L33 Synaptic Transmission

Question 1

What is the synaptic region?

Answer 1

Where one neurone connects to another. Pre-synaptic neurone to post synaptic neuron.

Question 2

What are the 2 ways to explain the process of synaptic transmission?

Answer 2

1. Electrical- potential goes directly from one cell to the next.
2. Chemical - chemical is released by presynaptic neuron

Question 3

What are the evidence for the chemical transmission of impulses theory?

Answer 3

1- the existence of the synaptic cleft ( people thought this was so chemicals could diffuse across)

2- Synaptic delay - which wouldn’t happen if the process was electric ( it would be faster if electric)

3-Otto Loewi experiment - he put a frogs heart into a beaker and attached it to a vagus nerve when he stimulated the vagus nerve the heart slows down. He then attached another heart to the heart in the beaker and only stimulated the vagus nerve of the first one. His experiment showed both hearts to slow down thus he postulated that the first heart slowing down released chemicals causing the second heart to slow down.

Question 4

What are gap junctions?

Answer 4

the membranes of adjacent cells joined together. The membrane proteins are joined togetehr causing a continuity the two neurones are connected togteher via their connected protein. These gap junctions can act as electrical synapses.

Question 5

What are advantages to jap junctions?

Answer 5

Very very quick

Question 6

What are the disadvantages of gap junctions?

Answer 6

Not very flexible as in it cant inhibit, modify.

Question 7

Where do you tend to find electrical synapses?

Answer 7

Places like the heart where you don’t need that flexibility.

Question 8

What is characteristic of a chemical pre-synaptic neuron?

Answer 8

Lots of mitochondria

Vesicles containing neurotransmitter.

Question 9

What is characteristic of a chemical post-synaptic neuron?

Answer 9

Post-synaptic receptors

Question 10

What are the stages of chemical synaptic transmission?

Answer 10

The arrival of an action potential in the axon causes it to become depolarised, this opens calcium channels. This leads to an influx of calcium.

These calcium ions cause contractions of microtubules which cause vesicles to migrate towards the pre-synaptic membrane. Here they release their contents via exocytosis.

The transmitter diffuses across the synaptic cleft
(down its concentration gradient) and binds to postsynaptic receptors.

Question 11

Why is it difficult to study the effects of a pre-synaptic neuron on a postsynaptic neuron?

Answer 11

A single postsynaptic neuron can receive synaptic input from several thousand pre-synaptic neurones.

(The junctions between neurons and skeletal muscle are therefore easier to study- one muscle cell receives input from one motor neurone)

Question 12

What is an end plate potential?

Answer 12

The action potential which causes depolarization of the muscle fibres. It’s like a small little hump before the big peak on an EMG.

Question 13

How can you isolate an endplate potential?

Answer 13

Using a substance called curare. which is a plant extract.

Question 14

What does curare do?

Answer 14

It destroys action potentials on muscles (but leaves the endplate potential) so it paralyses the individual.

Question 15

Who discovered curare?

Answer 15

Sir Bernard Katz - he got a Nobel prize for it.

Question 16

After Acetylcholine has been released into the synaptic cleft what proceeds to happen at a neuromuscular junction?

Answer 16

At the neuromuscular junction, Ach binds to the receptors on the sarcolemma, opening sodium channels.
This leads to an influx of sodium ions and so an endplate potential. If the threshold is reached, an action potential is generated.

Question 17

How were interactions between the pre and postsynaptic neurones elucidated and by whom?

Answer 17

They were elucidated by Sir John Eccles using cat and spinal cord motor neurons.

Question 18

What does IPSP stand for?

Answer 18

inhibitory postsynaptic potential

Question 19

What does an IPSP cause to the action potential?

Answer 19

A hyperpolarisation. (inhibitory postsynaptic potential )

Question 20

What does an excitatory postsynaptic potential (EPSP) do to an action potential?

Answer 20

It causes depolarization of the action potential.

Question 21

How do IPSPs (inhibitory postsynaptic potentials ) work?

Answer 21

The neurotransmitter opens either chloride channels causing them to diffuse in making the inside or the neurone more negative or poatssium channels may open allowing potassium ions (K+) to leave the neurone making ithe inside of the neurone more negative than the outside ( reducing potential difference). In many cases both happen.

Both cause hyperpolarisation.

Question 22

What are the ways affect protein channels?

Answer 22

Directly- Neurotransmitters bind to membrane protein channels , causing them to change shape and allow different ions through.

using secondary messenger model- sometimes Neurotransmitter binds to specialised receptor which opens channel. This is called an enzyme cascade recation. Binding to the specialised receptor causes the secondary mesenger to open the ion channel.

Question 23

What are the ways in which neurotransmitter be inactivated once it has bound to the post-synaptic receptor and done it’s job of causing action potential?

Answer 23

1. Diffusion ( neurotransmitter falls off and diffuses away)
2. Reuptake (by presynaptic neurone)
3. Enzymatic breakdown (Acetylcholinesterase is used to break down Ach)

Question 24

What substance allows for the reuptake of noradrenaline?

Answer 24

Monoamine oxidase

Question 25

Name some classic neurotransmitters

Answer 25

Ach 
Dopamine
Glutamate- used by rods and cones in our retina
GABA- major inhibtory neurotransmitter in the body
Noradrenaline
Adrenaline 
Seratonin
Histamine 
Oxytocin

Question 26

What are the two basic types of actylcholine receptors?

Answer 26

Nicotinic - occur at neuromuscular junction. Open Na+ channels thus is excitory.

Muscarinic- occur on heart - open K+ and Cl- channels and are therefore inhibitory.

Same neurotransmitter, but two different effects depending on the receptor.

Question 27

What are some diseases caused by a defect in synaptic transmission?

Answer 27

Parkinson’s disease - lack of dopamine

Schizophrenia - too much dopamine

Myasthenia gravis (muscle weakness)- destruction of Ach receptors

Depression - low levels of seratonin and nor-adrenalin.

Question 28

True or false- synaptic transmission is the process by which most theraputic drugs have their effect?

Answer 28

True

Question 29

What are drugs that enhance the effectiveness of a neuron called?

Answer 29

Agonists

Question 30

What are drugs that supress specific neurons called?

Answer 30

Antagonists

Question 31

What are some examples of therapeutic drugs?

Answer 31

L-dopa - a drug that stimulates the production of dopamine for those with parkinsons.

Botox- botulimun toxin - relaxes muscles by breaking open vesicles containing Ach thus allowing it not to be released and so muscles cannot contract . Used in quint or blepharit spasms.

Atropine- Ach receptor blocker - it allows pupil to dilate by relaxing sphincter pupilli from contracting. (extract from bella donna plant)

Prozak- selective serotonin reuptake inhibitors - used for fighting depression