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Neuro 1 > Neurophysiology BSC > Flashcards

Neurophysiology BSC Flashcards

1
Q

soma

A

cell body
perikaryon
- stains dark due to ribosomes called “nissl bodies”

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2
Q

case study: history of imparied glucose tolerance and HTN. recently noticed tingling and burning in feet. blood glucose is 146 (normal is 125). has decreased vibratory sensation and fasciculation in both feet

A

underlying cause: cumulative damage to neurons and glia = peripheral neuropathy, diabetic neuropathy (type of polyneuropathy)

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3
Q

fasciculation

A

twitch

= decreased motor innervation

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4
Q

tingling

A

PNS, decreased sensory innervation

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5
Q

peripheral neuropathy

A
  • positive: pain and dysethesia (abnormal sensations)
  • negative: loss of sensation or reflex; weakness and muscle atrophy
  • irritative: fasciculations (twitching) and paresthesia (tingling and burning)
  • this can involve one nerve or many nn.
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6
Q

mononeuropathy

A
  • involving only isolated nn.
  • often due to trauma or pressure
  • radiculopathy: damaged nerve roots
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7
Q

polyneuropathy:

A

due to metabolites, toxins, demyelinating disease and chronic infections

  • can affect the axon, myelin or synapse
  • becomes more senstivie to mononeuropathy
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8
Q

diabetic neuropathy

A
  • hyperglycemia serves as a trigger: inflammatory, metabolic and ischemic
  • pro-oxidative and pro-inflammatory
  • affects many cell types, but often causes axonal demylination
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9
Q

Parts of PNS

A
  • spinal and cranial nerves

- glial cells: Schwann cells

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10
Q

resting membrane potential

A

-65 mV

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11
Q

synaptic potentials

A

the incoming signal of a neuron that is received at the synapse of the dendrites

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12
Q

capacitator of neurons?

A

the lipid bilayer

- allows for storage of charges on opposite sides

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13
Q

resistor of neurons?

A

ion channels - allow a certain amount of current to flow across the membrane

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14
Q

conductance vs. resistance?

A 
conductane = flow of ion across the membrane
resistance = halting of flow of ion across the membrane
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15
Q

depolarization

A

decreased internal negativity

- due to inward Na+ current

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16
Q

hyperpolarization

A

increasing internal negativitiy

- due to outward K+ current

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17
Q

time constant

A

= how long it takes to reach final voltage

  • dependent on number of channels: many open channels lead to lower time constant
  • results in high conductance and low resistance
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18
Q

temporal summation

A

based on the time constant of the summation

- multiple signals conducted quickly may be summed to result in an AP

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19
Q

length constant

A

the distance required for the current to decline

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20
Q

spatial summation

A

decreased length constant, can result in increased summation of AP’s

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21
Q

what types of axons are first affected in neuropathy?

A

longest axons

“stocking and glove” - results in defects in sensation/strength of hands and feet first

22
Q

autonomic vs. motor loss in PND

A

motor neurons can be lost causing atrophy
Autonomic neurons can be lost:
- efferent: results in sweat loss, dry, cracked skin
- afferent: changes in senation and pain

23
Q

nodes of ranvier

A

junction between schwann cells

  • high concentration of voltage gated Na+ channels
  • allows for saltatory conduction
24
Q

nerve-conduction studies

A

stimulating electrodes are placed on the skin overlying a nerve

  • if the recording is then taken along the nerve: then can measure the APs (SNAP: sensory nerve action potential)
  • if placed on muscle, then it is detecting a CAMP, compound motor action potential
25
Q

myelin damage

A

slowed conduction

ectopic propogation

26
Q

axon damage

A

failure of propogation
ectopic propogation
decreased SNAP amplitude

27
Q

PNS regeneration

A
  1. schwann cells downregulate the myelin and the myelin sheath is broken down in response to injury.
  2. schwann cells rearrange themselves into endoneurial tubes
  3. macrophages phagocytose myelin debris
  4. anterograde degeneration of axon occurs (wallerian degeneration: axon distal to wound degenerates)
  5. retrograde signaling causes soma to reorganize and organelles are reorganized (chromatolysis): neuron must produce a large amount of amount of proteins
  6. during regeneration, many neurites sprout and are guided by schwann cells until a connection is made
    7 schwann cell redifferentiate
28
Q

sx: generalized neuronal changes, cognitive decline, headache, vomiting, nausea

A

could be due to intracranial pressure changes or neuronal swelling

29
Q

oligodendrocytes

A

white (and gray) matter

- form myelin sheaths

30
Q

astrocytes

A

provide mechanical and metabolic support and response to injury in CNS

  • are the endfeet of the CNS that provide a covering of endothelial cells, induce the formation of tight junctions in formation of blood brain barrier
  • control the brain ECF by buffering glucose and K+
  • store glucose and release it for energy
  • take up excess K+ ; have a lower membrane potential than neurons (-85 mV)
31
Q

microglia

A

phagocystose things in response to injury in CNS

32
Q

Ependymal cells

A

line the walls of ventricles and secrete CSF

33
Q

endothelial cells

A
  • in the CNS there are no clefts or fenestrae, they have continuous tight junctions
  • reduced paracytosis
  • reduced transcytosis
34
Q

what are the two types of astrocytes?

A
  1. fibrous astrocytes: are found in white matter and are associated with myelin; long thin processes
  2. protoplasmic astrocytes: short frilly processes and are found in gray matter
35
Q

primary brain injury

A
  • mechanically induced

i. e. contusions, axonal injury, vascular injury, cranial n. injury

36
Q

secondary brain injury

A

not mechanically induced, will take 12,24 hours to form

- intracranial hemorrhage, swelling, hypoxic injury, infection, ROS injury

37
Q

Cerebral edema

A
  • net accumulation of water in the brain
  • glial cells uptake K+. Cl- and water follow into astrocytes.
  • generalized edema: increased total intracranial pressure; if pressure excedes arterial pressure then blood flow can stop, if occurs slowly it will activate sensors in medulla to increase arterial pressure
  • focal edema: displaces nearby structures
    sx: headache, vomiting, altered conviousness, focal neurological problems
    tx: hyperventilation (resp. alkalosis induces vasoconstriction) or osmolytes like mannitol (draw water out)
38
Q

how are neural scars formed?

A

reactive gliosis: movement and proliferation of glial cells to the area, can result in scar or plaque formation.

39
Q

excess glutamate….

A

glutamate can be released by ischemia, anoxia, hypoglycemia or trauma and results in excitotoxicity

40
Q

how does xs glutamate affect the neuron?

A
  • inhibits Na/K ATPase
  • result in large increase in extracellular K and intracelluar Na
  • results in accidendtal membrane depol and release of NT
41
Q

how does xs glutamate affect astrocytes?

A
  • astrocytes want to take up glutamate, but to do this they need Na/K ATPase
  • thus there is diminished glutamate uptake
42
Q

how does xs glutamate affect post-synaptic terminals?

A

glutamate opens Na and K permeable ion channels

- this leads to neuronal damage

43
Q

how does xs glutamate affect cell swelling

A

neuron cell bodies and dendrites swell b/c Na+ enters and Cl- and water passively follows

44
Q

fast vs. slow synaptic potential

A
  • fast is most common and involves point-to-point contact through ligand-gated ion channels
  • slow synaptic potentials are less common. they are diffuse . normally occurs between branched and projecting neurons. requires G protein coupled receptors, can be electrically silent
45
Q

EPSP

A

Depolarizing response that brings membrane closer to threshold for firing an action potential

46
Q

IPSP

A

Hyperpolarizing response that moves the membrane away from threshold

47
Q

Potentiation

A
  • occurs with brief, high-freq action potentials occuring over long periods of time
  • results in presynaptic terminal releasing more NT with each action potential
  • results in entry of too much Ca2+ and residual Ca2+ increases vesicle exocytosis.
  • high intracellular Ca2+ induces kinases
48
Q

depression

A

due to long, high frequency APs, cause depletion of synaptic vesicles

or due to low-requency APs: moderate intracelluar Ca2+ levels induce phosphatases

49
Q

short vs. long term synaptic plasticity?

A

Short-term: Lasting seconds

Long-term: Lasting days, weeks or longer
Dendritic spines
Changes shape, number and diameter
Changes electrical properties and substrate concentrations

50
Q

long-term memory

A

Sensitivity of a synapse to past activity influences long-term effectiveness

  1. Long-Term Potentiation: Increases the amplitude of EPSPs
  2. Long-Term Depression: Decreases the amplitude of EPSPs

Neuro 1 (14 decks)

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