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MBBS II HNNS > L06, 07 - Neurotransmitters > Flashcards

L06, 07 - Neurotransmitters Flashcards

1
Q

Describe the structure of electrical synapses and how signal is transduced?

A

Gap junction channels link presynaptic and postsynaptic membrane:
6 connexins form 1 connexon

> > pores to allow ionic current to pass through down potential difference

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2
Q

3 physiological functions of electrical synapses?

A

1) No delay = minimize time between stimulus and response
2) Synchronize electrical activity among neurons: e.g. coordinate hormone secretion with neuronal activity
3) Coordinate/ relay intracellular signalling: allow ATP, secondary messengers to pass through

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3
Q

Electrical synapse only allows transduction of signal in one direction. T or F?

A

False

Most gap junctions allow bidirectional flow

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4
Q

List the sequence of events that occur in chemical synapse signal transduction?

A
  1. Transmitter molecules (e.g. glutamate, GABA) are synthesized, stored in synaptic vesicles
  2. Action potential reaches presynaptic terminal
  3. Presynaptic terminal depolarizes&raquo_space; voltage-gated Ca2+ channels open
  4. Rapid influx of Ca2+ down concentration gradient through channels into presynaptic terminal
  5. Ca2+ causes vesicles to fuse with presynaptic membrane, exocytosis into synaptic celft
  6. Transmitter bind to postsynaptic channels, cause excitatory/ inhibitory potential, later degraded by enzymes in cleft
  7. Vesicular membrane endocytosed from plasma membrane
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5
Q

Explain why chemical synapse signal conduction has delay?

A

delayed ~0.5 ms – time required for:
 Secretion of neurotransmitter
 Diffusion of neurotransmitter
 Response of the postsynaptic cell to it

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6
Q

Describe how quanta of neurotransmitters can lead to firing of postsynaptic action potential?

A

1 quanta of nuerotransmitter = 1 miniature end plate potentials (MEPPs)

Sum of MEPPs = End Plate Potential (EEP)

If EEP is over the threshold for triggering postsynaptic membrane potential = fire

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7
Q

How does high or low calcium concentration in the synaptic cleft influence postsynaptic AP firing?

A

Low extracellular [Ca]:
- No response to presynaptic depolarization, failure to trigger postsynaptic response

High extracellular [Ca]:
- Unit response remains the same (same threshold), but less failure in response of postsynaptic neuron

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8
Q

List 4 proteins for fusion of neurotransmitter vesicles with presynaptic membrane?

A
  1. NEM-sensitive fusion protein (NSF)
  2. Soluble NSF-attachment proteins (SNAPs)
  3. SNAP receptors (SNARE)
  4. Synaptotagmin
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9
Q

Describe how SNAP and SNARE work to facilitate neurotransmitter vesicle fusion at presynaptic membrane?

A

1) SNAP + NSF prime the vesicles: e.g. SNAP binds to Syanaptobrevin (SNARE) on vesicle membrane
2) SNAP on vesicle membrane bind to SNAREs on presynaptic plasma membrane: e.g. Syntaxin, SNAP-25
3) Binding forms macromolecular complex across 2 membranes&raquo_space; docking and fusion

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10
Q

Describe the role of Synaptotagmin in neurotransmitter release?

A
  • Binds to Ca in synaptic cleft and become activated
  • Ca-synaptotagmin complex insert into membrane and bind to other proteins

> > final step to fuse vesicle and plasma membrane

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11
Q

List the 3 proteins involved in the budding and recycling of neurotransmitter vesicles in the presynaptic membrane?

A
  • Clathrin
  • Dynamin
  • Synapsin
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12
Q

Briefly summarize the function of Clathrin in neurotransmitter vesicles?

A
  • Coats vesicles at cytosolic side

- Can assemble into coated pits to initiate membrane budding/ endocytosis of vesicle

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13
Q

Briefly summarize the function of Dynamin in neurotransmitter vesicles?

A
  • For pinching off vesicle membrane during budding endocytosis
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14
Q

Briefly summarize the function of Synapsin in neurotransmitter vesicles?

A
  • Bind to synaptic vesicle and cross link with cytoskeleton

> > keep vesicle tethered without degradation for recycling

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15
Q

Describe the common molecular mechanism for neurotoxins to exert effect?

A

toxin = proteases: cleave presynaptic SNARE proteins

> > limit vesicle-plasma membrane fusion

> > limit release of neurotransmitters

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16
Q

MoA of Botulinum toxin?

A

Botox cleaves SNAP-25, synaptobrevin and syntaxin on presynaptic membrane

> > abolish neurotransmitter release at motor neurons

> > block skeletal and visceral muscles: weakness, respiratory failure, viceral motor dysfunction

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17
Q

MoA of tetanus toxin?

A

Tetanus toxin cleaves synaptobrevin

> > Blocks release of inhibitory transmitters from interneurons in spinal cord

> > loss of synaptic inhibition on spinal motor neurons

> > hyperexcitation of skeletal muscle

18
Q

2 medical uses for Botox?

A
  1. Reduce dynamic wrinkles by reducing muscle tone

2. Face slimming : cause disuse atrophy of massater to slim face

19
Q

MoA of α-latrotoxin?

A

Bind to neurexins e.g. synaptotagmin&raquo_space; cause spontaneous vesicle fusion without Ca

Bind to CL1&raquo_space; activate Ca-mediated intracellular signals

> > > spontaneous synaptic vesicle discharge without extracellular Ca

20
Q

What is defective in Congenital myasthenic syndromes? Inheritance pattern?

A

Defect in Choline acetyltransferase (ChAT) = Defect in ACh synthesis (cannot transfer choline to acetate) / packaging

autosomal recessive

21
Q

List some symptoms and signs of Congenital myasthenic syndrome?

A

episodic apnea

weakness of the eye muscle (double vision)

mouth and throat muscles (difficulty chewing or swallowing)

22
Q

Treatment of Congenital myasthenic syndrome?

A

AChE inhibitors:

prophylactic pyridostigmine

23
Q

Name one condition that causes loss of presynaptic V-gated Ca channels?

A

Lambert-Eaton myasthenic syndrome (LEMS)

Common complication of lung SCC

> > defective Ca influx and Ca-mediated Ach release

24
Q

List 3 monoamine neurotransmitters?

A

Norepinephrine
Dopamine
Histamine

25
Q

List 2 amino acid neurotransmitters? Precursor?

A

Glutamate
GABA

Glutamine and Glutamate

26
Q

List 3 peptide neurotransmitters?

A

Endorphin
Enkephalin
Substance P

27
Q

Name 2 exogenous neurtransmitters that mimic the action of glutamate and GABA?

A

Glutamate: Monosodium glutamate (umami)

GABA: Benzodiazepines mimic GABA action

28
Q

Describe the synthesis and recycling of small neurotransmitters like Ach? think what’s made at the ER, transport, terminal

A

RER: synthesize enzyme e.g. choline acetyltransferase

Slow axonal transport to terminal

Synthesis and packaging of neurotransmitter at terminal

Reuptake after release

29
Q

Describe the synthesis of peptide neurotransmitters?

A

RER: pre-propeptide and enzymes made

Microtubule transport to terminal

Enzymatic processing of pre-propeptide

Extrasynaptic degradation by proteases: no reuptake

30
Q

Describe the general structure and action of ligand-gated receptors?

A

4 transmembrane helices or 3 transmembrane helices + pore loop

Bind to neurotransmitter&raquo_space; conformational change&raquo_space; multimeric ion channel open

31
Q

Describe the action of nicotinic receptors?

A
  1. Ach bind to specific site
  2. Channel opens, allow Na+ to enter postsynaptic neuron
  3. Depolarization
32
Q

List 3 types of ionotropic glutamate receptors?

A
  1. AMPA
  2. NMDA
  3. Kainate
33
Q

List some toxins that can cause neurotransmitter blockage?

A

 α-bungarotoxin (snake)
 α-neurotoxin (cobra)
 Erabutoxin (sea snake)
 Curare (plant toxin)

34
Q

Which ions interfere with NMDA receptor function?

A

Mg2+

Interferes with binding of Na+ and Ca2+ needed for depolarization

35
Q

Explain how presynaptic neuron stimulation can form synaptic memory?

A

High-frequency stimulation of presynaptic cell

> > Increase synaptic strength

> > more AMPA receptors respond to glutamate to trigger membrane depolarization

> > long-term higher sensitivity of post-synaptic neuron

36
Q

Describe the action of ionotropic GABA receptors?

A
  • Binding of GABA to receptor
  • Conformational change causes Cl- influx into postsynaptic neuron
  • Hyperpolarize, inhibit postsynaptic neuron
37
Q

Compare Spatial and temporal summation?

A

Spatial = several excitatory postsynaptic potentials (EPSPs) arrive at axon hillock simultaneously

Temporal = sum up postsynaptic potentials created in rapid succession at the same synapse

38
Q

Compare the speed and length of response between ionotropic and metabotropic receptors?

A

Ionotropic = Rapid, short acting response

Metabotropic = Slow, prolonged response

39
Q

Compare the action between ionotropic and metabotropic receptors?

A

Ionotropic = Ligand- gated ion channels, allow ion influx

Metabotropic = G-protein coupled receptor, require secondary messengers

40
Q

Summation of Excitatory and Inhibitory post synaptic potentials (EPSP and IPSP) occur in postsynaptic neurons. T or F?

A

True

EPSP and IPSP are integrated together for moment-to-moment control of AP firing

MBBS II HNNS (57 decks)

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