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Neurophys BSC Flashcards

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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
autonomic peripheral nerve disease
efferent: lose sweating, dry cracked skin afferent - chages in sensation, pain
26
Propagation
–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
27
unmyelinated axons
–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
28
myelination
–Schwann cells surround axons with compacted layers of myelin sheath
29
nodes of ranvier
–The junction between two adjacent Schwann cells –Nodes present every millimeter –High concentration of voltage-gated Na+ channels
30
internodal segment
the myelin between two nodes
31
saltatory conduction
–Action potentials traveling along internodalparts of the axon –Depolarize each node to threshold, generating action potentials at each node sequentially
32
nerve conduction studies
–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)
33
Nerve damage
•Myelin damage –Slows conduction –Compare to normal conduction velocities •Axon damage –Failure of propagation –Ectopic propagation –Decreased SNAP amplitude
34
CNS ## Footnote Neurons, dendrites, synapses
Gray matter Collect, integrate, transmit information; synthesize macromolecules
35
cns axons
White matter Conduct information
36
cns oligodendrocytes
White (and gray) matter Form myelin sheaths
37
cns ## Footnote Protoplasmic astrocytes
Gray matter Provide mechanical and metabolic support, response to injury
38
cns fibrous astrocytes
White matter Provide mechanical and metabolic support, response to injury
39
cns microglia
Gray (and white) matter Phagocytosis, response to injury
40
cns ependymal cells
Walls of ventricles Line ventricles and choroid plexus, secrete cerebrospinal fluid
41
blood brain barrier
•Endothelial cells –No clefts or fenestrae * Continuous tight junctions * Reduced paracytosis –Reduced transcytosis –Thick basement membrane •Astrocytes –Endfeetprovide a nearly continuous covering
42
astrocytes glucose
–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
astrocytes k
»Inward K+ channels •Voltage-gated »Limit K+ accumulation »Lower membrane potential than neurons (-85 mV) –Neurotransmitters
44
astrocyte processes
numerous and elaborate
45
fibrous astrocytes
–White matter –Long and thin processes
46
protoplasmic astrocytes
–Gray matter –Short and frilly processes
47
primary brain injury
(mechanically induced) –Contusions and lacerations –Axonal injury –Vascular injury –Cranial nerve injury
48
cerebral edema
–Net accumulation of water within the brain –Not cell swelling alone
49
edema classification
–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
cerebral edema treatments and symptoms
•Symptoms –Headache, vomiting, altered consciousness, focal neurological problems •Treatments –Hyperventilation (respiratory alkalosis induces vasoconstriction) –Osmolytes(Mannitol)
51
scar formation
•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
synaptic transmission
1. Synthesis of neurotransmitter 2. Concentration and packaging of neurotransmitter 3. Release of neurotransmitter from presynaptic cell into synaptic cleft 1. Ca2+ sensitive 4. Binding of neurotransmitter to receptors in postsynaptic cell membrane 5. Termination of neurotransmitter action
53
neurotransmitters small molecules
Small molecules –Amines and amino acids –Made in presynaptic cytoplasm * Locally available substrates * Enzymes arrive by slow axonal transport
54
neuropeptide neurotransmitters
–Arrive by fast axonal transport •Packaged into vesicles in the cell body
55
termination of neurotransmitter
–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
Excitotoxicity
•Excessive accumulation of neurotransmitter in the brain extracellular fluid postsynaptic neuron sees this as normal firing
57
excitotoxicity - glutamate
–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
Excitation
•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
axonal degeneration
get no twitch
60
excitation steps
61
synaptic plasticity
•Activity-dependent changes in the effectiveness of synapses
62
synaptic plasticity - potentiation
–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
synaptic plasticity - depression
Depression –Due to long, high-frequency action potentials •Depletion of synaptic vesicles –Due to low-frequency action potentials •Moderate intracellular Ca2+ induces phosphatases
64
synaptic plasticity time
•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
myelin degenaration
loss of conductance
66
damage to neurons and glia
endothelial cell damage, peripheral neuropathy (positive negative or irriative symptoms) are complications from diabeetus
67
long axons are more susceptible to
ischemia
68
losing efferent means you cannot
vasoconstrict
69
replaglinide
release more insulin
70
intracranial bleeding
lesion on ct scan
71
intracranial pressure changes
mental confusion hydrocephalus (decreased motor function) obtusion
72
neuronal swelling
neuron wont fire
73
focal edema
specific changes cranial nerves, visual, auditory etc
74
bbb passage
glucose ions gases transporters that only allow certain thigns
75
lactate
can be used by some neurons...energy?
76
what is activated with excitation?
g proteins
77
synaptic plasticity is
how we store info
78
potentiation cause
cells to respond more in the future
79
kinases
positively influence cell signaling
80
depression causes
cell to respond less in the future
81
phosphatases
inhibit cell signaling

Neuro (10 decks)

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