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Neuro > Neurophys BSC > Flashcards

Neurophys BSC Flashcards

1
Q

soma

A

May have one, two, or many processes; typically one axon, many dendrites

Nucleus, Golgi apparatus, Nissl substance, cytoskeleton, mitochondria

Synthesize macromolecules, integrate electrical signals*

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2
Q

axon

A

Single, cylindrical; may be many centimeters long; may be myelinatedor unmyelinated

Cytoskeleton, mitochondria, transport vesicles

Conduct information to other neurons

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3
Q

axon terminal

A

Vesicle-filled apposition to part of another neuron; most are axodendritic or axosomatic, but other configurations occur

Synaptic vesicles, mitochondria

Transmit information to other neurons

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4
Q

peripheral neuropathy

A

Symptoms

–Positive

•Pain and dysesthesia

–Negative

•Loss of sensation or reflex; weakness

–Irritative

•Fasciculationsand paresthesia

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5
Q

mononeuropathy

A

–Involving isolated nerves

•Radiculopathy is damaged nerve roots

–Due to trauma or pressure

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6
Q

polyneuropathy

A

–Due to metabolites, toxins, demyelinating diseases and chronic infections

–Can affect the axon, myelin or synapse

–Become more sensitive to mononeuropathy

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7
Q

diabetic neuropathy

A

•Hyperglycemia serves as trigger

–Inflammatory, metabolic and ischemic

  • Pro-oxidative and pro-inflammatory
  • Variably affects cell types
  • Variable presentation of disease
  • PNS cells more susceptible
  • Predominantly axonal

–Variable degrees of demyelination present

World

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8
Q

membrane potential equilibrium

A
  • Current of an ion moving out of a cell is equal and opposite to the current moving into a cell.
  • Determined by:

–Charge and concentration

•Resting Membrane Potential (-65 mv)

–Inward Na+ current

–Outward K+ current

•Closer to K+ equilibrium potential because of greater K+ permeability

–Maintained by Na/K-ATPase

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9
Q

Ion concentrations

A

Ion

Extracellular Concentration (mM)

Intracellular Concentration (mM)

Equilibrium Potential*(37°C)

Na+

140

15

+60 mv

K+

4

130

−94 mv

Ca2+

  1. 5
  2. 0001†

+136 mv

Cl−

120

5

−86 mv

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10
Q

capacitor

A

the lipid bilayer

stores charges on opposite sides

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11
Q

resistor

A

ion channels

allow an amount of current flow across the membrane

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12
Q

resistance

A

opposite of conductance

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13
Q

hyperpolarization

A

increasing internal negativity

due to outward k current

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14
Q

voltage gated na channels

A

–Open

•In response to membrane depolarization

–Inactivated

•Closed and will not reopen in response to depolarization

–Deinactivatedor resting

•After the membrane is repolarized, return to a confirmation that allows them to be opened in response to depolarization

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15
Q

voltage gated k channels

A

–Open

  • Slowly, in response to depolarization
  • Do not inactivate
  • Remain open as long as membrane is depolarized

–Resting

•After membrane is repolarized

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16
Q

action potential steps

A
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17
Q

summation - time constant

A

–How long to reach final voltage

•Usually 10 msecor less

–Dependent on number of channels

–Many open channels lead to lower time constant

•High conductance, low resistance

–Few open channels lead to higher time constant

•Low conductance, high resistance

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18
Q

temporal summation

A

–Based on time constant

–Brief conductance changes may only partially charge the membrane

–Multiple signals spread over time may reinforce each other

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19
Q

length constant - summation

A

the distance required for the current to decline

a few hundred micrometers

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20
Q

spatial summation

A

inputs that are physically close may reinforce each other

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21
Q

summation chart

A
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22
Q

neuromuscular junction

A

•Motor axon

–Unmyelinated at terminus

–Multiple terminal branches

  • Protected by Schwann cells
  • Contain vesicles filled with neurotransmitter (acetylcholine)
  • Muscle fiber

–Contains ligand-gated ion channels

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23
Q

neuropathy

A

–Longest axons first

•”Stocking and glove” defects in sensation and strength

–Motor deficit

•Muscle atrophy

–Loss of trophic effect on skeletal muscle

•Fibrillation or fasciculation

–Neurotransmitter loss from damaged axon or Schwann cells

–Sensory deficit

•Paresthesia

–Tingling sensation

•Pain

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24
Q

Motor peripheral nerve disease

A

atrophy

foot deformity (claw toe derofmity)

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25
Q

autonomic peripheral nerve disease

A

efferent:

lose sweating, dry cracked skin

afferent - chages in sensation, pain

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26
Q

Propagation

A

–The generation of an action potential in one area generates action potentials in adjacent areas containing the necessary channels

–Will not be generated backwards due to the refractory period

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27
Q

unmyelinated axons

A

–Slow

–Inward Na+ current spreads from trigger zone

•Depolarizes adjacent areas of the membrane

–Dependent on density of Na+ channels to reach threshold

•Abundant in axons

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28
Q

myelination

A

–Schwann cells surround axons with compacted layers of myelin sheath

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29
Q

nodes of ranvier

A

–The junction between two adjacent Schwann cells

–Nodes present every millimeter

–High concentration of voltage-gated Na+ channels

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30
Q

internodal segment

A

the myelin between two nodes

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31
Q

saltatory conduction

A

–Action potentials traveling along internodalparts of the axon

–Depolarize each node to threshold, generating action potentials at each node sequentially

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32
Q

nerve conduction studies

A

–Stimulating electrodes placed on the skin overlying a nerve

–Recording electrodes placed

•Along the nerve

–Detecting a compound sensory nerve action potential (SNAP)

•Overlying a muscle belly innervated by the nerve

–Detecting a compound motor action potential (CAMP)

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33
Q

Nerve damage

A

•Myelin damage

–Slows conduction

–Compare to normal conduction velocities

•Axon damage

–Failure of propagation

–Ectopic propagation

–Decreased SNAP amplitude

34
Q

CNS

Neurons, dendrites, synapses

A

Gray matter

Collect, integrate, transmit information; synthesize macromolecules

35
Q

cns

axons

A

White matter

Conduct information

36
Q

cns

oligodendrocytes

A

White (and gray) matter

Form myelin sheaths

37
Q

cns

Protoplasmic astrocytes

A

Gray matter

Provide mechanical and metabolic support, response to injury

38
Q

cns

fibrous astrocytes

A

White matter

Provide mechanical and metabolic support, response to injury

39
Q

cns

microglia

A

Gray (and white) matter

Phagocytosis, response to injury

40
Q

cns

ependymal cells

A

Walls of ventricles

Line ventricles and choroid plexus, secrete cerebrospinal fluid

41
Q

blood brain barrier

A

•Endothelial cells

–No clefts or fenestrae

  • Continuous tight junctions
  • Reduced paracytosis

–Reduced transcytosis

–Thick basement membrane

•Astrocytes

–Endfeetprovide a nearly continuous covering

42
Q

astrocytes

glucose

A

–Glucose

»Store virtually all the glycogen in the brain

•Released in absence of blood glucose as lactate

»Preferentially take up blood glucose and release as lactate

43
Q

astrocytes

k

A

»Inward K+ channels

•Voltage-gated

»Limit K+ accumulation

»Lower membrane potential than neurons (-85 mV)

–Neurotransmitters

44
Q

astrocyte processes

A

numerous and elaborate

45
Q

fibrous astrocytes

A

–White matter

–Long and thin processes

46
Q

protoplasmic astrocytes

A

–Gray matter

–Short and frilly processes

47
Q

primary brain injury

A

(mechanically induced)

–Contusions and lacerations

–Axonal injury

–Vascular injury

–Cranial nerve injury

48
Q

cerebral edema

A

–Net accumulation of water within the brain

–Not cell swelling alone

49
Q

edema classification

A

–Generalized

  • Increases total intracranial pressure
  • Activates sensors in medulla to increase arterial pressure
  • If it exceeds arterial blood pressure, blood flow to brain stops

–Focal

•Displaces nearby structures

50
Q

cerebral edema treatments and symptoms

A

•Symptoms

–Headache, vomiting, altered consciousness, focal neurological problems

•Treatments

–Hyperventilation (respiratory alkalosis induces vasoconstriction)

–Osmolytes(Mannitol)

51
Q

scar formation

A

•Astrocyte Activation

–Hyperplasia and hypertrophy

•Microglia Activation

–Migrate toward injury

–Increased phagocytosis

•Reactive Gliosis

–Scar or plaque formation

–Trauma, stroke, neurotoxins, inflammatory demyelination, neurodegenerative disorders

52
Q

synaptic transmission

A
  1. Synthesis of neurotransmitter
  2. Concentration and packaging of neurotransmitter
  3. Release of neurotransmitter from presynaptic cell into synaptic cleft
  4. Ca2+ sensitive
  5. Binding of neurotransmitter to receptors in postsynaptic cell membrane
  6. Termination of neurotransmitter action
53
Q

neurotransmitters small molecules

A

Small molecules

–Amines and amino acids

–Made in presynaptic cytoplasm

  • Locally available substrates
  • Enzymes arrive by slow axonal transport
54
Q

neuropeptide neurotransmitters

A

–Arrive by fast axonal transport

•Packaged into vesicles in the cell body

55
Q

termination of neurotransmitter

A

–Uptake

•Presynaptic cell

–Serotonin, dopamine, norepinephrine

•Glial cells

–Glutamate

•Postsynaptic cell

–Neuropeptide receptor endocytosis

–Degradation

•Enzymes present in the synaptic cleft

–Acetylcholine and neuropeptides

56
Q

Excitotoxicity

A

•Excessive accumulation of neurotransmitter in the brain extracellular fluid

postsynaptic neuron sees this as normal firing

57
Q

excitotoxicity - glutamate

A

–Induced by ischemia, anoxia, hypoglycemia or trauma

–Neuron

  • Inhibits Na/K-ATPase
  • Large increases in extracellular K and intracellular Na
  • Membrane depolarization
  • Release of neurotransmitter

–Astrocytes

•Glutamate uptake requires Na/K-ATPase

–Transporter may run in reverse and dump glutamate

–Post-synaptic Terminals

  • Glutamate opens Na+ and K+ permeable ion channels
  • Leads to neuronal injury

–Cell Swelling

  • Induced in neuron cell bodies and dendrites
  • Na+ enters and Cl-and water passively follow
58
Q

Excitation

A

•Fast Synaptic Potentials

–Point-to-point

–Ligand-gated ion channels

•Slow Synaptic Potentials

–Slow and diffuse

–Branched and projecting neurons

–G-protein coupled receptors

–Can be electrically silent

g proteins are activated

59
Q

axonal degeneration

A

get no twitch

60
Q

excitation steps

A
61
Q

synaptic plasticity

A

•Activity-dependent changes in the effectiveness of synapses

62
Q

synaptic plasticity - potentiation

A

–Due to brief, high-frequency action potentials

–Presynaptic terminal releases more neurotransmitter with each action potential

  • The entry of too much Ca2+
  • Residual Ca2+ increases vesicle exocytosis
  • High intracellular Ca2+ induces kinases
63
Q

synaptic plasticity - depression

A

Depression

–Due to long, high-frequency action potentials

•Depletion of synaptic vesicles

–Due to low-frequency action potentials

•Moderate intracellular Ca2+ induces phosphatases

64
Q

synaptic plasticity time

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
65
Q

myelin degenaration

A

loss of conductance

66
Q

damage to neurons and glia

A

endothelial cell damage, peripheral neuropathy (positive negative or irriative symptoms) are complications from diabeetus

67
Q

long axons are more susceptible to

A

ischemia

68
Q

losing efferent means you cannot

A

vasoconstrict

69
Q

replaglinide

A

release more insulin

70
Q

intracranial bleeding

A

lesion on ct scan

71
Q

intracranial pressure changes

A

mental confusion

hydrocephalus (decreased motor function)

obtusion

72
Q

neuronal swelling

A

neuron wont fire

73
Q

focal edema

A

specific changes

cranial nerves, visual, auditory etc

74
Q

bbb passage

A

glucose

ions

gases

transporters that only allow certain thigns

75
Q

lactate

A

can be used by some neurons…energy?

76
Q

what is activated with excitation?

A

g proteins

77
Q

synaptic plasticity is

A

how we store info

78
Q

potentiation cause

A

cells to respond more in the future

79
Q

kinases

A

positively influence cell signaling

80
Q

depression causes

A

cell to respond less in the future

81
Q

phosphatases

A

inhibit cell signaling

Neuro (10 decks)

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