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61 Cards in this Set

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  • Back
label this neuron.
What do the red and black arrows represent?

label this neuron.

What do the red and black arrows represent?

red= action potential
black= synaptic potential

red= action potential

black= synaptic potential

There are two types of signals used for communication for neurons. What are these signals and where are these of signal produced?

Chemical signals at the synapses.

Electrical signals along dendrites, axons and cell body.

Most cells in the body have a negative RMP, however only a few respond when there is a transient change to this potential and so are said to be 'excitable'.

What are the cells?

Neurons, Muscle cells and some endocrine cells.

What are the two methods used to measure neuron membrane potential?

Which one can measure current?

microelectrode recording technique, where one FINE microelectrode (with saline solution) is pierced into the neuron, and a reference microelectrode on the outside.

patch-clamp technique where glass pipette is put on the surface of the membrane, putting pressure on it to form a channel with it. This one measures not only the voltage but also current.

What are the three main things that affect resting membrane potential?

1. Unequal concentration of Na+ and K+ inside and outside the cell.

2. Unequal permeability of the cell membrane to these ions

3. Electrogenic action of the Na-K pump (only to a small degree).

How does Na/K pump contribute to RMP?

What goes in and what goes out? how many?

What happens to RMP if this stops?

3Na+ carried outside, 2 K+ carried inside.

Overall, there is 1 positive charge leaving the cell, which is what contributes to making the intracellular matrix more negative.

If Na/K pump stops, it will hardly affect the RMP as it only contributes so little to it

There are two types of channels in the cell. What type of channels are they?

leak and mechanical channels

On the cell membrane of neurons, which ion (Na+ or K+) has the most 'leak' channels?

What does this mean about the permeability of the cell to that ion?

K+ has more leak channels than Na+, so neurons are more permeable to K+ than Na+.

What is the concept of equilibrium potential?

What equation would you use to find this for a particular ion?

It is an intracellular potential at which the net flow of ions is zero, in spite of a concentration gradient and permeability.

The Nernst equation is used to find this.

What is the nernst equation used for?

When can it be used?

What is the equation itself and what is E[ion] proportional to?

It is used to find the equilibrium potential for ions (E[ion]). It can only be used if the cell is permeable to only one ion.

E[ion] = 2.3 x RT/zF x log (ion[o]/ion[i])

R and F are constants. T is temperature, and E[ion] is proportional to this because temperature increases diffusion, hence increasing E[ion].

z is for charge of the ion, and E[ion] is inversely proportional to this, because bigger charge means less E[ion] needed to balance diffusion.

Nernst equation can be simplified to:

E[ion] = a x log (ion[o]/ion[i]).

What would a be equal to for K+,Na+,Ca2+,Cl-?

K+ (a) = 61.5mV

Na+ a = 61.5mV

Cl- a = -61.5mV

Ca2+ a = 30.7mV

A typical neuron cell has more K+ leak channels than Na+ leak channels.

How does this affect RMP?

Cells more permeable to K+, so RMP will be closer to the equilibrium potential of K+.

What is the equilibrium potential for K+, Na+ and Cl-?

E(k) = -80mV

E(Na) = +60mV

E(Cl) = -65mV

What is the goldman equation, and what is it used for?

Goldman equation can be used to find RMP, as it takes into account both concentration gradients and relative permeability of the resting cell membrane to K+ and Na+ ions.

note Vm is resting membrane potential, P is for permeability to that ion.(...

Goldman equation can be used to find RMP, as it takes into account both concentration gradients and relative permeability of the resting cell membrane to K+ and Na+ ions.

note Vm is resting membrane potential, P is for permeability to that ion.(P[k+]/P[Na+] = 40/1, so P[K+] = 40 and P[Na+] = 1).

At rest, what is the permeability of K+ of the membrane compared to Na+

Membrane is 40 times more permeable to K+ compared to Na+.

What type of neuron cell is this?
Where is it found?

What type of neuron cell is this?

Where is it found?

Purkinje cell found in the cerebellum.

What type of neruon is this?
Where is it found?

What type of neruon is this?

Where is it found?

Pyramidal cell, found in the cerebral cortex.

What is hyperpolarisation and depolarization?

Hyperpolarization is when is when the potential in neurons become more negative.

Depolarization if it becomes less negative.

What is an action potential?

Brief fluctuation in membrane potential caused by transient opening of voltage gated ion channels which spread like a wave along the axon.

Also known as a 'spike', 'nerve impulse', 'discharge'.

When does an action potential occur?

After the membrane potential reaches certain voltage called the threshold (~ -55mV).

Action potentials can be regarded as a form of 'language' by which neurons communicate. Why is this so?

Because the information is coded in the frequency of action potentials.

What causes the RMP to shift to a threshold value (around -55mV)?

a stimulus which can be physical (electric current or stretch) or chemical (synaptic excitation).

What are the stages of action potentials?

1. Slow depolarization from RMP to threshold value (-55mV).

2. Then rapid depolarization to around +30 mV (reversal of polarisation or 'overshoot').

3. Repolarization towards RMP

4. After hyperpolarization (goes below -70mV) and then back to RMP.

What is Absolute and Relative refractory period and when do they occur?

In the absolute refractory period, the cell is not 'excitable'. So this is during the stages of rapid depolarization after threshold, and repolarization.

In the relative refractory period, another action potential can be induced, but the stimulus must be stronger than the previous. This is during the final stage where after hyperpolarisation occurs. The potential is below RMP at this point, hence stronger stimulus required to increase this to threshold value.

Explain the mechanism of the rapid depolarization after threshold, and also repolarization.

When MP reaches threshold, sudden activation of voltage gated Na+ channels so permeability of Na+ is now 20 times higher than K+, so MP shift towards E[Na+] -> overshoot.

Opening of voltage gated Na+ channels is short lasting as channels quickly inactivate.

Then followed by opening of voltage gated K+ channels, leading to repolarization and AHP ( now the ratio of P[K+] to P[Na+] is 100:1)

When does the influx of Na+ stop during depolarization?

When the inside potential is positive and attracts Na+ less.

Na+ channels inactivate.

Explain the mechanisms of the activation and inactivation of voltage gated Na+ channels.

Na channel has two separate gates, an activation gate and inactivation gate. 
At start, the activation gate is closed and inactivation gate opened, activation gate will open during depolarization. 
After that, an inactivation gate closes and th...

Na channel has two separate gates, an activation gate and inactivation gate.

At start, the activation gate is closed and inactivation gate opened, activation gate will open during depolarization.

After that, an inactivation gate closes and then goes back to its initial stage when the membrane repolarises.

Each action potential is an all or none event. What does this mean?

The action potential is always measured to be 100mV. There is no in between value, it is either 100mV or does not exist, hence it does not depend on the stimulus intensity, provided the stimulus is suprathreshold.

What does it mean if the stimulus is supra threshold?

The stimulus is able to bring the membrane potential to threshold.

How can electrical currents generate an action potential using two electrodes (cathode and anode?).

Current goes from +ve -> -ve (this is the direction of positive charge, negative charge goes in the opposite direction).

Only when the current goes accross the membrane and inside the axon can it change the RMP. At the anode (+, attract anions) the negative charges accumulate, so MP becomes more negative, so hyperpolarisation occurs. at the cathode (- , attract cations) positive charge accumulates, so MP becomes more positive, so depolarization occurs.

note depolarization goes in both directions of the axon.

How are APs generated physiologically in CNS neurons?

Where is it first generated and why?

What causes this depolarization and where does it come from?

In CNS neurons, APs are first generated in the axon initial segment because it has the lowest threshold.

Depolarization is evoked by EPSPs, excitory postsynaptic potentials which spread passively from dendrites and transmitted actively along the axon away from cell body.

What are the characteristics of mylenated and unmylenated neurons? (ie, size, transport of AP)

unmylenated axons are smaller in diameter, and AP transmission is slow and continuous.

mylenated axons are bigger in diameter, AP transmission is fast and saltatory.

If current generated by an outside source flows through cell membrane from outside to inside, what occurs?

What about from inside to outside?

Outside to inside, hyperpolarization.

Inside to outside, depolarization.

There are two stages of action potential transmission. What are they?

1. Passive spread

2. Active generation of action potential

If there was a depolarised region in the axon, what would happen?

(ie ----------++++----------- , + means polarized region, this is intracellular, extracellular is opposite).

How would this affect action potentials?

How far would this spread?

There would be a passive flow of current from + to - . So adjacent areas are getting depolarized.

This passive depolarisation spreads only a short distance. It dissipates as it flows along the axon.

So where the current is generated into the axon, is where depolarization is strongest.

Depolarises to threshold, then further with opening of voltage gated ion channels, leading to an action potential. Note that in electrical stimulated responses, action potential travels in both directions!!

What is the speed of AP transmission in unmyelinated axons?

Why is this so compared to myelinated axons?

What is the speed of AP transmission in myelinated axons?

1 metre per second.

Slower, because although passive current is fast, AP must be regenerated at every point on the membrane, which is what makes it slower.

20 to 100 m/s for myelinated axons.

Which cells form the myelin sheath in PNS and CNS?

How is the axon myelinated? '

How does this affect depolarisation accross the axon?

Schwann cells in the PNS.

Oligodendrocytes in the CNS.

Mylelination is discontinuous. Intereupted at nodes of Ranvier.

Myelin acts as insulation layer and reduces disipation of current as it flows along the axon.

Why is myelinated axons faster at AP transmission compared to non myelinated AP?

What is the process of AP transmission called?

myelinated axons segmented, current flows out only at the nodes of ranvier, so this is the only point where depolarization occurs and an AP is regenerated, hence why it is faster as it is not continuously regenerated along the whole axon which occurs in non myelinated axons.

This process is called 'saltatory conduction'.

Why under physiological conditions does AP conduct in only one direction?

This is due to the absolute refractory period, by the time it is done (1-2ms) the AP has already moved down the axon and is 3 nodes ahead (myelinated).

What happens when APs pass each other when transmitted from the opposite directions?

What is the direction that AP is transmitted from the body and electrical stimulation?

orthodromic direction when AP comes from the cell body, antidromic direction when produced by electrical stimulation.

They cancel out (called collision) due to the absolute refractory period. ( because as they get closer together, they will still be in the refractory period, and hence they will not be able to go any further as during this period, another signal cannot be produced, so the APs extinguish each other.)

How are APs generated in sensory neurons?

Stimulus acts on receptors in sensory neurons ( eg mechanical stimulus acting on muscle spindle).

This evokes graded depolarisation known as the 'receptor potential' (graded because bigger stretch = bigger amplitude).

This potential spreads passively to the 'trigger zone' where APs are generated.

AP spreads along axon towards CNS. Strength of stimulus is coded in the amplitude of the receptor potential and frequency of APCs.

There are two types of messages that can be sent from one excitable cell (eg muscle cell, neuron) to another excitable cell.

What are they called?

Which one is more common?

Example of where the less common one is found?

Chemical synapses which are more common.

Electrical synapses which are less common, found in retina.

This shows synaptic transmission between neurons. 
What is the link between the axon of one neuron and dendrite of the other called?

This shows synaptic transmission between neurons.

What is the link between the axon of one neuron and dendrite of the other called?

Axo-dendritic synapse

What type of neuron is this?
What is the name of the synaptic connection between the neuron axon and the muscle fibre?

What type of neuron is this?

What is the name of the synaptic connection between the neuron axon and the muscle fibre?

This is a motor neuron.

It is called the neuromuscular junction, or also known as the 'end plate'.

What are the steps of a synaptic response between neuron and muscle fibre?

What is the neurotransmitter in the neuromuscular junction?

Action potential reaches the presynaptic knob (presynaptic potential).

Voltage gated Ca+ channels open, Ca+ goes down its electrochemical gradient (into the cell).

This causes the neurotransmitter vesicles to exit by exocytosis.

Neurotransmitters then activate postsynaptic receptors.

This opens the chemically gated channels, which are NON selective, allowing Na+ and K+ to diffuse down their electrochemical gradient.

So postsynaptic potential produced, causing AP to be produced at the end plate.

Acetylcholine (ACh) is the neurotransmitter

Note that end plate potential is ALWAYS suprathreshold, it always causes an action potential.

There are two main types of chemical synapses in the CNS. WHat are they?

Excitatory synapse, depolarisation of post synaptic membrane, (EPSP - Excitatory post synaptic potential)

Inhibitory synapse, hyperpolarisation of post synaptic membrane (IPSP - Inhibitory post synaptic potential)

What are the neurotransmitters for EPSP and IPSP.

What are the mechanisms (ie what channels open?)

EPSP - Mainly Glutamic acid (glutamate) or ACh. Opens channels selective for Na+ K+ and sometimes Ca+.

IPSP - Mainly GABA (Gamma-aminobutyric acid) or glycine.

Opens channels selective for K+ or Cl- channels.

Neurotransmitters can be classified into two groups (based on chemical structure), what are they?

What are some examples?

Small molecule neurotransmitters, where action is fast and direct on post synaptic receptors.

Includes : amino acids (glutamate, GABA, glycine), ACh, Amines (serotonin (5-Ht), noradrenaline, dopamine), ATP.

Neuropeptides, large molecules where action is slow and indirect (metabotropic) on post synaptic receptors, OR modulatory action (sometimes called neuromodulator) on the effects of other neurotransmitters. More diffuse action (volume transmission).

eg neuropeptide y (NPY), Substance P, kisspeptin, Endorphins

What are the two factors that determine synaptic activity?

1. Type of neurotransmitter or neuromodulator

2. Type of receptors on post synaptic membrane.

Which EPSP neurotransmitter is most widely utilised in the brain?


There are four different post synaptic receptors that glutamate can activate, what are they?

What would happen if too much glutamate is released?

AMPA, NMDA, Kainate receptor, and metabotropic (slow) glutamate receptor.

Note that these are hybrid molecules (receptor + channel).

This will lead to excessive depolarisation and overeaction of neurons.

Of the four post synaptic receptors, NMDA being one of them is different to the others. WHY?

Excessive activation of this channel may cause damage to the neuron. HOW? what is this called?

Because other receptors (AMPA, Kainate etc) are permeable to Na+ and K+ ions, whereas NMDA is permeable to Na+ K+ and Ca2+ ions.

If activated for too long, excessive entry of Ca2+ damages the neuron, this is called exitotoxicity. Too much Ca+ can kill neurons.

Leads to stroke, epilepsy, traumatic brain injury.

How is the neutransmitter inactivated?

It can diffuse away from the synapse. (not a major process).

Enzymatic degradation in the synaptic cleft (Acetylcholine esterase breaking down ACh, monoamine oxidase (MAO) degrades biog Enix amines, peptides cleave neuropeptides.)

Re-uptake , most common (for most amino acids and amines) and recycling. This involves neurotransmitters transporters (in the presynaptic membrane or adjacent cells ie glia cells) Can be taken up by where it came from or adjacent cells (astrocytes, glia cells). Otherwise taken up back into the presynaptic terminals which is one form of glutamate transport. Another form moves glutamate to synaptic vesicles.

How many synapses do neurons receive? What type of synapses?

How strong are the signals these synapses produced and what happens to them as they travel to the axon initial segment?

They recieve 1000 synapses, which can be excitatory or inhibitory.

These individual synapses produce small post synaptic potentials (0.1mV) at axon initial segment.

Potential decays as it goes from dendrite to axon initial segment, so EPSPs must be enhanced to bring the potential at the axon initial segment to threshold.

Chemical synapses have 3 key features, what are they?

1. Specificity - specific neurotransmitters have specific effects on postsynaptic membrane.

2. Complexity - Type, time course, stregth, location, timing etc.

3. Plasticity - Structure and function changes over time, associated with development, aging, learning etc.

Neurotransmitters and neurotransmitter receptors help with the complexity of human sensory, behavioural and cognitive function. How so?

Because there is a diverse range of neurotransmitters and neurotransmitter receptors in the nervous system, which contributes to this complexity of sensory functions etc.

What is the main function of the ion channels activated by EPSPs?

To bring the membrane potential away from the RMP.

IPSPs can increase permeability to chloride and potassium ions in postsynaptic membrane, however both have different effects. How so?

Increasing potassium permeability will cause hyperpolarisation.

Increasing chloride permeability DOES NOT hyperpolarise the membrane, this is because the equilibrium potential of Cl- (-61.5 mV) is quite close to the resting membrane potential. Rather it decreases cell membrane resistance, hence shunting the current induced by excitatory synapses, making the current less efficient (more disipation!) to bringing the cell membrane potential to threshold.

What is spatial summation and temporal summation?

Spatial summation is when two excitatory potentials from separate presynaptic neurons add up to enhance the amplitude of EPSPs to reach threshold.

Temporal summation is when repeated same excitatory potential adds up (however not too frequently due to absolute refractory period) and enhance the amplitude of EPSPs to reach threshold.

By doing this, it helps the cell produce an action potential at the axon initial segment.

Difference between indirect and direct gating?

Direct gating is when neurotransmitter binds to receptor/ion channel complex, open the ion channel. Effects are very fast and short lasting.

Indirect gating is when transmitter binds to receptor (G protein coupled receptor or Metabotropic receptors), activating biochemical pathway, (eg GTP G protein) which produces second messengers such as cAMP, which activates protein kinase, which then phosphorylates specific ion channels. Slower, long lasting.