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PHYSIOLOGY > Lecture 5: Synaptic Transmission > Flashcards

Lecture 5: Synaptic Transmission Flashcards

1
Q

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

A
  • another neuron (synapse)
  • a muscle (neuromuscular junction)
  • a gland
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2
Q

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

A

innervate

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3
Q

nerves that innervates muscle fibers are called ?

A

motorneurons

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4
Q

what is a synapse?

A

the junction b/w a presynaptic neurons and postsynaptic neurons

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5
Q

what are the 2 types of synaptic transmission?

A

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

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6
Q

what does it mean that synaptic transmissions are unidirectional?

A

the go from the presynaptic neuron —> postsynaptic neuron

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7
Q

in electrical gap junctions, how is voltage transferred?

A

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

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8
Q

in chemical synapses, how are signals transferred?

A

through ion channels from the pre to post synaptic neurons

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9
Q

gap junctions are especially abundant in what muscle types

A

cardiac and smooth muscle

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10
Q

neuron that conducts the action potential towards the synapse

A

presynaptic neuron

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11
Q

neuron whose action potentials are propagated away from the synapse

A

postsynaptic neuron

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12
Q

synaptic knob contains ______

A

synaptic vesicles

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13
Q

space b/w the pre and post-synaptic neurons

A

synaptic cleft

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14
Q

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

A

gap junctions (communicating junctions)

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15
Q

how are gap junctions functionally different in non-muscle tissues

A

they permit the unrestricted passage of small nutrient molecules between cells

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16
Q

what is synaptic delay

A

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)

17
Q

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

A
  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
18
Q

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

A

ligand gated ion channels for FAST neurotransmission
GPCRs for slower transmission

19
Q

what causes the end of the signal?

A
  • 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)
20
Q

common excitatory NTs

A

acetylcholine (ACh)
Norepinephrine

21
Q

common inhibitory NT

A

GABA (G-aminobutyric acid)

22
Q

What is a cholinergic synapse and what does it do

A

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

23
Q

what is acetylcholinesterase important for

A

The breakdown of NT in the synaptic cleft

24
Q

synaptic vesicles are organized by ______ proteins

A

snare

25
Q

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

A

density

26
Q

what are the steps in Cholinergic response

A
  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
27
Q

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

A

SNAP/SNARE

28
Q

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

A

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

29
Q

describe the post synaptic organization in the skeletal muscle membrane

A
  • the crest has several folds with ACh receptors
  • Voltage-gated Na+ channels in the valleys of the folds
30
Q

the excitatory adrenergic synapse employs what NT?

A

Norepinephrine (NE) aka noradrenaline

31
Q

what is the receptor type for norepinephrine

A

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

32
Q

explain the steps that occur at the excitatory adrenergic synapse

A
  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
33
Q

what type of receptors are GABA receptors?

A

Channel receptors

34
Q

explain what happens at the inhibitory GABA-ergic synapse

A
  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
35
Q

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

A

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

36
Q

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

A

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

37
Q

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

A

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.

38
Q

Explain Ivermectin Neurotoxicity

A

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

PHYSIOLOGY (25 decks)

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