissue and cell types, including germ cells
embryonic stem cells
(blank) are self-renewing, and they can give rise to a full range of cell classes within certain tissues (e.g. neural and glial cell types)
neural stem cells (somatic stem cells)
(blank) cannot self-renew continuously and typically give rise to one class of progeny.
progenitor cells
(blank) are non-dividing cells that will differentiate into neurons
neuroblasts
Neurons that migrate through laminated structures, such as the hippocampus. cerebral or cerebellar cortex, use (blank) as a cellular guide.
radial glia
Genetic mutations of extracellular matric molecules appear to disrupt (blank) in the cerebellum
neuronal migration
Disruptions of migration in the cerebral cortex can lead to (blank)
epilespy
Disruptions of migration in the neural crest cells can lead to (blank)
congenital megacolon
What is a specialize structure at the tip of the extending axon? What do they do?
growth cone
explore the environment and respond to local cues by changing the speed or direction of growth (of a axon)
What do the growth cones of axons contain that are fine finger like processes that are used to explore the environment
filopedia
The first axonal pathways may be established by (blank) with subseqent fibers following their path.
pioneer fibers
Cues that guide axons can be divided into 2 broad categories. What are they?
extracellular adhesive molecules
diffusible molecules
How do diffusale molecules work as guides?
they set up attractive or repellent gradients for growing axons
The growth cones contain receptors (integrins) which bind to (blank) or (blank) and induce a signaling cascade within the growth cone which promots axon extension.
laminin
fibronectin
Axon extension is also influenced by molecules on cell surfaces called (blank)
cell adhesion molecules (CAM).
N-CAMs are expressed by (blank) and Ng-CAMs are expressed by (blank)
neurons
glial cells
What are a class of cell surface receptors that bind to each other in a calcium-dependent manner?
cadherins
Are tropic hormones diffusible or extraextracellular adhesive molecules?
tropic hormones
What do tropic hormones do? What is a very important class of tropic hormone?
they are a diffusible molecule that guides growing axons to a source
netrins
What is sort of werid about netrins?
netrins have a positive chemotropic action on some axons but a negative growth inhibiting action on other axons
Netrins and the slit-robo signalin system guide axons across the midline to form (blank)
commissures
What are ephrins?
chemotropic molecules that establish a gradient over the superior colliculus to guide the nasal and temporal retinal axons, resulting in a retinotopic map.
What are these:
collapsins, semaphorins, and CNS myelin-associated proteins
negative chemotropism
What is the chemoaffinity hypothesis?
in structures containing topographic maps, each cell carries a unique identification tag which is recognized by complementary tags on retinal axons
What are responsible for the segregation of temporal retinal axons to the anterior pole of the superior colliculus, and nasal retinal axons to the posterior colliculus?
chemotropic and chemorepellent molecules in the superior colliculus
several members of the ephrin family are expressed in a gradient over the superior colliculus and repel nasal retinal axon, but not (blank)
temporal axons
The expression of (blank) and (blank) molecules in gradients are a major factor in the establishment of topographic maps in the nervous system
tropic and repellent molecules
Synapses are formed at an astonishing speed in the developing nervous system. Neurotransmission occurs within (blank) after synaptic contact
hours
So a ton of synapses are made and only a few are retained (synpatic turnover). What makes these synapses in the neuromuscular junction? What makes these synapses in the CNS?
agrin
neurotrophic factors, trophic interactions between pre- and postsynaptic sites play an important roles in synapse stabilization and elimination
Information about the sites of neuromuscular junctions is retained in the (blank) even after destruction of the muscle or the nerve fiber terminal.
extracellular matrix
(blank) are essential for the development of proper connections between developing nerves and their targets.
trophic interactions
Why when we have a bunch of neurons do a lot of them die?
neurons have to compete for access to a limited supply of neurotrophic factors in their target. The death of neurons is done via apoptosis
T or F
The final number of neurons which innervate a target is not fully determined in advance, but depends on neuron-target interactions in each developing individual.
T
What do trophic hormones do?
determine the survival of motor neurons and elaboration of their processes
What is the most important trophic hormone?
neurotrophins
What are the four growth factors of neurotrophins?
nerve growth factor
brain-derives neutrophic factor,
neurotrophins-3
neutrophin -4
T or F
neurotrophins bind to different tyrosine kinase receptors
T
How do neurotrophins work?
they are released from dendrites, bind to and activate receptors on terminals, are internalized and transported retrogradely to the cell body where gene expression is modified
Most neurons in the central nervous system seem to utilize (one/many) different neurotrophic factos and do not critically depend for their survival on one single factor.
many
(blank) can stabilize synapses and thereby regulate the connections formed with targets in response to altered patterns of activity or injury.
neurotrophic factors
In addition to the target-derived (retrograde) mode of neurotrophic support, (blank) also provide trophic support to neurons in the form of neutrophic factors transported anterogradely by axons and released from terminals similiar to peptide neurotransmittes.
afferents
What are neurodegenerative diseases believe to involve dysfunction of trophic interactions?
amyotrophic lateral sclerosis
parkinsons disease
huntingtons disease
alzheimers disease
What are neutrophic hormones important for?
survival of injured neurons and the mechanism of axon regeneration