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Physiology > Receptor And Synaptic Potentials > Flashcards

Receptor And Synaptic Potentials Flashcards

1
Q

What does the Axon hillock do?

A

Can convert graded EPSPs to (all or none) action potential

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2
Q

What does the Axon terminals do?

A

Axon terminals converts electrical signals (e.g., action potentials ) to chemical signals

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3
Q

What do Axons do?

A

Axon conducts action potentials to axonal terminals. Propagation of action potentials hastened with myelination and increased axonal diameter

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4
Q

What do dendrites do?

A

Dendrites convert chemical signals into graded summating postsynaptic potentials (i.e., EPSPs, IPSPs)

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5
Q

What is a graded potential?

A
  • Amplitude graded- dependent on stimulus intensity
  • Decay over time and distance
  • Ligand gated ion channels
  • Example ligsnds - neurotransmitters (e.g., acetylcholine )
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6
Q

What dies graded potential vary in amplitude?

A
  • stimulus due to Ligand binding to receptor at synapse (e.g. acetylcholine)
  • Occur at dendrites, soma, terminal, neuromuscular junction
  • Amplitude relates to stimulus intensity
  • Signal amplitude decays with from point of initiation
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7
Q

What is excitatory postsynaptic potentials (EPSPs)?

A

Input is excitatory —> depolarization of membrane potential (Vm)

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8
Q

What is inhibitory postsynaptic potentials (IPSPs)?

A
  • Input is inhibitory —> no depolarization as membrane potential (Vm) pushed further from threshold
  • Hyperpolarization: inhibitory neurotransmitters (e.g., GABA) can cause influx of negative ions (e.g., Cl-)
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9
Q

How are inputs integrated on the some/cell body?

A
  • Summation

- EPSP/IPSP

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10
Q

What is summation?

A

When multiple signals arriving at the trigger zone are superimposed (summed)

  • temporal
  • spatial
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11
Q

What is temporal summation?

A

Change in frequency of stimulation (time)

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12
Q

Explain a temporal summation

A
  • Single presynaptic neuron fires many times in quick succession
  • Increased frequency- graded potentials sum together
  • If summed graded potentials reach threshold —> generates action potential.
  • Depends on passive properties (time constant) of cell membrane
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13
Q

What is spatial summation?

A

Multiple inputs at different locations on neuron (space)

  • PSPs arriving at the trigger zone (axon hillock) at the same time can summate.
  • Sufficient spatial summation of EPSPs can trigger action potentials
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14
Q

What are the series of events caused by an EPSPs and spatial summation ?

A
  1. Three excitatory neurons fire. Their graded potentials separately are all below threshold.
  2. Graded potentials arrive at trigger zone together and sum to create a suprathreshold signal.
  3. An action potential is generated
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15
Q

What is an action potential?

A
  • All-or-none (I.e., present-or-absent), amplitude often less subject to modulation (I.e., largely independent of stimulus size)
  • Voltage gated ion channels
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16
Q

List sequentially major synaptic events that move an action potential from the pre- to post-synaptic potentials

A

Graded potentials > threshold > action potentials

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17
Q

What are the Action potential (AP) features?

A
  1. All-or-none: action potentials ONLY occurs if stimulus > threshold, if not then no AP
  2. Stimulus magnitude: has greater impact on frequency of firing of action potentials
  3. Amplitude: generally no loss in action potential (AP) amplitude during conduction over the length 9f the axon (but, amplitude can be modulated at the terminal)
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18
Q

In the conversion of graded to action potentials, voltage of summated EPSPs must be above threshold, why?

A

Voltage of summated EPSPs must be above threshold at which a certain # of voltage gated Na+ channels open and initiate an action potential

19
Q

What is propagation of the action potential?

A

AP initiated at axon hillock
(Summation/EPSP/IPSP > action potential)

  • but how is that signal then sent down an axon?
    1. Depolarization in one area
    2. Followed by repolarization in that area with depolarization moving dish (wave of action potential )
    3. That area then has a period of resting and repolar8zation cint8nues to move down
20
Q

What role does the Axon hillock/threshold have in propagation ?

A

Axon hillock/threshold

  • Voltage-gated Na+ channels largely absent on soma and dendrites. Hillock (junction of soma and axon) is heavily populated with voltage-gated Na+ channels
  • if graded potentials depolarization > threshold, signal converted to action potential
21
Q

What events occur during propagation of action potential

A
  • membrane depolarization rapid influx of Na+
  • depolarization of one axonal region —> positive charge flows to adjacent regions and propagate depolarization
  • Voltage gated Na+ channels open in adjacent region and AP moves down axon
  • Action potential propagates without losing amplitude
22
Q

What happens after an action potential is propagated?

A

Refractory period of action potential

-in refractory region, voltage gated Na+ channel inactivation gate closed

23
Q

Summarize the steps of the propagation of the action potential

A
  1. A graded potential above threshold reaches the trigger zone
  2. Voltage-gated Na+ channels open and Na+ enters the axon.
  3. Positive charge flows into adjacent sections of the axon by local current flow
  4. Local current flow from the active region causes new sections of the membrane to depolarize p
  5. The refractory period prevents backward conduction. Loss of K+ from the cytoplasm repolarizes the membrane
24
Q

How does conduction of action potential along an axon occur?

A
  • passive

- saltatory in myelinated axons

25
Q

Describe the distribution of voltage-gated channel

A

Unmyelinated axon

Dense distribution at impulse initiation zone

Myelinated axon

Dense distribution at impulse initiation zone

Dense distribution between nodes of Ranvier

At Nodal-paranodal-juxtaparanidal region(node of ramvjer before terminal)

Na+ = nodal +terminal

K+ = paranodal + juxtaparanodal

Ca +2= terminal

26
Q

How does a myelin sheath effect conduction of action potential?

A

Rapid conduction in myelinated axons

27
Q

How is velocity affected by axonal diameter?

A

High intracellular resistance = short length constant

This causes lower velocity in small diameter neurons

Low intracellular resistance = long length constant

Tsmall very similar to Tlarge

28
Q

Contrast the amplitude of action and graded potentials

A

Graded potentials- amplitude varies with intensity of stimulus, I.e., the response is graded

Action potential- Once the threshold is reached, the amplitude of an action potential is not dependent on the initial stimulus, I.e., it is an all or none phenomenon

29
Q

Contrast the threshold of graded and action potentials

A

Graded potentials- there is no threshold

Action potential- there is a threshold

30
Q

Contrast the refractory period of graded and action potentials

A

Graded potentials- there is no refractory period

Action potential- there is a refractory period

31
Q

Contrast the duration of graded and action potentials

A

Graded potential- Duration is dependent on the initial stimulus

Action potential- duration is constant

32
Q

Contrast conduction of graded and action potential

A

Graded potential- conduction decreases with decreases with distances (decremental conduction)

Action potential- conduction is not decremental

33
Q

Constrast the depolarization occurrences of graded and action potentials

A

Graded potential- can be depolarizing or hyperpolarizing

Action potential- are always initiated by depolarization

34
Q

Contrast the summation of graded potentials and action potentials

A

Graded potential- summation can occur

Action potential- no summation occurs

35
Q

Contrast the mediation of graded potentials and action potentials

A

Graded potentials- are mediated by a receptor (ligand gated)

Action potential- Are mediated by voltage-gated ion channels

36
Q

What are electrical events at a synapse ?

A
  • Action potential in presynapse result in calcium ion influx at axonal terminal/presynapse
  • Neurotransmitter stored within vesicles released into synaptic cleft as free neurotransmitter (T)
  • Neurotransmitter (T) binds to ligand-gated ion channels - provokes graded potential
  • Conversion of signals electrical (presynaptic) —> chemical —> electrical (postsynaptic)
37
Q

What is the neuromuscular junction ?

A

Functional interface between a motor neuron and a muscle cell

38
Q

What happens at the neuromuscular junction?

A
  • Nerve impulse converted to a muscle action potential

- Where disease, inhibition, by drugs/poisons occurs (botulism, curare,etc.), yielding weakness or spasm

39
Q

List the steps involved in in neuromuscular transmission in skeletal muscle and point out location of each step

A
  • Acetylcholine released from synaptic vesicles into synaptic cleft
  • ACh diffuses across cleft
  • ACh binds to nicotinic receptors in the sacrolemma
  • Na+ influx through nicotinic receptors (ligand-gated ion channels)
  • Channels induced graded endplate potential (EPP)
  • The EPP migratesacross motor endplate surface (membrane)
40
Q

What is the graded response to the neuromuscular junction ?

A

Graded response

-Under normal conditions ACh released results in suprathreshold EPP

41
Q

Describe the action potential of the neuromuscular junction

A

EPP migrated along muscle cell surface to activate voltage-gated Na+ channels present

-Depolarization of muscle cell surface due to opening of voltage-gated channels, triggering action potentials

42
Q

What is Myasthenia Gravis?

A

Severe muscle weakness

  • Autoimmune disease: Auto-antibodies bind to and decrease # nicotinic acetylcholine (ACh) receptors at skeletal muscle neuromuscular junction (NMJ)
  • Muscular weakness is elicited due to a decrease in the response of the muscle fiber to acetylcholine
43
Q

What are the symptoms of Myasthenia Gravis?

A
  • Weakness of the eyelids, eye muscles, oropharyngeal muscles, and limb muscles. Increased during exercise and reduced by rest
  • Diplopia (“double vision”), ptosis(“drooping”) of Both eyelids after repeated blinking exercises
44
Q

What are the treatments for Myasthenia Gravis?

A

Anticholinesterase drugs (e.g., neostigmine). Inhibition of acetylcholinesterase allows released ACh to remain at the NMJ (unhydrolyzed) for a longer time and increases the chances of its interaction with the nAChRs

Physiology (36 decks)

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