Unit 2- Excitable cells Flashcards

1
Q

Describe the basic structure and function of a neurone.
How do they:
-Receive signals
-Integrate incoming signals
-Communicate signals to target cells

A
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2
Q

What can speed up cell communication?

A

1- Myelination:Insulation
>Depolarisation at Nodes of Ranvier only→saltatory conduction (impulse jumps from node to node)
> Impulse doesn’t travel whole axon / no need to depolarise along whole length of axon unlike non-myelinated neurone
2- Axon diameter
> Bigger diameter Less resistance to flow of ions
>Larger membrane = more ion channels
3- Temperature
> Increases rate of movement of ions Na+ and K+ as more kinetic energy (active transport /
diffusion)
> Higher rate of respiration (enzyme activity faster) so ATP produced faster and energy
released faster→active transport faster
»But proteins could denature at a certain temperature

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3
Q

Define membrane potential? What are the 3 factors that mainly determine this?

A
  • Distribution of charge across the cell membrane
    1. Conc of ions on the inside and outside cell
    2. Permeability of cell membrane to ions e.g. specific ion channels
    3. Activity of electrogenic pumps that maintain the ion conc across the membrane
    >Inside of cell is more negative : Polarised
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4
Q

How is a neuronal resting potential generated? -70mv

A
  • Sodium-potassium ion pump actively transports:
    > 3 sodium ions out of axon
    > 2 potassium ions into axon
  • Electrochemical (concentration) gradient created e.g. higher conc. of potassium ions inside axon than outside, higher conc. of sodium ions outside axon than outside
  • Membrane more permeable to potassium ions (open K+ channels) than sodium ions (closed Na+ channels)
  • Potassium ions move out of axon by facilitated diffusion
    > Inside of axon negatively charged relative to outside; axon is polarised = resting potential
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5
Q

How are graded potentials generated?

A

-Temporary local changes in membrane potential
-Dependent on strength and duration of triggering event
-Short distant signals
-Spread by passive current flow, potential reduces as it moves away from triggering stimulus
-Dependent on specific ion channels activated in cell membrane
- *If generator potential reaches threshold (-55) it triggers an action potential

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6
Q

How are action potentials generated?

A
  • Stimulus
    1. RESTING POTENTIAL: Na+ inactivation gate opens , activation gates are closed
    2. At threshold (around -50mV), Na+ activation gate rapidly opens and permeability of Na+ rises
  • Na+ inactivation gate starts to slowly close and the K+ activation gate starts to slowly open
    3. ACTION POTENTIAL BEGINS : Na+ enters cell causing depolarisation
    4.At peak (+30mv) of action potential, Na+ inactivation gate closes and K+ activation gate is open
    4. The permeability of Na+ falls. At the same time, K+ activation gates open and K+ permeability rises. K+ leaves cell causing repolarisation
    5. Na+ activation gate is closed and inactivation gate is open at RMP. Further outward movement of K+ through still-open K+ channel briefly hyperpolarises membrane.
    6. Once K+ channels close, membrane returns to resting potential by Na+/K+ pump
  • Note: bigger stimulus will cause more frequent action potentials but they will all be the same size
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7
Q

What is the refractory period? What is the need for it?

A

-After AP where membrane is not as exitable
-K+ channels are open Na+ channels closed
-Requires greater stimulation to reach threshold
- Importance:
1. Produces discrete and discontinuous
impulses > process info properly
2. Limits frequency of impulse transmission at a low intensity > higher intensity stimulus causes higher frequency of action potentials but only up to certain intensity, prevents overwhelming hindering survival.
3. Unidirectional action potential , action potential in 1 way so resting potential re-generated.

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8
Q

What is synapse? 3 Types ?

A
  • The connections between neurons are called synapses.
  • The synaptic connections between neurons & skeletal muscle cells are generally called neuromuscular junctions.
  • The connections between neurons & smooth muscle cells or glands are known as neuroeffector junctions.
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9
Q

Describe the process of synaptic transmission. Neurone > Neurone

A

*influx of calcium.
* Facilitates formation of the
docking complex.
* Once docking is accomplished, additional proteins, under the influence of elevated intracellular calcium levels, associate to form a fusion pore.

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10
Q

Describe the process of synaptic transmission.
Neurone > Muscle

A
  • AP depolarizes the presynaptic neurone, → influx of calcium through the voltage-gated membrane channels.
  • Synaptic vesicles fuse with the presynaptic membrane & release ACh into the synaptic cleft.
  • ACh binds to receptors on the postsynaptic membrane & opens ion channels. Ion flux then occurs, & a depolarizing potential END PLATE POTENTIAL spreads over the surface of the muscle fiber.
  • EPP triggers the release of calcium (from sarcoplasmic reticulum), which elicits the movement of actin & myosin filaments, resulting in muscle contraction.
  • Synaptic transmission is terminated by acetylcholinesterase → acetate & choline.
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11
Q

What are excitatory/inhibitory post synaptic potentials?

A
  • If a neurotransmitter is excitatory and produces a depolarizing PSP, we refer to the PSP as an
    excitatory postsynaptic potential (EPSP).
  • If the neurotransmitter is inhibitory and produces a hyperpolarizing PSP, the
    PSP is an inhibitory postsynaptic potential (IPSP).
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12
Q

What is spatial and temporal summation?

A

-The sum of excitatory or inhibitory post synaptic potentials
* Spatial summation occurs when subthreshold impulses from two or more synapses trigger an AP because of synergistic interactions.
* Temporal summation occurs when a series of subthreshold EPSPs in one excitatory fiber produce an AP in the postsynaptic cell.
* This occurs because the EPSPs are superimposed on each other temporally before the local region of membrane has completely returned to its resting state.

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13
Q

When are action potentials more likely? (Action potential propagation)

A

-expression of voltage-gated Na+ channels at dendrites vs. soma vs. axon hillocks.

  • It begins in the initial segment of the axon where the axon leaves the neuronal soma.
  • The membrane of the initial segment has seven times as great a concentration of voltage-gated sodium channels as the soma and, therefore, can generate an action potential with much greater ease than can the soma.
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14
Q

What are the criteria for neurotransmitters?

A
  1. Must be synthesized & stored in pre-synaptic neurons.
  2. Released from presynaptic endings of the neuron in response to the appropriate stimulus (such as an action potential).
  3. There is binding and recognition of the putative neurotransmitter molecule on the postsynaptic target cell.
  4. Mechanism exists for the inactivation and termination of the biological activity of the neurotransmitter.
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15
Q

What are some of the key neurotransmitters?

A

> ACH ( Acetyl choline) - made from choline + acetyl CoA = muscles
GABA : Inhibitory
Glutamate : Exitatory

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16
Q

Compare excitatory / inhibitory synapses?

A

> An excitatory transmitter promotes the generation of an action potential in the postsynaptic neuron, while an inhibitory transmitter prevents it.
Exitatory:
1. Opening of sodium channels
2. Depressed conduction through chloride or potassium channels, or both.
3. Various changes in the internal metabolism of the postsynaptic neuron to excite cell activity or, in some instances, to increase the number of excitatory membrane receptors or decrease the number of inhibitory membrane receptors.

> Inhibitory:
1. Opening of chloride ion channels through the postsynaptic neuronal membrane.
2. Increase in conductance of potassium ions out of the neuron.
3. Activation of receptor enzymes that inhibit cellular metabolic functions or that increase the number of inhibitory synaptic receptors or decrease the number of excitatory receptors.

17
Q

What is special about Acetylcholine?

A
  • The neurotransmitter Acetylcholine (ACh) is excitatory at the neuromuscular junction in the skeletal muscle, causing muscles to contract.
  • In contrast ,it is inhibitory int the heart, where it slows heart rate.
  • These opposite effects are possible because two different types of ACh receptor proteins are found in the two locations.