Neuroscience and Clinical Semester 1 Week 2: Neural conduction and synaptic transmission Flashcards

1
Q

What is the resting membrane potential?

A

The difference in electrical charge between the inside and outside of a neuron at rest, typically around -70mV. It arises due to an uneven distribution of ions across the membrane.

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2
Q

What are the two main types of ions?

A
  • Cations (positive ion)
  • Anions (negative ion)
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3
Q

The solutions inside the cell (intra-cellular) and outside the cell (extra-cellular) are mostly composed of water and which ions?

A
  • Potassium (K+)
  • Sodium (Na+)
  • Calcium (Ca2+)
  • Chloride (Cl-)
  • Larger organic and inorganic ions (A-) (mainly inside)
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4
Q

How does the passive process establish the resting membrane potential?

A
  • At rest, the membrane is relatively impermeable to many ions, except potassium (K+)
  • The potassium ions move from high concentration to low concentration through the membrane, causing an uneven distribution of charge.
  • Selective diffusion of potassium establishes a membrane potential.
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5
Q

How does the active process establish the resting membrane potential?

A
  • Sodium-potassium pump
  • Transports Na+ out and K+ in
  • 3 Na+ for every 2 K+ - Leaving behind a negative potential -> passive process
  • Requires energy supplied by ATP
  • Other pumps redistribute Ca2+ and Cl- (amongst other things)
    *Too much calcium will kill a neuron
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6
Q

Depolarisation

A

If the membrane potential is made less negative

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7
Q

Hyperpolarisation

A

If the membrane potential is made more negative

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8
Q

What voltage-gated channels?

A

Ion channels that open in response to a change in the membrane potential.

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9
Q

Action potentials

A
  • Sodium channels open - sodium ions flow in, causing the membrane to be more positive. (up curve)
  • If the membrane is depolarised beyond the threshold, an action potential process is triggered.
  • Action potential triggered
  • Sodium channels close and potassium channels open
  • Potassium ions flow out (down curve)
  • Restores resting membrane potentia
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10
Q

What is the absolute refractory period?

A
  • brief time during and after an action potential when a neuron cannot fire another action potential, no matter how strong a stimulus is.
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11
Q

What is the relative refractory period?

A
  • the period that follows the absolute refractory period. During this time, the neuron can fire another action potential, but it requires a much stronger stimulus than usual.
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12
Q

How do action potentials travel down an axon?

A
  • Action potentials propagate by the passive flow of charge
  • Action potentials are regenerated continuously as it goes down the axon
  • When one part of a membrane is depolarised, this opens adjacent sodium channels further down the axon and triggers another action potential and so on.
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13
Q

How is the process of action potentials travelling down the axon sped up by myelin?

A

The action potential travels down an axon more quickly when there is myelin, and the myelin acts as insulation and allows the action potential to travel further along the axon before needing to be regenerated.

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14
Q

What is a synapse?

A

A point of specialised contact between two neurons where a process (axon) of the presynaptic cell contacts the receiving area of the postsynaptic cell.

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15
Q

Structure of Synapse

A
  1. Presynaptic element
    Vesicles - contain neurotransmitter
    60+ suspected neurotransmitter candidates identified so far
  2. Synaptic cleft
    Physical space between presynaptic and postsynaptic cell, 20-40nm
  3. Postsynaptic element
    This may be:
    - A dendrite (axodendritic synapse)
    - A cell body (axosomatic synapse)
    - A terminal bouton (axo-axonal synapse) - a synapse on a synapse
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16
Q

Synaptic transmission 1: Neurotransmitter synthesis and storage

A

Neurotransmitters are synthesised in the neuron and stored in high concentrations in synaptic vesicles located in the presynaptic terminal.

17
Q

Synaptic transmission 2: Arrival of action potential

A

When an action potential travels down the axon, it depolarises the presynaptic membrane, causing voltage-gated calcium channels to open. Calcium ions then flood into the cell.

18
Q

Synaptic transmission 3: Vesicle fusion and neurotransmitter release

A

The influx of calcium facilitates the binding of vesicles to the presynaptic membrane, causing them to undergo exocytosis and release neurotransmitters into the synaptic cleft.

19
Q

Synaptic transmission 4: Endocytosis and vesicle recycling

A

After neurotransmitter release, vesicle membranes are retrieved from the presynaptic membrane through endocytosis, and new vesicles are formed using these retrieved membrane components.

20
Q

Synaptic transmission 5: Binding to postsynaptic receptors

A

Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane, which can result in excitatory or inhibitory effects on the postsynaptic neuron.

21
Q

Synaptic transmission 6: Neurotransmitter inactivation

A

Neurotransmitters are inactivated through mechanisms such as enzymatic degradation, reuptake into the presynaptic neuron, or diffusion away from the synaptic cleft.

22
Q

Speed of synaptic transmission

A

Action potential to secretion < 200 μs
Diffusion across synapse, 1-2 ms

23
Q

What are receptors and how do they work?

A
  • Neurotransmitters bind to receptors on the postsynaptic element and this results in the opening of ion channels (types of transmembrane proteins).
  • The channels allow certain ions to flow through them, which have either a +ve or -ve charge.
  • It is the flow of charged particles through the channels opened by neurotransmitters that produce the effect on the postsynaptic cell.
  • The effect of neurotransmitters on the cell is dependent on which kind of channel they open.
24
Q

What are the two types of receptors?

A

1) Ionotropic
Receptors directly associated with an ion channel (physical connection)

2) Metabotropic
A ‘biochemical cascade’ links the receptor to the ion channel (no physical connection, chemicals connect them)

25
Q

How does synaptic activation affect the likelihood of action potentials?

A

1) If channel opening causes entry of +vely charged ions:
- Depolarisation; ‘excitatory postsynaptic potential’
- Makes cell more likely to fire an action potential
- Substance referred to as excitatory neurotransmitter (e.g. glutamate)

2) If channel opening causes entry of –vely charged ions
- Hyperpolarisation; Inhibitory postsynaptic potential
- Makes cell less likely to fire an action potential
- Substance referred to as inhibitory neurotransmitter (e.g. GABA)

26
Q

How are neurotransmitters inactivated?

A

The neurotransmitter is removed from the synaptic cleft either by:

  • Reuptake -> active transport back into presynaptic element
  • Diffusion
  • Glial cells
  • Breakdown by enzymes - products actively transported into presynaptic element or into glial cells

If taken back to presynaptic element, the neurotransmitter can be resynthesised

27
Q

How can drugs interfere with synaptic transmission?

A
  • Causing release (amphetamine)
  • Mimicking the action ([agonists] barbiturates )
  • Blocking the action ([antagonists] ketamine)
  • Blocking reuptake (cocaine)
  • Medical uses e.g. Fluoxetine (depression; blocks the reuptake of 5-HT)