ch 7 Flashcards
ganglion
collection of neuron cell bodies outside CNS
somatic motor nerve
skeletal muscle nerve
autonomic motor nerve
smooth muscle or cardiac that stims glandular secretion
central nerv system
brian and spinal
periperal nerv system
nerves ganglia and nerve plexuses outside of CNS
neuron
smallest unit of nervous system able to signal
neuron general function
respond to chem and physcial stim
conduct electrochem impulses
release chem regulator
enable perceptions of senses
neurons cannot
divide but they can repair
retrograde
back towards the nucleus of the axon
towards
anterograde
forwards toward the axon terminal
away
retrograde uses
dynactin
dynein
anterograde uses
kinesin
kinesin impairment disease
ALS,
HSP
IPN
dynein impairment disease
ALS
IPN
dynactin impairment diseases
PS
IPN
multipolar neuron
interneruon and ermm
many dendrite
one axon
bipolar neuron
usually small
one dendrite
one axon
pseudounipolar
one process
somatic or smth
sensory
anaxonic
multiple dendrites, no axon
function categories of neurons
interneuron
sensory
interneruon
intermediaries between sensory (afferent) and motor (efferent) neurons
sensory neuron
transmit sensory information from the body’s periphery to the central nervous system
brings signal to spinal cord from pns
autonomic motor neuron
controls involuntary bodily functions, such as heart rate, digestion, and sweating
cns/spine to peripheral
somatic motor neruon
cns/spine to pns
neuroglia
support cells of nervous system
outnumber neuron 10:1
neuroglia of PNS
schwann cell, satellite cell
schwann cell form
myelin sheath
schwann cell function
wrap around a lot and insulate
satellite cell
insulate cell body
like sweater
support and nourish neurons in the PNS, and are essential for maintaining nerve health
PNS regen (2 steps)
distal portion of nerve degenerates
proximal schwann cell will form a regen tube
neurotrophins
promote neuronal growth in the fetal brain
neruotrophins in adults
maintain sympathetic ganglia and regen of sensory neruons
guillain barre syndrome
demyelinating disease
makes neruons slower/damaged/death
causes muscle weakness
hard to breath and maintain bp
microglial cell
phagocytic
clean up the CNS
oligodendrocyte
wraps around structures with cell body
makes up white matter
astrocyte
regulate external environment
make sure bad shit don’t pass thru
form blood brain barrier
ependymal cell
line ventrical of brain
make and circulate cerebral spinal fluid
blood brain barrier made of
made of paricyte and astrocyte
blood brain barrier highly permeable to
warer, glucose, nicotine, alc, glucose, lipid soluble substances (o2, co2), anesthetics
blood brain barrier slightly perm to
na, k, cl, waste products of urea and creatinine
what takes up potassium in the extracell fluid of the brain
astrocytes
what prevents glutamate from lingering in synapses and firing for too long by taking it up and turning it into glutamine
astrocytes
how is glucose taken up in brain capillaries
thru astrocytes
what makes up scar tissue in the brain
astrocytes
what guilds fetal neuronal development
astrocytes
mulitple sclerosis
demyleination
t cells become inflammatory and attack the neuron
brain tumors arise from
meninges
metastasis
glial cells
gliomas
tumors of glial cell grow rapidly and are highly malignant
depolarization
voltage becomes less neg. more pos
repolarization
voltage returns to original negative value
hyperpolarization
voltage becomes more negative than RMP
local potential
local distrubances in membrane potential
short range
exittatory
action potential in more likely to happen
inhibitory
action potential is less likely to happen
action potential
dramatic, transient change in membrane
steps of action potential
1 resting -70mv
gates closed
2 local potential
slight influx of na
3 threshold is met at - 55mv
4. na voltage gated channels open
5.depolarization
hit +30mv na rushes into cell
6. at +30 na gates close
7. k channels open
8. k leaves cell- repolar
9.k close and k eflux stop- channels inactive
10 hyperpolarization
11 restored
thereshold is the
minn amount of energy to activate
what start depolarization event
hitting -55mv
sodium will enter cell
absolute refractory period
no stim will tigger new action potential
time after an action potential when a cell is unable to generate another action potential
relative refractory period
a new action potential can only be triggered with an unusally strong stim
resting period
saltatory conduction
leaping, only go forward
the transmission of an impulse from node to node along a myelinated axon, allowing for faster and more efficient conduction compared to unmyelinated axons.
speed of singal depends on
diameter of fiber (large diameter fast)
presence of myelin
thin unmyelin neuron speef
1.0 m/sec
thick myelinated neuron speed
100 m/sec
nociceptive neruon
feel pain
synapses
small sapce bn two cells where they communicate of neuron and other cell
axodentritic synpase
axon and dendrite
axosomatic synaps
axon and cell body
axoaxonic synpase
axon and axon terminal
electrical synapse cells joined by gap junctions
not touching
ions freely flow, quick, no integration
in smooth and cardiac muscle
chemical synpase
presynaptic neuron releases neruotrasnmitter to postsynaptic cell
junction between neurons that uses neurotransmitters to transmit signal
release of neurotransmitter steps
1 action potentials reach axon term
2 volt gated ca channels open
3 ca binds to sensor in cyto
4 ca protein complex release
neruotransmitters classes
aminos
peptide
biogenic amines
acetyl choline
acetylcholine found where
in neuromuscular junctions,
autonomic nerv system,
some neuron in the CNS
cholinergic receptors types
nicotinic
muscarinic
nicotinic receptor
ligand gated
all ANS postganglionic neruon
skeletal muscle
regions of brain
muscarinic receptros
g protein coupled receptor
cardiac and smooth muscle/glands
excitatory cholinergic synapse steps (6)
1 AP reaches knob and opens ca channels
2 ca influx causes exocytosis of synaptic vesicle, releasing Ach
3. empty vesicle refills w ACh
4. ACh diffuses and binds to receptor and opens channels (na in and k out)
5. Na influx may start AP
6. ACh breaks down
botulism toxin prevents
release of ACh due to cleavage of SNARE proteins
monoamine neurotransmitters derived from
amino acids
monoamine neurotransmitters
catecholamines (from tyrosine, dopamine, norepinephrine)
serotonin (form tryptophan)
histamine (histidine)
norepinephrine released by
sympathetic nervous system
makes brain alert
norepinephrine binds to
adrenergic receptors- g coupled
alpha (smoov) and beta (cardiac and smov)
norepinephrine can be stimulated by
epinephrine and ampetamines
excitatory adrenergic synapse steps
1 unstim adrenergic receptor is bond 2 g protein
2. Norepi binds to receptor, g protein dissociates
3. alpha g-pro binds to adenylte cyclase (ATP to cAMP)
4. cAMP deploarizes postsynap neuron, changed enzyme activation metabolism, transcribes metabolic enzymes
serotonin implicated in
mood, appetite, behavior, cerebral cirulation
serotonin used by
neurons in the raphe nuclei
dopamine involved in what part of brain
nigrostriatal dopamine system- substantia nigra
midbrain
dopamine important in
control and intitiation of movements
degeneration of dopamine neurons may cause and treatment
parkinsons
treated by l dopa and MAOIs
mesolimbic dopamine system-ventral tegmental area involved in
emotional reward associated with addictions
glutamate
most excitatory neruotransmiters in brain
major energy use in brain
astrocytes take that hoe up
glutamate receptors type
ion channels
NMDA and AMPA open stuff blocked by mg
gaba freq
most common neurotrans in brain - 1/3
gaba use
inhibitory, causes hyperpolarizaiton
opnes cl- channels
involved in motor control
degen of GABA secreating neurons in cerebell leads to
huntingtons
how signal stops
presynaptic cells stops releasing neruotransmitters
how neurotransmitters are cleaned up
diffusion- get absorbed
reuptake
degrade
spacial summation
input from many neurons
temporal summation
many stim from one neuron
local action potential
short dist
pos or neg
graded
synaptic plasticity
ability of synapse to change in responce to activity
somatic motor neuron
controls voluntary movements
Long-term potentiation
(LTP)
- Repeated stimulation
enhances excitability - Insertion of AMPA
glutamate receptors
Long-term depression (LTD)
– Low frequency of
stimulation
* Removal of AMPA
glutamate receptors
Qualitative information depends on
which neurons fire
Labeled line code:
a neuron only carries one type of
information
Quantitative information is
information about the
intensity of a stimulus
1st step of action potential
resting membrane -70mv
channels are closed
step after resting membrane
local potential- slight influx of NA
after slight influx of NA (step 2)
thershold is met at -55mv
after threshold is met (step 3)
NA volt gate channels open
after Na volt gate channels open
Depolarization
na rush into cell until +30mV
after depolarization
at +30mV, Na channels close
after NA channels close
k volt gates open and leave (repolarization)
after repolarization
k channels close and k efflux stops
k channels close leading to
hyperpolarization
after hyperpolarization
RMP is restored with NA/K pumps
excitatory cholinergic synapse step 1
AP reaches knob and opens gated Ca channels
excitatory cholinergic synapse step 2
ca influx causes exocytosis of synaptic vesicle, releasing ach
excitatory cholinergic synapse step 3
empty vesicle refills with ACh
excitatory cholinergic synapse step 4
ACh diffuses across cleft, binds to receptor and opens channels
Na influx, k influx
excitatory cholinergic synapse step 5
na influx starts action potential
excitatory cholinergic synapse step 6
ach breaks down
schizophrenia is associated with
too much dopamine in mesolimbicc dopamine system
