Nerves and Synapses Flashcards

1
Q

Neurones resting state?

A

The outside of the membrane is positively charged compared to the outside
Membrane is polarised - difference in charge (potential difference or voltage)
Voltage across the membrane at rest is called resting potential = -70mV
Maintained by sodium-potassium pumps and potassium ion channels

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2
Q

Work of sodium-potassium pumps and potassium ion channels to maintain resting rate?

A

Sodium-potassium pump - actively transport three sodium ions out (membrane not permeable to sodium ions so they don’t diffuse back in) for every two potassium ions moved in - negative charge inside neurone - sodium ion electrochemical gradient - requires ATP
Potassium ion channel - allow facilitated diffusion of potassium ions (K+) out of the neurone, down the concentration gradient - membrane permeable so some diffuse back out

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3
Q

Action potential?

A

Stimulus - Excites the neurone cell membrane - sodium ion channels open. Membrane becomes more permeable to sodium - sodium ions diffuse into the neurone down the sodium ion electrochemical gradient - makes the inside of the neurone less negative
Depolarisation - Potential difference reaches threshold - (-55mV), more sodium ion channels open - more sodium ions move rapidly into the neurone
Repolarisation - Potential difference of +30mV causes the sodium ion channels to close and potassium ion channels to close - membrane is more permeable to potassium - potassium ions diffuse out - down the gradient - membrane back to its resting potential
Hyperpolarisation - potassium ion channels are slow to close - ‘overshoot’ - too many potassium ions diffuse out of the neurone - potential difference becomes more negative than the resting potential
Resting potential - ion channels are reset - sodium-potassium pump returns the membrane to the resting potential and maintains it

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4
Q

Wave of depolarisation?

A

Action potential - some sodium ions that enter neurone diffuse sideways
Sodium ion channels in the next region of the neurone open and sodium ions diffuse into that part
Causes wave of depolarisation
Wave moves away from the parts of the membrane in the refractory period because those parts can’t fire an action potential

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5
Q

Discrete impulses?

A

During the refractory period, ion channels are recovering can’t be opened
Acts as a time delay between one action potential and the next:
Action potentials dont overlap, pass along as discrete (separate) impulses
Limit to the frequency at which the nerve impulses can be transmitted
Action potentials are unidirectional (only travel in one direction)

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6
Q

All or nothing?

A

Once the threshold is reached, an action potential will always fire with the same change in voltage, no matter ow big the stimulus is
No threshold reach, no action potential
A bigger stimulus will only affect the frequency of the action potentials

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7
Q

Factors that affect the speed of conduction of action potentials by neurones?

A

Myelination
Axon diameter
Temperature

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8
Q

Myelination?

A

Myelin sheath - electrical insulator - made of Schwann cell
Between the Schwaan cells are patches of are mebrane - nodes of Ranvier - sodium ion concentrated
In a myelinated neurone, depolarisation only happens at the nodes of Ranvier - sodium ions can get through the membrane here
Neurones cytoplasm conducts enough enough electrical charge to depolarise the next node - impulse ‘jumps’
Saltatory conduction - really fast
In a non-myelinated neurone - impulse travels as a wave along the whole length of the axon membrane (depolarisation along the whole length of the membrane)
This is slower

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9
Q

Axon diameter?

A

Action potentials conducted along axons with bigger diameters - less resistance to the flow of ions - depolarisation reaches other parts of the neurone cell membrane quicker

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10
Q

Temperature?

A

Speed of conduction increases with temperature - ions diffuse after - only up to 40 degrees as proteins begin to denature

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11
Q

Structure of synapses?

A

A junction between two neurones or neurone and effector cell
Tiny gap between cells is called synaptic cleft
Presynaptic neurone has a swelling called a synaptic knob - contains synaptic vesicles filled with chemicals called neurotransmitters

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12
Q

Process of synapses?

A

Action potential reaches end of a neurone - neurotransmitters released - into the synaptic cleft - diffuse across the postsynaptic membrane - bind to specific receptors - trigger an action potential in neurone or muscle contraction in effector muscle cell or hormone secretion in gland cell effector
Receptors only on the postsynaptic membrane - impulses are unidirectional
Neurontrnasmitters are removed from the cleft so the response stops - taken back into the presynaptic neurone - broken down by enzymes
Neurotransmitters - acetylcholine (ACh) and noradrenaline - synopsis that use ACh are called cholinergic synapses

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13
Q

How ACh transmits a nerve impulse across a synapse?

A

Action potential arrives at the synaptic knob of the presynaptic neurone
Stimulates voltage-gated calcium ion channels in the presynaptic neurone to open
Calcium ions diffuse into the synaptic knob
Influx of calcium ions into the synaptic knob causes the synaptic vesicles to move to the presynaptic membrane. They fuse with the presynaptic membrane.
Vesicles release ACh into the synaptic cleft - excytosis
ACh diffuses across the synaptic cleft and binds to the specific cholinergic receptors on the postsynaptic membrane
Sodium ion channels in the postsynaptic neurone open
Influx of sodium ions into the postsynaptic membrane causes depolarisation. Action potential on the postsynaptic membrane is generated if the threshold is reached.
ACh is removed from the synaptic cleft so the response doesn’t keep happening. Broken down by the enzyme acetylchloinesterase (AChE) and the products are reabsorbed by the postsynaptic neurone and are used to make more ACh

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14
Q

Types of neurotransmitters?

A

Excitatory - depolarise the postsynaptic membrane - make it fire an action potential if threshold is reached -ACh at cholinergic synapses in the CNS
Inhibitory - hyper polarise the postsynaptic membrane (make potential difference more negative) - prevents action potential firing - ACh at cholinergic synapses in the heart - potassium ion channels open on postsynaptic membrane - hyperpolarises

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15
Q

Summation?

A

The effect of neurotransmitter released from many neurones is added together to reach the threshold
Both types of summation mean synapses accurately process information, finely tuning the response

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16
Q

Spatial summation?

A

Many neurones connect to one neurone
Small amount of neurotransmitter released from each added together reaches the threshold in the postsynaptic neurone to trigger an action potential
If the neurone release an inhibitory neurotransmitter then the total effect might be no action potential

17
Q

Temporal summation?

A

Two or more nerve impulses arrive in quick succession from the same presynaptic neurone
Action potential more likely because more neurotransmitter is released into the synaptic cleft

18
Q

Neuromuscular junction?

A

Synapse between a motor neurone and a muscle cell

Use the neurotransmitter ACh) - bind to cholinergic receptors called nicotinic cholinergic receptors

19
Q

Process of Neuromuscular junction?

A

Same as cholinergic synapse except for:
Postsynaptic membrane has lots of folds that form clefts - store the enzyme that breaks down ACh (acetylychoilesterase) AChE
Postsynpatic membrane has more recptors
ACh is always excitatory at a neuromuscular junction - motor neurone fires an action potential it normally triggers a response in a muscle cell

20
Q

Ways in which drugs effect synaptic transmission?

A
  • Some are same shape as neurotransmitters so they mimic their action at receptors (agonists) - more receptors are activated - nicotine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain
  • Some block receptors so they can’t be activated by neurotransmitters (antagonists) - fewer receptors can be active - could cause paralysis of muscles
  • Some inhibit the enzyme that breaks down neurotransmitters - more neurotransmitters in the synaptic cleft to bind to receptors - longer activation - loss of muscle control
  • Some stimulate the release of neurotransmitter from the presynaptic neurone so more receptors are activated - amphetamines
  • Some inhibit the release of neurotransmitters from the presynaptic neurone - fewer receptors are activated - alcohol