Lecture 5: Synaptic Transmission

Question 1

a neuron can terminate at one of three structures…..

Answer 1

• another neuron (synapse)
• a muscle (neuromuscular junction)
• a gland

Question 2

when a neuron terminates in a muscle or gland, the neuron is said to _______ the structure

Answer 2

innervate

Question 3

nerves that innervates muscle fibers are called ?

Answer 3

motorneurons

Question 4

what is a synapse?

Answer 4

the junction b/w a presynaptic neurons and postsynaptic neurons

Question 5

what are the 2 types of synaptic transmission?

Answer 5

electrical (gap junction)
- transfer of electrons
chemical
-NTs

Question 6

what does it mean that synaptic transmissions are unidirectional?

Answer 6

the go from the presynaptic neuron —> postsynaptic neuron

Question 7

in electrical gap junctions, how is voltage transferred?

Answer 7

via the touching of the pre and post-synaptic membranes (direct connection via intercellular channels)

Question 8

in chemical synapses, how are signals transferred?

Answer 8

through ion channels from the pre to post synaptic neurons

Question 9

gap junctions are especially abundant in what muscle types

Answer 9

cardiac and smooth muscle

Question 10

neuron that conducts the action potential towards the synapse

Answer 10

presynaptic neuron

Question 11

neuron whose action potentials are propagated away from the synapse

Answer 11

postsynaptic neuron

Question 12

synaptic knob contains ______

Answer 12

synaptic vesicles

Question 13

space b/w the pre and post-synaptic neurons

Answer 13

synaptic cleft

Question 14

a gap between two adjacent cells linked by small connecting tunnels formed by connexons

Answer 14

gap junctions (communicating junctions)

Question 15

how are gap junctions functionally different in non-muscle tissues

Answer 15

they permit the unrestricted passage of small nutrient molecules between cells

Question 16

what is synaptic delay

Answer 16

the time needed for the conversion of an electrical signal (AP) from the presynaptic neuron to an electrical signal (EPSP or IPSP) in the post-synaptic neuron by chemical means (via NT receptor interaction)

Question 17

what are the steps in excitation-secretion coupling in chemical synapses

Answer 17

1. An action potential depolarizes the axon terminal
2. Depolarization opens the voltage-gated Ca+ channels and Ca+ enters the pre-synaptic axon terminal (aka synaptic knob)
3. Ca+ entry triggers the exocytosis of NT into the synaptic cleft
4. NT diffuses across the synaptic cleft and binds to receptors on the post synaptic cell
5. binding of NT receptor initiates a response in the post-synaptic cell

Question 18

2 main types of receptors at the post-synaptic membrane?

Answer 18

ligand gated ion channels for FAST neurotransmission
GPCRs for slower transmission

Question 19

what causes the end of the signal?

Answer 19

• removal of the NT
  HOW?
  
  • diffusion (NT moves away from synaptic cleft)
  • Enzymatic degradation (inactivation by enzymes within the cleft)
  • Reuptake (NT is taken back up into the presynaptic axon terminal. Either gets Recycled or destroyed)

Question 20

common excitatory NTs

Answer 20

acetylcholine (ACh)
Norepinephrine

Question 21

common inhibitory NT

Answer 21

GABA (G-aminobutyric acid)

Question 22

What is a cholinergic synapse and what does it do

Answer 22

miniature transducer that converts presynaptic electrical signal into ACh that then diffuses across the synaptic cleft. ACh triggers another electrical signal on the post-synaptic side as it interacts with ACh receptors

Question 23

what is acetylcholinesterase important for

Answer 23

The breakdown of NT in the synaptic cleft

Question 24

synaptic vesicles are organized by ______ proteins

Answer 24

snare

Question 25

post synaptic ______ of the NT in the synaptic cleft affects response

Answer 25

density

Question 26

what are the steps in Cholinergic response

Answer 26

1. nerve signals cause voltage-gated Ca+ channels to open at the synaptic knob 2. Ca+ triggers exocytosis of the synaptic vesicles and the release of ACh 3. reserve synaptic vesicles move upwards to the active site and release their ACh 4. ACh diffuses across the synaptic cleft and binds to ACh receptors - (ligand-gated Na+ channel or a GPCR) 5. ACh receptor opens allowing Na+ ions to follow their concentration gradient into the postsynaptic cell 6. this results in depolarization of the post-synaptic cell and an AP might be generated 7. once membrane potential reaches -50mV, AP begins

Question 27

During synaptic vesicle fusion, bound Ca+ triggers _________ protein interaction to bring the vesicles into position for fusion with the presynaptic cell membrane

Answer 27

SNAP/SNARE

Question 28

the opening of ACh receptors at the neuromuscular junction results in ________

Answer 28

EPP (End plate potential) - EPP depolarizes the membrane and initiates APs

Question 29

describe the post synaptic organization in the skeletal muscle membrane

Answer 29

- the crest has several folds with ACh receptors - Voltage-gated Na+ channels in the valleys of the folds

Question 30

the excitatory adrenergic synapse employs what NT?

Answer 30

Norepinephrine (NE) aka noradrenaline

Question 31

what is the receptor type for norepinephrine

Answer 31

transmembrane protein associated with a G-protein **NOT an ion gate

Question 32

explain the steps that occur at the excitatory adrenergic synapse

Answer 32

1. unstimulated NE receptor is bound to G protein 2. binding of NE causes G protein to be released 3. G protein binds to adenylate cyclase, activating the enzyme and converts ATP to cAMP (2nd messenger system) 4. cAMP produces an internal chemical that binds to a ligand-gated Na+ channel, cell is depolarized

Question 33

what type of receptors are GABA receptors?

Answer 33

Channel receptors

Question 34

explain what happens at the inhibitory GABA-ergic synapse

Answer 34

1. GABA binds to Cl- channel or GPCR 2. Binding causes them to allow Cl- ions to pass 3. Cl- influx results in hyperpolarization (reduces the neuron's excitability) and makes the RMP more negative, inhibiting neuron firing

Question 35

Tetanus is an example of a pre/post-synaptic disorder

Answer 35

Tetanus is a PREsynaptic disorder - tetanus toxin damages synaptobrevin (which prevents the release of GABA) -an unchecked GABA system causes an imbalance b/w inhibition and excitation symptoms: painful muscle spasms, stiff immovable muscles, muscle contraction

Question 36

what is Myasthenia Gravis and what is its mechanism of action?

Answer 36

MG is a chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscles, resulting in weakness of the skeletal muscles. mechanism: autoimmune reaction w/ ACh receptors reduces the effectiveness of ACh in the synaptic cleft

Question 37

why does administering a reversible cholinesterase inhibitor improve symptoms of myasthenia gravis?

Answer 37

reducing the activity of the esterase increases the half-life of ACh. A longer half-life of ACh in the synaptic cleft improves the effectiveness of ACh by increasing the probability of ACh interacting with the receptors that are still functioning.

Question 38

Explain Ivermectin Neurotoxicity

Answer 38

ivermectin is an anti-parasitic macrocyclic lactone with high affinity to GABA gated Cl- ion channels - kills parasites by inhibiting their nerve activity leading to paralysis and death The mammalian BBB normally is able to keep the drug from entering the CNS - except some dog breeds such as Collies - Collies have a mutation in the MDR1 gene which allows ivermectin to pass through the BBB -macrocyclic lactones (ivermectin) bind with high affinity to the GABA gated Cl- channels -an accumulation of ivermectin causes neurological symptoms