Exam 4: Nervous System Flashcards
4 functions of the nervous system
coordination/regulation
interpretation - sensory info comes in and it interpreted to see if strong enough signal to warrant a response
immediate response, short lived
memory/learning - remember by repetition or a major event
4 components of the nervous system
brain
spinal cord
peripheral nerves
sensory organs
CNS
brain and spinal cord - both do reflex action and conduction
- integration
PNS
tracts with info coming in and out
- sensory and motor pathways
somatic
autonomic - parasympathetic, sympathetic
somatic nervous system
voluntary - skeletal, visceral, striated
autonomic nervous system
involuntary
heart beat - BP
postural reflexes
2 types of cells in nervous tissue
neurons - conductive cells
- not the highest concentration of cells in nervous system
neuroglia (glial cells) - support cells
- myelinating cells, help recycle neurotransmitters back into neurons
- act as BBB
every neuron has many glial cells
dendrites
receive info
axon hillock
more dense
- sets threshold: need strong enough signal
neurofibrils
provide structural support for neuron
Nissl cells
- little dots
- produce proteins
- in action when growing neurofibrils if you have to repair an axon
bipolar neurons
- special senses
- several diff inputs coming in but goes out as one signal
- lots in retina - diff rods and cones
multipolar neurons
motor
interneurons - many dendrites, many axons
- many extensions
pseudounipolar neurons
sensory
many in touch receptors
nonconductive cells
support the conductive neurons
glial cells of CNS
more varied and are structurally different than in PNS
- will not regenerate even if neural body survives
(as a mature brain, a child’s brain could still grow)
glial cells in PNS
can regenerate if still part of damaged cell body
types of neuroglia in the PNS
satellite cells and schwann cells
types of neuroglia in CNS
ependymal cells
astrocytes
microglia
oligodendrocytes
Schwann cells
- only myelinates one region of the axon, that is it
- ions cannot go through the myelination but there are channels because you depolarize
saltatory conduction
“jumping” from node to node of ranvier
- when open channels Na rushes into the cell and goes node to node
what diameter produces a quicker conduction
thicker diameter - multi lane highway
satellite cells
helps control what gets into neuron
- may absorb certain nutrients or molecules from blood and direct to neuron
- make sure nutritional support
protect neuron
oligodendrocytes
- like schwann cells but handle things differently
- myelinate axons but cell body not involved
- can myelinate more than one axon at many points on an axon
- more likely to scar over when damaged instead of encouraging growth
Astrocytes
absorb nutrients, interact with blood vessels
- recycle neurotransmitters to original neuro to make more
(without astrocytes you would not be able to recycle)
microglia
become the immune system of these cells
- if large infection permeability altered, but usually no macrophages or neutrophils in CNS
ependymal cells
- produce CSF - surrounded by ventricle in brain , central canal of spinal cord
- CSF: lower sugar levels but proportional to what is in the bloodstream
damage to PNS
- macrophages come in to clean up infection
- schwann cells not injured but no longer have axon, begin to proliferate and form a schwann tube
- associate together - tunnel to original target location formed
- secrete growth factors and direct reforming of axon back tp its target site
- send STRONG signals to bring it back can take months
if amputation - damage to PNS
- schwann cells still form schwann tube trying to direct to foot (leg was amputated i this case)
- they forma tangle since there is no foot to get to, keep sending signal (phantom pain)
- try to bring person into therapy to train brain that there is no foot there
- can get collateral nerve
what are schwann cells designed to do
regenerate neurons
- CANNOT give you more but can help you regenerate them
damage to CNS
- portions of oligodendrocyte
- takes long time to clean up bc you have microglia, not macrophages
- does not put out growth factors, puts out inhibitory factors
in a mature brain: enhances interaction btw certain neurons, inc how well they communicate, cannot grow new areas
in younger brains: more likely to regrow
OMGO and NOGO
inhibitory
MAG
can be stimulatory or inhibitory based on the receptor
process by which the overlying ectoderm form the neural plate and then the neural tube
- begins in third week of development
neurulation
two types of neural tube formation
primary and secondary
primary neurulation
involves neurulation, forms majority of spinal cord to S2
- thickening of midline at dorsal area - neural plate
- after thickening you get neural crest and neural groove
- eventually fuses together
- area forming neural tube gives you spinal cord as you go anteriorly you get brain
secondary neurulation
involves cavitation (hollowing out) of a solid mass of cells that fuses with primary neural tube forming region inferior to S2
Homeobox (HOX) genes
crucial to determining cranial vs caudal differentiation
activation of HOX genes
carried out by secretion of retinoic acid (RA) from the notochord mesodermal cells
no RA =
low RA=
high RA =
no RA = no expression of HOX
low RA = high HOX -inc development of neural tube, get brain, formation of face and skull over the brain
high RA = slows HOX - stay just at spinal cord
vitamin A and accutane
linked to craniofacial abnormalities
- this is increased RA which will slow HOX gene production - lacking differentiation
tonus medullaris
end point of spinal cord
what anchors the end f the spinal cord in secondary neurulation
phylum terminale (connective tissue) comes down and connects to sacral region
cauda aquina
collection of extended spinal nerves
- supply innervation
when they sample CSF why do they do a lumbar puncture
they do NOT run the risk of going in and hitting spinal cord since it is not there and the nerves are more centrally located
neural tube defects
primary and secondary
BOTH have to do with neurulation - NONE cavitation
what do primary neural tube defects result from
anterior opening failing to close
ex: anencephaly: exposes forebrain to amniotic fluid and degeneration occurs of the tissue
what causes secondary neural tube defects
when inferior opening fails to close
spina bifida/dysraphism
- can get minor discoloration - looking at the darker myelination nerve endings
- open spina bifida: bulging out skin not completely forming, see meninges and part of spinal nerves bulging out
diff effects on daily life not survivability
secondary neural tube defect worse case scenario
craniorachisis: - closure failure of entire neural tube - not survivable - get extra proteins released into amniotic fluid, toxins if tissue is dying - the mother will be ill - developmental issue not genetic folic acid helps prevent
alpha fetal protein tests
detection of neural tube defects
- recommended for all pregnant women
what can abnormally high alpha fetal protein results indicate?
- multiple fetuses
- a fetus more advanced in development
- neural tube abnormality
what has been shown to be protective against neural tube defects
folic acid
- folate is a coenzyme in many pathways - lack of folic acid can hit many places
