Chapter 3 Flashcards

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1
Q

neurophysiology

A

study of the electrical and chemical signaling communication process

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2
Q

action potential

A

rapid electrical signal that travels along the axon of a neuron within a neuron

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3
Q

resting cell

A
  • inside of a resting cell is more negatively charged than the extracellular fluid on the outside
  • resting membrane potential = -50 to -80 millivolts (mV)
  • neuron at rest = balance of electrochemical forces
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4
Q

ions

A

electrically charged molecules

  • anions: negatively charged
  • cations: positively charged
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5
Q

lipid bilayer

A

2 layers of fatty molecules that make up the cell membrane

  • where specialized proteins (receptors) float
  • build natural boundary against other molecules -> semipermeable via ion channels
  • two opposing forces that drive ion movement through cell membrane: diffusion and electrostatic pressure
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6
Q

diffusion

A

ions flow from areas of high to low concentration (move down concentration gradient)
- cell membranes permit some ions/substances to pass through but not all

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7
Q

electrostatic pressure

A

ions flow towards oppositely charged areas

  • like charges repel each other (e.g. + +)
  • opposite charges are attracted to each other (e.g. + -)
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8
Q

ion channels

A

proteins that span the membrane and allow ions to pass

  • open all the time for potassium (K+) ions only
  • gated: open and close in response to voltage changes, chemicals, or mechanical action
  • neuron shows selective permeability to K+ - can enter and leave freely
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9
Q

ion pump

A

located at the cell membrane, actively pumps ions to maintain resting potential
- sodium potassium pump: 3 Na+ out for every 2 K+ in

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10
Q

establishment and maintenance of resting potential

A
  • at rest, K+ ions move into negative interior of cell because of electrostatic pressure
  • K+ ions build up inside cell and diffuse out through the membrane
  • K+ reaches equilibrium (movement out = movement in) aka resting membrane potential -60 mV (range: -50 to -80 mV)
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11
Q

distribution of ions

A
  • K+: more found inside (cell interior)
  • Na+, Cl-, Ca+: more outside (extracellular fluid)
  • they are exchanged through specialized ion channels in cell membrane; large & negatively charged proteins stay inside neuron
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12
Q

action potentials

A

brief but large changes in membrane potential of axons
- function: transmit information within a neuron
- originate in axon hillock, propagated along axon
- all-or-none property: neurons fire at full amplitude or not at all
+ does NOT reflect increased stimulus strength
+ stimulus strength increases -> action potential frequency increases

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13
Q

hyperpolarization

A

increase in membrane potential (interior of membrane becomes even more negative compared to the outside)

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14
Q

depolarization

A

decrease in membrane potential (interior of cell becomes less negative)
- process through which action potentials are generated

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15
Q

generation of an action potential

A
  • stimulus is sent out from cell body -> sodium channels open and Na+ ions surge in
  • inside of cell becomes more positive
  • when threshold (-40 mV) is reached -> membrane triggers an action potential and send the electrical signal down the axon
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16
Q

return to resting potential

A
  • action potential = Na+ ions moving into the cell -> at peak, concentration gradient pushing Na+ ions in = positive charge driving them out
  • membrane shifts from resting state to active state and back (depolarization)
  • voltage-gated Na+ channels open and more Na+ ions enter
  • membrane reaches equilibrium (+40 mV) -> inside of cell becomes positive
  • voltage-gated K+ channels open -> K+ ions move out -> resting potential restored
17
Q

refractory period

A

time during which stimulus given to neuron, no matter how strong, will not lead to an action potential
- Na+ channels are inactivated
- types:
+ absolute refractory period: complete insensitivity to stimuli; about 1-2 millisecond
+ relative refractory phase: reduced sensitivity; only strong stimulation produces an action potential

18
Q

ion channels-blocking toxins

A
  • tetrodotoxin (TTX - found in pufferfish) and saxitoxin (STX): block voltage-gated Na+ channels -> prevent production of action potentials, leading to paralysis and death
  • batrachotoxin (found in poison arrow frogs): forces Na+ channels to stay open -> prevent restoration to resting potential & block neuronal transmission, leading to paralysis
19
Q

speed of action potentials along axons

A
  • as fast as 150 m/s for some neurons
  • factors:
    + size: larger diameter allows depolarization to spread faster through the interior
    + species: vertebrates have much faster conduction thanks to nodes of Ranvier, aka small gaps in the myelin sheath
    + myelin insulation provides resistance to ion flow -> with these nodes, action potentials can jump from node to node instead moving down entire membrane channel by channel like in insects (SALTATORY CONDUCTION)
20
Q

multiple sclerosis

A

demyelinating disease

  • myelination: process in which glial cells wrap axons with a fatty sheath (myelin) to insulate and speed conduction
  • immune system attacks myelin sheath and causes communication problems between brain and rest of the body
  • results: nerve deterioration and permanent damage to body
  • theories: genetics? virus?
  • no cure yet
21
Q

neurotransmitter

A

chemical messenger that transmits information between neurons through synapses

22
Q

postsynaptic potentials

A
  • excitatory postsynaptic potential (EPSP): produces small local depolarization, pushing cell closer to threshold
  • inhibitory postsynaptic potential (IPSP): produces small hyperpolarization, pushing cell further away from threshold
    + result from chloride ions (Cl-) entering the cell and making the inside more negative
  • integration of excitatory and inhibitory inputs = INFORMATION PROCESSING
23
Q

transmission at a chemical synapse

A
  • action potential travels down the axon to the axon terminal
  • voltage-gated calcium channels open and Ca2+ enter
  • synaptic vesicles fuse with membrane and release transmitter into the cleft
  • transmitters cross the cleft and bind to postsynaptic receptors -> cause an EPSP or IPSP
  • transmitter is inactivated (by enzymatic degradation) or removed (by transposter for reuptake and recycling) -> action is brief
  • transmitter may activate presynaptic autoreceptors, decreasing release
24
Q

summation of action potentials from pre-synaptic neurons

A
  • spatial summation: summing of potentials that come from different parts of the cell
    + if overall sum of EPSPs and IPSPs can depolarize cell at axon hillock -> action potential occurs
  • temporal summation: summing of potentials that arrive at the axon hillock of postsynaptic neuron at different times
    + the closer together in time they arrive, the greater the summation
25
Q

electrical synapses

gap junctions

A

allow axon potentials to jump directly to the postsynaptic region without first being transformed into a chemical signal with no time delay
- for behaviors that require fastest possible responses like defensive reflexes