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Science for Medicine > SfM - How Nerves Work > Flashcards

SfM - How Nerves Work Flashcards

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Biology 101 flashcards
1
Q

what are the components of the CNS?

A

brain
spinal cord
peripheral nerves

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2
Q

what are the components of the peripheral NS?

A

nerves & ganglia outside the brain and spinal cord

somatic/autonomic NS

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3
Q

what are the main regions of the brain?

A
  • cerebrum (frontal, temporal, parietal, occipital lobes)
  • cerebellum
  • diencephalon (thalamus, hypothalamus)
  • brainstem (midbrain, pons, medulla)
  • meninges
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4
Q

how many spinal nerves are there?

A
  • 31

8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal

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5
Q

what is the organisation of spinal cord?

A

spinal cord –> root –> ganglion –> ramus –> nerve

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6
Q

where are sensory fibres located?

A

sensory fibres are found only in dorsal side (dorsal root)

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7
Q

where are motor fibres located?

A

motor fibres are found only in ventral side (ventral ramus)

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8
Q

when do the fibres mix?

A

Fibres mix in the ramus and go onto create the spinal nerves

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9
Q

what are the main regions of a neurone?

A

dendrites, cell body, axon hillock, axon, synapse

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10
Q

what is the role of astrocytes?

A

maintain the external environment for the neurones, produce blood-brain barrier

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11
Q

what is an oligodendrocyte?

A

forms myelin sheaths in the CNS

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12
Q

what is the role of microglia?

A

phagocytic hoovers mopping up infection

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13
Q

what is the resting membrane potential?

A

-70mV

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14
Q

what are the main factors that influence the RMP?

A
  • mainly the leaky K+ channels

Na+K+ pump has influence but it is closer the K equilibrium

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15
Q

what happens if there is higher extracellular K conc?

A
  • reduces concentration gradient
  • so K+ enters cell
  • therefore RMP reduced
  • causes depolarisation
  • unregulated AP firing
  • All muscles in body contract, atrial fibrillation
  • brain is protected from high K+ - blood brain barrier (astrocytes)
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16
Q

How does the Na/K pump influence RMP?

A
  • open Na channels = cell depolarises
  • open (more) K channels = depolarisation/hyperpolarisation
  • open Cl channels = cell hyperpolarisation
  • open Ca channels = cell depolarises
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17
Q

definitions of

  • depolarisation
  • repolarisation
  • hyperpolarisation
A
  • membrane potential becomes more + (moves closer to Na+ equilibrium +60)
  • MP moves from a more +ve to a more -ve value (closer to RMP -70)
  • MP overshoots, surpassing RMP (closer to K+ equilibrium -90)
18
Q

what is the role of a graded potential?

A

graded potentials are changes in membrane potential that vary in size - related to size of the stimulus

19
Q

examples of graded potentials

A
  • generator potentials - sensory receptors
  • postsynaptic potentials - synapses
  • endplate potentials - NMJ
20
Q

are graded potentials decremental?

A

Following some local stimulus, ion channels open creating a potential difference. This current leaks out along the rest of the membrane, meaning that the further away from initial site of depolarisation you go, the smaller the membrane potential.

21
Q

how are graded potentials graded?

A
  • if you have a stronger stimulus initially = more channels opened –> bigger current flow & bigger potential
22
Q

can graded potentials be depolarising?

A
  • GPs can be depolarising or hyperpolarising
  • can excite or inhibit a cell for firing an AP
  • more likely to fire an AP = excitatory - EPSP
  • less likely to fire AP = inhibitory - IPSP
23
Q

what ions are involved in IPSP/EPSP?

A

K+ leaves = hyperpolarise = IPSP
Cl- enters = hyperpolarise = IPSP
Na+ enters = depolarise = EPSP
Ca2+ enters = depolarise = EPSP

24
Q

what generates fast IPSP?

A

GABA binds to ionotropic GABA receptors triggers opening of ion-pore = hyperpolarisation

25
Q

what generates slow IPSP?

A

GABAb is a metabotropic receptor which activates K+ channels, K+ leaves cell - becomes more -ve

26
Q

what generates fast EPSP?

A

glutamate binds to ionotropic Na+K+ - huge Na influx -> depolarisation

27
Q

what generates slow EPSP?

A

Glutamate binds to leaky K+ channels (metabotropic R) and closes them –> depolarisation = Slow EPSP

28
Q

can graded potentials summate?

A

yes, graded potentials can add onto each other

- important in synaptic integration for AP generation

29
Q

what do spatial summation and temporal summation mean?

A
  • spatial summation - when multiple presynaptic neurons release NT and is enough to evoke AP
  • Temporal summation - when one presynaptic neurone releases NT many times enough to evoke AP
30
Q

what does synaptic integration mean?

A
  • process of summing all neuronal inputs together to determine if initial segment (axon hillock) reaches threshold for AP generation
31
Q

what are the main characteristics of APs?

A
  • threshold of -55mv
  • are all or none
  • can only encode stimulus intensity in frequency
  • self-propagate
32
Q

what does self-propagation mean?

A
  • AP can efficiently travel to next bit and open voltage-dependent Na+ channels - elicits an AP in the next neuron
33
Q

is there back flow of AP?

A

there is some backflow of current but doesn’t evoke an AP as the previous channels are kept in refractory state

34
Q

why are APs not decremental?

A
  • myelin sheath prevents current leaking out
35
Q

what cells produce myelin?

A
  • PNS - Schwann cells

- CNS - oligodendrocytes

36
Q

what is the role of saltatory conduction?

A
  • saltatory conduction is involved in speeding up conduction
  • propagates AP in Nodes of Ranvier
  • NoR are uninsulated, meaning ions can be exchanges to regenerate APs
37
Q

what is the effect of demyelination?

A
  • MS & Guillain-Barre Syndrome are diseases of demyelination
  • damage of myelin sheath means AP will leak out = local current decays quicker = fails to depolarise next node to threshold = conduction fails
38
Q

what is a compound action potential?

A
  • signal recorded (extracellularly) from a large population neuronal axons
  • have a mixture of small/large non-/myelinated axons
  • this means that different APs will arrive at different speeds (fastest arrive first as a wave, then 2nd fastest…)
39
Q

what are the characteristics of a fast conductor?

A
  • myelination
  • large diameter
    examples
    all A-fibres are myelinated and fairly large diameter (involved in proprioception, motoneurons, touch, fast pain)
40
Q

steps to evoke an AP

A
  1. AP comes down axon (mediated by Na+ channels)
  2. AP opens voltage gated Ca2+ channels in presynaptic terminal
  3. Triggers fusion of vesicles (Ca2+ dependent exocytosis)
  4. Acetylcholine released and diffuses across cleft
  5. Binds to nicotinic ACh receptors - evokes GRADED post-synaptic potentials by opening channels
  6. Opens ligand-gated Na+/K+ channels - more Na+ flows in
  7. Evokes local graded excitatory end plate potential
  8. EPP depolarises adjacent membrane to threshold
  9. Opens voltage-gated Na+ channels - evoking new AP
  10. ACh removed by acetylcholinesterase
41
Q

how can toxins impact APs?

A
  • tetrodotoxin - blocks Na+ channels = blocks AP
  • joro spider toxin - blocks Ca2+ = stops NT release
  • botulinum toxin - disrupts release machinery = blocks NT release
  • curare - blocks ACh receptors = prevents EPP
  • anticholinesterases - block ACh breakdown = increase transmission at NMJ
42
Q

what are the differences with CNS synapses?

A
  • have a wider variety of neurotransmitters (ACh, nor/epinephrine, dopamine, glutamate…)
  • have a range of small post-synaptic potentials (fast EPSPs - ionotropic, slow EPSPs - metabotropic), fast/slow IPSPs)
  • variation of anatomical arrangement of synapse (axo-somatic/axo-dendritic/axo-axonal)
  • variations on connectivity of neurones (convergence = many neurones synapse onto 1 neurone, divergence = one neurone synapses onto many neurons, feedback inhibition - presence of inhibitory interneuron)

Science for Medicine (9 decks)

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