5.2 Nervous tissue: Action potentials Flashcards

1
Q

Describe action potential in neurons

A

Principal way neurons send signals
* Means of long-distance neural communication

  • Occur primarily in muscle cells and axons of neurons
  • Brief reversal of membrane potential with a change in voltage of ~100 mV

*Action potentials (APs) do not decay over distance

In neurons, also referred to as a nerve impulse

Involves opening of specific voltage-gated channels

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2
Q

What channels regulate action potential

A
  • Only leakage channels for Na+ and K+ are open at rest
  • Each voltage-gated K+ channel has one voltage sensitive gate
    • Closed at rest
    • Opens slowly with depolarization
  • Each voltage-gated Na+ channel has two voltage sensitive gates
    • Activation gates: closed at rest; open with depolarization, allowing Na+ to enter cell
    • Inactivation gates: open at rest; block channel once it is open to prevent more Na+ from entering cell
    • *two gates 3 states: closed, open and inactivated
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3
Q

Stages of action potential

A
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4
Q
A
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5
Q

describe the absolute refractory period

A

*size of AP is not important, no addition action portnetial can be generated during the absoulte refractory period

  • Time from opening of voltage-gated Na+ channels until resetting of channels (involves opening the inactivation gate)
  • Ensures that each AP is an all-or-none event
  • Enforces one-way transmission of nerve impulses
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6
Q

relative refractory period

A

Most voltage-gated Na+ channels have returned to resting state

  • Some voltage-gated K+ channels are still open
  • Threshold required for initiating an AP generation is elevated
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7
Q

what is the role of the Na+/K+ pump in the action potential

A
  • Repolarization restores resting electrical conditions of neuron
  • Only a small amount of Na+ and K+ cross the membrane during an AP (e.g. 0.012% percent of the Na+ outside the cell enters)
  • Ionic redistribution is restored by the Na+/K+ pumps
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8
Q

describe Threshold and the All-or-None Phenomenon

A

Not all depolarization events produce APs

  • For an axon to “fire,” depolarization must reach threshold voltage to trigger AP
  • Threshold:
  • Membrane is depolarized by 15 to 20 mV
  • Na+ permeability increases
  • Na+ influx exceeds K+ efflux
  • The positive feedback cycle begins

• All-or-None: An AP either happens completely, or does not happen at all

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9
Q

Describe propogation of action potential

A
  • propogation allows AP to be transmitted from origin down entire axon length twds terminal
  • Na+ influx through voltage gates in one membrane area -> local currents that cause opening of Na+ voltage gates in adjacent membrane areas
  • Once initiated, an AP is self-propagating

* In nonmyelinated axons, each successive segment of membrane depolarizes, then repolarizes

*Propagation in myelinated axons differs

• Since Na+ channels closer to the AP origin are still inactivated, no new AP is generated there

– AP occurs only in a forward direction

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10
Q

How does strength of stimulus intensity relate to action potential

A

*APs are alike & are independent of stimulus intensity

-Strong stimuli can generate APs more often than weaker stimuli

• CNS determines stimulus intensity by frequency of impulses

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11
Q

Conduction velocity

A
  • vary widely • Effect of axon diameter

Larger diameter fibers: less resistance to local current flow and faster impulse conduction

Effect of myelination – Myelin sheaths insulate & prevent leakage of charge –

Saltatory conduction: Voltage-gated Na+ channels located at nodes of Ranvier • APs jump rapidly from node to node (30X faster than non-myelinated)

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12
Q

How does voltage decay in bare plasma membrnae, unmyelinated axn and myelinated axon?

A

Bare PM: doesnt have voltage gated channels like dendrites, voltage decays bc current leaks across

Unmyelinated: voltage gated Na and K channels regenerate ap at point along axon, votlage does not decaay

*Conduction is slow because movements of ions & of the gates of channel proteins take time & must occur before voltage regeneration occurs.

Myelinated axon: keeps current in axons (voltage doesn’t decay much). APs are generated only in nodes of Ranvier & appear to jump rapidly from node to node.

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13
Q

What are the classifications of nerve fibers

A

Group A:

  • 150 m/s (~300mph)
  • large diameter, myelinated
    • Ex: somatic sensory motor fibers

Group B:

  • 15 m/s (30 mph)
  • intermediate diamter, lightly myelinated
    • ANS motor fibers serving isceral organs and smaller somatic sensory fibers from skin (pain and touch)

Group C

  • 1 m/s (2 mph)
  • Smallest diameter, unmyelinated
    • include some ANS motor fibres serving visceral organs and smaller somatic sensory fibers from skin (pain &
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14
Q

how does multiple sclerosis related to AP

A

Multiple sclerosis (MS) = autoimmune disease -> affects primarily young adults

• Myelin sheaths in CNS are destroyed when immune system attacks myelin

– Turns myelin into hardened lesions called scleroses -> Impulse conduction slows and eventually ceases -> Demyelinated axons increase Na+ channels, causing cycles of relapse and remission

  • Symptoms: visual disturbances, weakness, loss of muscular control, speech disturbances, incontinence
  • Treatment: drugs that modify immune system activity
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15
Q

describe the synpase

A
  • junction that mediates information transfer from one neuron to another or an effector cell
  • Presynaptic neuron: conducts impulses toward synapse
  • Postsynaptic neuron: transmits impulses away from synapse

*in PNS: postsynaptic cell may be a neuron, muscle cell, or gland cell

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16
Q

where can neurons synpase?

A
  • with another neuron
  • on skeletal muscle fibers (meuromuscular junctions)
  • on gland cells (neuoglandular synpases)
17
Q

Where can synapse occur on the neuron?

A
  • axodendritic (most common)
  • axosomatic (onto cell body itself)
  • less common types: axoaconic, dendrodendritic, dendrosomatic
18
Q

describe chemical synapses

A
  • most common
  • specialized for release of neurotransmittes into synaptic cleft

Composed of two parts

  • Axon terminal of presynaptic neuron: contains synaptic vesicles filled with neurotransmitter
  • Receptor region on postsynaptic neuron’s membrane: receives neurotransmitter
  • Two parts separated by fluid-filled synaptic cleft

*Electrical impulse changed to chemical across synapse, then back into electrical

19
Q

how does transmittion occur accorss the synaptic cleft

A

Synaptic cleft prevents nerve impulses from directly passing from one neuron to next

– Chemical event (as opposed to an electrical one)

– Depends on release, diffusion, and receptor binding of neurotransmitters

– Ensures unidirectional communication between neurons

20
Q

How is information transfered across chemical synpase?

A

*example is for graded potential, if was going via acon would be an action potential

  1. AP arrives at terminal
  2. voltange gated Ca channels open and Ca enters the axon temrinal
  3. Ca entry causes neurotransmitter containing vesicles to release contents via exocytosis
  4. neurotransmmitter diffuses across synpatic cleft and binds to receptors on post synaptic membrane
  5. binding of neurotranmisster open ion channles creating a grade potential
  6. effects terminated by reuptake, enzymatic degredation of duffusion away from synapse
21
Q

If synapse on dendrite cell = ___ potential

if synapse on axon = ____ potential

if synapse on cell body = ___ potential

A
  • if synapse on dendrite or cell body = graded potential
  • if synapse on axon = action potential
22
Q

describe information transfer across chemical synpase

A
  1. AP arrives at axon terminal
  2. voltage gated Ca chennels open & Ca enters axon terminal
  3. Ca entry causes neurotransmitter containing synpatic vesicles to release contents by exocytocic
  4. Neurotransmitter diffuses across synaptic cleft and bind to speciifc receptors on postsynaptic membrane
  5. binding of neurotransmitter opens ion channels, resulting in graded potentials
  6. neurotransmitter effects are terminated by reuptake through transport proteins, enzymatic degradation or diffusion away from synpase
23
Q

what is synaptic delay

A
  • Neurotransmitter must be released, diffuse across synapse, and bind to receptors
  • Synaptic delay (0.3-0.5 milliseconds)
  • Synaptic delay is rate-limiting step of neural transmission
24
Q

Describe electrical synapses

A
  • Less common than chemical synapses
  • Neurons are electrically coupled (gap junctions)
  • Communication is very rapid
  • May be unidirectional or bidirectional
  • Are important in stereotyped movements e.g. jerky movements of the eyes, axoaxonal synapses in hippocampus, brain regions for emotions and memory and in embryonic nervous tissue
25
Q

Postsynaptic potentials

A

Graded potentials strength determined by: Amount of neurotransmitter released and Time neurotransmitter is in area

Types of postsynaptic potentials:

EPSP: excitatory postsynaptic potentials

IPSP: inhibitory postsynpatic potentials

26
Q

describe excitatory synpases and EPSP

A

Neurotransmitter binds chemically gated channels that allow simultaneous flow of Na+ & K+ in opposite directions

Na+ influx > K+ efflux (Causes a net depolarization)

• EPSP helps trigger AP at axon hillock

27
Q

describe inhibitory synapses and IPSP

A
  • Neurotransmitter opens chemical gated channels for either K+ or Cl–
  • Causes a hyperpolarization
  • Reduces postsynaptic neuron’s ability to produce an AP
28
Q

describe summation os integration

A
  • A single EPSP cannot induce an AP E1
  • EPSPs can summate to reach threshold
  • IPSPs can also summate with EPSPs to cancel each other out

*lcan have a ton of sympases on a single axon hillock

  • if have two stimuli separated in time can caue EPSP that od not add together
29
Q

What is temporal summation

A

Temporal summation: One or more presynaptic neurons transmit impulses in rapid-fire order

*2 excitatory stimuli close in time cause EPSPs that add together.

*sends another signal quick enough to get an AP

30
Q

What is spatial summation

A

Spatial summation: Postsynaptic neuron is stimulated by a number of terminals at same time

*multiple signals from different synapses -> these are graded potentials, can be depolarizing or hyperpolarizing

31
Q

What is synaptic potentiation?

A
  • type of integration
  • Repeated use increases efficiency of neurotransmission (Long-Term Potentiation)
  • Ca2+ concentration increases in presynaptic terminal & postsynaptic neuron
32
Q

What are the steps of synaptic potentation

A
  1. Glutamate binds to AMPA and NMDA channels
  2. Net Na+ entry throuhg AMPA channels depolarizes the psot syaptic cell
  3. Depolarization ejcts Md2+ form NMDA receptor channel and opens channel
  4. Ca2+ enters cytoplasm throuhg NMDA channel
  5. Ca2+ activates second messenger pathways
  6. paracrine from post synaptic cell enhances glutamate release
33
Q

describe presynaptic inhibition integration

A
  • Release of excitatory neurotransmitter by one neuron may be inhibited by activity of another neuron via an axoaxonic synapse

• Less neurotransmitter is released & smaller EPSPs are formed