The synapse: mechanisms of communication between neurons

Question 1

Myasthenia Gravis: symptoms

Answer 1

dysfunction of synaptic transmission. Causes fluctuating muscle weakness, problems chewing (dysphagia) and talking (dysarthria) and respiratory weakness

Question 2

Synapse

Answer 2

the place where neurons come into close proximity with other neurons
pre synaptic- before the synapse
post synaptic- after the synapse

Question 3

Axodendritic synapse

Answer 3

the terminal buttons synapses with a dendrite of the post synaptic neuron

Question 4

Axosomatic synapse

Answer 4

the terminal button synapses with the cell body (soma) of the post synaptic neuron

Question 5

Axoaxonic

Answer 5

the terminal button synapses with the axon of the post synaptic neuron

Question 6

presynaptic membrane

Answer 6

the membrane of the presynaptic terminal button

Question 7

post synaptic membrane

Answer 7

the membrane of the postsynaptic neuron

Question 8

dendritic spine

Answer 8

a ridge on the dendrite of the post synaptic neuron, with which a terminal button from a pre synaptic neuron forms a synapse

Question 9

synaptic cleft

Answer 9

the tiny gap between the presynaptic and postsynaptic membrane (approximately 20 nanometers wide)

Question 10

synaptic vesicles

Answer 10

tiny balloons filled with neurotransmitter molecules; found in the release zone of the terminal button

Question 11

microtubules

Answer 11

long tubes that run down the axon and guide the transport of synaptic vesicles from the soma to the axon terminal

Question 12

release zone

Answer 12

part of the interior of the presynaptic membrane to which synaptic vesicles fuse in order to release their neurotransmitter into the synaptic cleft

Question 13

Release of a neurotransmitter 1

Answer 13

1. vesicles contain neurotransmitter (NT) molecules
2. an action potential in the pre synaptic cell triggers vesicles to move toward the cell membrane
3. vesicles are guided towards the membrane by proteins

Question 14

Release of a neurotransmitter 2

Answer 14

Guiding proteins act like ropes that help fuse the vesicle and pre synaptic membrane together

Question 15

Release of a neurotransmitter 3

Answer 15

1. an influx of calcium ions into the pre synaptic terminal button induces fusion of the two membranes
2. neurotransmitter molecules are then released into the synaptic cleft

Question 16

Excitatory post synaptic potential (EPSP)

Answer 16

Excitatory post synaptic potentials (EPSPs) depolarise the post synaptic cell membrane
EPSPs increase the likelihood that an action potential will be triggered in the post synaptic neuron

Question 17

Inhibitory post synaptic potential (IPSP)

Answer 17

Inhibitory post synaptic potentials (IPSPs) hyperpolarise the postsynaptic cell membrane
IPSPs decrease the likelihood that an action potential will be triggered

Question 18

neural integration

Answer 18

the interaction between the effects of EPSPs and IPSPs

IPSPs tend to cancel out the effects of EPSPs

Question 19

Reuptake

Answer 19

the neurotransmitter is removed from the synaptic cleft via special transporter molecules in the terminal buttons. These molecules use energy to draw the neurotransmitter back into the cytoplasm of the pre synaptic neuron

Question 20

Enzymatic deactivation

Answer 20

an enzyme in the synaptic cleft destroys the remaining neurotransmitter molecules. Such deactivation seems to occur only for one type of neurotransmitter, called acetylcholine (ACh). The enzyme that destroys ACh in the synapse is called acetylcholinesterase (AChE); it does the job of breaking ACh into its constituents, acetate and choline

Question 21

Seven steps of neurotransmitter action at the synapse

Answer 21

1. neurotransmitter (NT) molecules are synthesised from their precursors by enzymes
2. NT molecules are stored in vesicles
3. NT molecules that leak from vesicles are destroyed by enzymes
4. action potentials cause vesicles to fuse with the presynaptic cell membrane, releasing their NT into the synaptic cleft
5. released NT binds with autoreceptors in presynaptic membrane, limiting further release of the NT
6. released NT binds with the receptors on postsynaptic membrane, causing ion channels to open
7. free NT molecules in the synaptic cleft are taken back up by transporter molecules in the presynaptic membrane, or destroyed by enzymes- reuptake or enzymatic deactivation

Question 22

Amino acids

Answer 22

Glutamate: the most common excitatory neurotransmitter in the CNS
GABA (gamma aminobutyric acid): the most common inhibitory neurotransmitter

Question 23

Monamines

Answer 23

Dopamine and Norepinephrine (catecholamines)
Serotonin (Indolamine)

present in groups of neurons that are located mostly in the brainstem

Question 24

Acetylcholine

Answer 24

Acetylcholine: the neurotransmitter that operates at synapses with muscles, as well as other parts of the CNS

Question 25

Agonist

Answer 25

increases the activity of the synapse

Question 26

Antagonist

Answer 26

decreases the activity of the synapse

Question 27

Agonists do the following…

Answer 27

1. increase the number of neurotransmitter (NT) molecules that are synthasised
2. increase the number of NT molecules stored in the vesicles
3. destroy the enzymes that attack NT molecules
4. increase the number of vesicles that fuse with the pre synaptic cell membrane
5. decrease the activity of autoreceptors
6. binding directly with the post synaptic membrane, causing ion channels to open
7. decreasing the amount of NT that is reuptaken or destroyed by enzymes

Question 28

Anatgonists can do any of the following

Answer 28

1. decrease the number of neurotransmitter (NT) molecules that are synthasised
2. decrease the number of NT molecules stored in the vesicles
3. cause NT to leak from vesicles where they are attacked by degrading enzymes
4. decrease the number of vesicles that fuse with the pre synaptic cell membrane
5. increase the activity of autoreceptors
6. block the inotropic receptor, preventing the ion channels from opening
7. increasing the amount of NT that is reuptaken or destroyed by enzymes in the synapse

Question 29

Myasthenia Gravis

Answer 29

Autoimmune disorder where the person’s own immune system destroys ACh receptors which are located on synapses with the muscles
Treated with anticholinesterase (AChE) inhibitors- these increase and prolong the effects of ACh on the post synaptic membrane
Also treated with immunosuppressive drugs or by removal of the thymus gland