Neurophysiology Flashcards
peripheral neuropathy
pain and dysesthesia
- loss of sensation or reflex;weakness
- fasciculations and paresthesia
mononeuropathy
involve isolated neurons
-trauma or pressure
radiculopathy
damage to nerve roots
polyneuropathy
metabolites, toxins, demyelinateing disease, chronic infections
can affect axon, myelin, or synapse
diabetic neuropathy
hyperglycemia is trigger
- pro-oxidative and pro-inflammatory
- PNS cells more susceptible
- predominantly axonal damage
- variable demyelination
resting membrane potential
-65
synaptic potential
slow, graded, local
action potential
brief, actively propagated and traveling
equilibrium
current of ion moving in and out of cell is equal
–determined by charge and concentration
establishment of RMP
inward Na
outward K
-closer to K - because it has greater permeability
maintained bt Na/K ATPase pump
capacitor
lipid bilayer
-stores charge on opposite sides
resistor
ion channels
-allow certain amount of ions to flow
conductance
flow of ion across membrane
resistance
opposite of conductance
depolarization
due to inward Na current
hyperpolarization
due to outward K current
voltage-gated Na channels
open - membrane depolarization
inactivation - closed and will not reopen
deinactivated or resting - after membrane repolarized, return to conformation that allows them to opened in response to depolarization
voltage gated K channels
open - slowly, response to depolarization
-do not inactivate
resting - after membrane repolarized
steps in AP
depolarization
- rising phase
- falling phase
- undershoot
- resting
temporal summation
multiple signal over time may reinforce eachother
spatial summation
multiples signals that are physically close may influence eachother
time constant
how long to reach final voltage
- depends on number of channels
- many open channels, lower time constant
length constant
distance required for current to decline
neuromuscular junction
unmyelinated at axon
- release of acetylcholine
- muscle fiber - ligand gated ion channels
muscle atrophy
due to loss of trophic effect on muscle
fibrillation or fasciculation
neurotransmitter loss from damaged axon or schwann cells
peripheral nerve disease
motor - muscle atrophy
autonomic nerves - sweating lost, dry, cracked skin
loss of efferent autonomics
lose sweating
dry cracked skin
loss of afferent autonomics
changes in sensation, pain
internodal segment
myelin between two nodes
saltatory conduction
AP - travels along internodal parts of axon
-speeds signal speed
nerve conduction studies
myelin damage - slow conduction
axon damage - failure of propagation, ectopic propagation, decreased SNAP amplitude
PNS regeneration
schwann cells dedifferentiate
- macrophage phagocytose
- anterograde degeneration (wallerian)
- retrograde signaling induces reorganization of soma (chromatolysis)
- regeneration - neurite sprouts guided by schwann cells until connection mae
- schwann cells redifferentiate
fibrous astrocytes
white matter
-long and thin processes
protoplasmic astrocytes
gray matter
-short and frilly processes
astrocytes
control brain ECF
- store all glycogen in brain
- limit K accumulation
membrane potential in brain
lower
-85
primary brain injury
at time of injury
-axonal injury, vascular injury, CN injury, contusion, laceration
secondary brain injury
within 12-24 hours
-swelling, infection, increased ICP, hypoxic injury
edema
glial cells - uptake of K, followed by Cl and water - swelling
generalized edema
increased total ICP
-increase arterial pressure
focal edema
displaces nearby structure
Sx of edema
headache, vomiting, altered consciousness, focal neuro problems
Tx of edema
hyperventilation - alkalosis induces vasoconstriction
osmolytes - mannitol
scar formation
astrocyte and microglia
-reactive gliosis - scar or plaque formation
neurotransmitter release
Ca induced
termination of signal
uptake or degradation
uptake to presynaptic cell
serotonin, dopamine, NE
neuropeptides
fast axonal transport
amines and amino acids
made in presynpatic cytoplasm
excitotoxicity
excessive accumulation of neurotransmitter in brain ECF
glutamate
inhibits Na/K ATPase
excitation
fast - ligand-gated ion channels
slow - GPCRs
EPSP
closer to threshold
IPSP
moves away from threshold
potentiation
repeated APs
-more neurotransmitter with each AP
depression
high frequency AP - depletion of vesicles
low frequency - intracellular Ca - induce phosphatase
memory
synapses physical site of memory storage
working memory
fleeting changes
long-term memory
sensitivity of synapse to past activity influences long-term effectiveness
long-term potentiation
increase amplitude of EPSPs
long term depression
decrease amplitude of EPSPs