Lecture 5: Neuronal Transmission 2 - Synapses and Circuits Flashcards

1
Q

How do sodium channels cause a positive feedback loop?

A

Increase in Na+ -> Depolarise membrane potential -> Open Na+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Do action potentials change in ‘strengths’/levels

A

Action potentials either happen or not. They do not change in that sense but can change in frequency i.e. how often they happen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is involved in action potential propagation/spread along the axon

A

They are all the same size along the axon.
As it moves down the axon, it depolarises the next bit of membrane and opens sodium channels. Spreads like a wave as sodium channels are activated. If enough channels are opened, the membrane potential reaches the threshold potential and the action potential propagates along. The area that has just generated an action potential cannot fire another as the Na+ channels are now inactivated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the action potential propagation speed

A

0.1 m/s to 100m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why is the action potential propagation speed so variable?
1) what is the membrane potential change affected by?
2)How far depolarisation can spread along the axon is affected by?

A

1)
– leakiness/resistance of membrane – slower if more charge can leak out
– capacitance of cell –how easy it is to change the membrane voltage. Large
membrane = large capacitance – takes a lot of charge to change membrane voltage.
2)
– membrane resistance - more leaky membrane -> depolarisation spreads
less far
– diameter (internal resistance to flow down the axon) – big diameters
conduct faster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What wraps myelin sheaths around an axon, how do myelin sheaths aid in neural conduction and what is this conduction called?

A

Oligodendrocytes wrap myelin sheaths around axons and the conduction is called saltatory conduction. Myelin insulates the membrane so less charge loss/leak therefore faster conductance because it does not need to regenerate the ion channels. Action potentials travel and jump across from one node of Ranvier to another = saltatory conduction. (salt=sodium boost). It’s faster and more efficient as there are fewer ion slow so less ATP needed for pump channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Label a neuron cell

A

-Cell body/axon
- action potential
- pre-synaptic (sending) cell
- axon terminals/dendrites
-synapses
- post-synaptic (receiving) cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain the stages of neuronal transmission

A

1.Action potential arrives at axon terminal
2. This depolarises the membrane which opens voltage-gated calcium channels. (-10mV)
3. Calcium inside the cell causes vesicles of neurotransmitter to fuse with membrane.
4. Neurotransmitter diffuses through synaptic cleft.
5. Neurotransmitter binds to ligand-gated sodium/potassium ion channel (cation channel)(activated when a molecules binds to it)
6. Ion flow through the channel, depolarising or hyperpolarising the post-synaptic membrane. (i.e. may trigger excitatory postsynaptic potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a ligand gated ion channel

A

A channel that is activated and opens when binding to a specific molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain excitation with glutamate

A

Glutamate is the major excitatory neurotransmitter in the brain. It makes the next cell more likely to fire.
Depolarisation of dendrites by ion flow through glutamate receptors generates an excitatory post-synaptic potential (EPSP) - drives membrane potential towards the threshold for action potential firing.
(60-70% of synapses in mammalian brains use glutamate as a neurotransmitter.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What receptor is essential for glutamate excitation and how does it do this?

A

AMPA receptors are glutamate receptors which when binded to, they open the ion channels (cation/ligand-gated) allowing sodium and potassium ions to come into the nerve cell/pre-synaptic terminal.
Sodium will come in more than potassium due to the size of the gradient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does the NMDA receptor work

A

NMDA receptors are ion channels that need to bind to glutamate AND be depolarised to open. It is blocked by a magnesium ion. They also let calcium in which cause changes to the synapse to make it work better or worse - important for associative learning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do Megabotropic glutamate receptors do

A

Bind glutamate and trigger lots of intracellular signalling pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is summation and why is it needed? Give the two types of summation.

A

A single esp/synapse being activated will not create enough of a depolarisation to let the membrane reach the threshold (-55mV) for the sodium/potassium voltage gated channels to open. Temporal summation can happen if the same axon fires a rapid burst of action potentials which keeps releasing vesicles of glutamate for longer period of time so repeated epsps which add up or spatial summation happens when signals from different synapses arrive at the same time and add up = increased depolarisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is summation different to action potentials

A

You can have different graded amounts of activity with epsp like big or small. Action potentials either happen or they don’t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe inhibition

A

Happens at the postsynaptic membrane - GABA is the main inhibitory transmitter in the brain and it opens chloride channels (GABAa receptors) which allow negative charge into the membrane, generating an inhibitory post-synaptic potential (IPSP) and/or making it harder to depolarise the membrane. It is harder for the threshold for action potential firing to be reached so the cell is less likely to fire an action potential.

17
Q

What is synaptic integration?

A

The summation (adding up) of excitatory and inhibitory inputs at the axon hillock (if it becomes more or less than -55mV).
Input: synapses
Computation: integration
Outputs: action potential

18
Q

In what ways can synaptic integration be influenced

A
  • distance of synapse from axon hillock
  • shape of neuron (e.g. small or complex)/surface area of neuron affects effective distance.
  • location relative to inhibitory inputs (gating).
19
Q

How is information coded in the nervous system through action potentials and synapses

A

short and small stimulus cannot sustain a series of depolarisation and action potentials firing. Larger and longer stimulus will sustain this.

20
Q

How do neuronal networks affect firing of neurons

A

The way neurons wire together affects computations they perform and information they represent.
e.g.
- feedforward excitation - simple straightforward activation from one cell to another.
- feedforward inhibition - exciting one neuron can increase inhibition in the next neuron.
- feedback/recurrent inhibition/lateral inhibition: increases activity of one cell but inhibits other cells at the same time.

21
Q

Example of feed forward excitation and inhibition

A

Knee jerk reflex - excitation of motor neuron excites interneuron in spinal cord and causes constriction in extensor muscle which inhibits motor neuron at flexor muscle so it relaxes.

22
Q

Example of lateral inhibition

A

mach bands illusion - in the retina, enhancing perceived contrast at the edges of objects, creating the illusion of brighter and darker bands at the boundaries of areas with different luminance