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PN3313 > SignalTransmission between neurons > Flashcards

SignalTransmission between neurons Flashcards

1
Q

What are the 2 categories of synaptic transmission?

A
  • Electrical

- Chemical

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2
Q

Where are electrical synapses found?

A

Muscles, glial cells and certain neurons requiring a coordinated response

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3
Q

Describe the structure of electrical synapses

A
  • Intercellular space narrows to form gap junctions
  • Gap junctions formed by 2 conexons of 6 connexins
  • small molecules e.g ions, can pass
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4
Q

How can electrical synapses between horizontal cells be inhibited?

A

Dopamine

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5
Q

What are the characteristics of electrical synaptic transmission?

A
  • Fast
  • Loss of voltage
  • Bidirectional (exitatory and inhibitory)
  • Graded
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6
Q

What are the characteristics of chemical synapses?

A
  • Presynaptic vesicles filled with vesicles
  • Postsynaptic membrane
  • Small synaptic cleft
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7
Q

What are the 4 types of chemical synapse?

A
  • Axo-dendritic
  • Axosomatic
  • Axoaxonic
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8
Q

Describe type 1 chemical synapses

A
  • Round synaptic vesicles
  • Dense basement membrane
  • Large active zone
  • Large post-synaptic density
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9
Q

Describe type 2 chemical synapses

A
  • Oval synaptic vesicles
  • Shallow basement membrane
  • Small active zone
  • Small post-synaptic density
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10
Q

Name the classical neurotransmitters

A 
Amino acids
- Glutamate 
- GABA
- Glycine
Amines 
- Ach
- Dopamine 
- Serotonin
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11
Q

Name non-classical neurotransmitters

A
  • Neuropeptides
  • Neurotrophins
  • Gaseos massengers
  • D-serine
  • Endocannabinoids
  • ATP/adenosine
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12
Q

What are the two neurotransmitter synthesis methods?

A
  • Neuropeptides broken down from precursor proteins after being synthesized. Packaged and processed in the Golgi aparatus and stored at the presynaptic terminal
  • Precursors combine with enzyme to form neurotransmitter
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13
Q

How are neurotransmitters transported to the pre-synaptic membrane?

A

Require special transporter proteins on vesicle membranes

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14
Q

How are neurotransmitters released from the pre-synaptic membrane?

A
  • Action potentials open voltage-gated Ca2+ channels
  • Binding of synaptotagmin triggers fusion of neurotransmitter vesicle
  • Activates Ca/Calmodulin dependent kinase II which acts on synapsin so more vesicles dock at the active zone
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15
Q

What are the two different types of receptors?

A

Ionotropic and metabotropic receptors

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16
Q

Describe ionotropic channels

A
  • Ligand-gated channels

- Extracellular neurotransmitter binding domain and membrane-spanning ion channel

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17
Q

Name 4 different ionotropic receptors

A
  • Nicotimic AChR
  • AMPA Glutamate receptor
  • NMDA Glutamate receptor
  • Glycine receptor
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18
Q

What is an agonist and antagonist?

A

Agonist - substance that binds to neurotransmitter receptors and mimics neurotransmitter actions
Antagonist - bind to but do not activate transmitter receptors, blocking the actions of neurotransmitters

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19
Q

What are EPSPs and what are they mediated by?

A

Lead to depolarisation of membrane potential, usually mediated by Ca2+ influx , causing post-synaptic neuron action potential

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20
Q

What are IPSPs and what are they mediated by?

A

Lead to hyperpolarisation of the membrane potential making it more difficult for the post-synaptic neuron to fire action potentials, mediated by Cl- influx or K+ outflow

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21
Q

What is synaptic delay?

A

Delay in change of post-synaptic membrane usually ~ 1ms

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22
Q

Describe metabotropic receptors

A

Alter intracellular metabolic reactions, often stimulate the production of second messengers (G-protein, cAMP, diacylglycerol), which in turn activate protein kinases, phosphorylating different substrate
proteins including ion channels

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23
Q

Which neurotransmitters have metabotropic receptors?

A

Glutamate, Adrenaline/noradrenaline, most seretonegic neurons all neuropeptide receptors

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24
Q

What are neuromodulators?

A
  • Work via metabotropic receptors
  • Can’t send fast transmission on their own but can alter fast synaptic transmission
  • Receptors can be pre/post synaptic
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25
Q

Describe muscarinic Ach receptors

A

1,3 and 5 - excitqatory, coupled to PKC leading to increase in Ca2+ causing smooth muscle to contract
2,4 - inhibitory, inhibit cAMP production and open K+ channels slowing down heart rate

26
Q

Describe what receptors peptide hormones may bind to and what effects these induce

A

G-coupled proteins or Receptor tyrosine kinases can activate

  • MAPK (differentiation and plasticity)
  • PLC alpha
  • PI3-Akt which promotes cell survival
27
Q

What are

a) autoreceptors
b) heteroreceptors

A

a) receptors on presynaptic terminals activated by own transmitter
b) activated by transmitters different to their own
Both typically metapotropic

28
Q

Give an example of a system with auto and heteroreceptors?

A

Histaminergic system

These can occur on non-histaminergic cells

29
Q

Name 2 presynaptic mechanisms of inactivation of a chemical transmission

A
  • Reuptake by transporters (dopamine, serotonin)

- Binding of inhibitory autoreceptor at presynaptic membrane inhibiting exocytosis (GABA, glutamate)

30
Q

Name 3 methods mechanisms of inactivation of a chemical transmission occuring in the synapse or involving glial cells

A
  • Diffusion from the synaptic cleft
  • Uptake by glial cells (glutamate, GABA)
  • Enzymatic decay of neurotransmitter (e.g Ach is broken down by AchE to acetate and choline, pumped by choline transporter)
31
Q

Name 2 postsynaptic mechanisms of inactivation of a chemical transmission

A
  • Internalisation of receptors

- Desensitization of receptors

32
Q

Describe the breakdown of glutamate

A
  • Internalised by astrocytes, broken down to glutamine by glutamine synthase and transported back to the neuron by glutamine transporters
  • recycled into glutamate by glutaminase
33
Q

Describe the mechanism of temporal integration

A
  • 2nd PSP rides on the back of the 1st one to become more effective
  • Currents flowing across membrane determined by post synaptic time constant, PSP dynamics and presynaptic firing frequency
34
Q

Describe the mechanism of spatial integration

A
  • Arrival of 2nd input coincides with 1st

- More currents flowing across membrane. Determined by postsynaptic length constant and distance between inputs

35
Q

What is a signal process and where are they typically found?

A
  • Receive both excitatory and inhibitory inputs

- Used in locomotion and processing of cyclic inputs

36
Q

What is short-term facilitation?

A
  • Where the 2nd PSP is larger
  • Can be due to accumulation of Ca2+ in presynaptic terminals, increase in reusable vesicles and/or calcium channel facilitation
37
Q

What is short-term anti-facilitation?

A 
- 2nd PSP is smaller 
Could be due to: 
- Depletion of presynaptic veiscles
- Desensitization of receptors 
- Saturation of postsynaptic receptors 
- Negative feedback of autoreceptors
38
Q

What is Hebbian long term potentiation?

A

After simultaneous firing of pre and post synaptic neurons EPSPs are enhanced

39
Q

Describe an example of early phase long term potentiation

A
  • Ca2+ increase causes retrograde messengers to enhance neurotransmitter release
  • New AMPARs are inserted into postsynaptic membrane enhancing affinity for glutamate
40
Q

What occurs during late phase long term potentiation?

A
  • Transcription of new genes and synapse formation

- Can involve CAMP pathway and cAMP kinase activation

41
Q

What is non-hebbian long term potentiation?

A
  • Does not require both pre and post synaptic activation

- Occurs via the activation of G-proteins and protein kinases

42
Q

What is long term depression?

A
  • Where synaptic transmission becomes weaker over time after conditioning stimulation
  • Uses internalisation/desensitization of AMPARs
43
Q

What is a neuromuscular junction?

A

Synapse between muscle and motor neuron

44
Q

Describe the strucute of a neuromuscular junction?

A

Motor neuron innervates muscle membrane at end plate, where axon looses myelin sheath and splits into many branches called synaptic boutons which transmit at junctional folds containing receptors

45
Q

What neurotransmitter is released by motor neurons?

A

Acetylcholine

46
Q

How does a motor neuron excite a muscle fibre?

A
  • Release of neurotransmitter opens postsynaptic Ach receptors
  • Causes EPSP (or end plate potential) which if compound EPSP (from many boutons) is large enough opens v gated Na channels causing action potential which spreads along the muscle fibre
47
Q

Describe the stucture of a synaptic bouton

A
  • Contains multiple release sites each capable of releasing neurotransmitter
48
Q

What is quantal release?

A
  • Neurotransmitter released in discrete ammounts called quanta
  • Each produces post synaptic potential of equal size called the quantal synaptic potential
  • Causes smooth grading of total EPSPs
49
Q

Give an example of a non-spiking synapse

A
  • Photoreceptor bipolar cell
  • Glutamate released at base level causing continuous depolarisation (-40mV)
  • Post-synaptic response is not linear
50
Q

What are voltage dependent NMDARs?

A
  • Have multiple binding sites for neuromodulators as well as glutamate
  • Mg binding site present inside which is blocked at hyperpolarisation which can be removed by depolarisation
  • Need both post and pre synaptic neuron to fire
  • If you change voltage level changes size of EPSPs
  • Important in long term potentiation
51
Q

What neurotransmitter have been shown to be released by glial cells?

A

Glutamate, ATP-adenosine, D-serine

52
Q

How do gial cells enact transmission?

A
  • Have some receptors which can be activated

- Release neurotransmitters which act very locally on neurons

53
Q

Give an example of gial transmission

A

hippocampal CA3–CA1 synapses

  • Glial glutamate activates presynaptic groups
  • Glial adenosine activates postsynaptic receptors
  • Changes transmitter release and contributes to LTP
54
Q

Which transmitters can enact retrograde signalling?

A 
Lipid derived (endocanabinoids) 
Gases 
peptides
GABA
Growhth factors
55
Q

How does retrograde signalling enact long term potentiation?

A

e. g Ca2+ influx through NMDAR
- Ca2+/Calmodulin activates NO synthase
- NO released
- Activates presynaptic guanylate cyclase
- Results in cGMP enhancing vesicle release
- PDE can degrade cGMP stopping the enhancing process

56
Q

Describe presynaptic inhibition

A
  • Neuron inhibited causing increased Cl- conduction and less Ca2+ entry
  • Less vesicle release therefore less postysynaptic EPSP
57
Q

Describe presynaptic facilitation

A
  • Neuron activated causing K+ current to become depressed

- More Ca2+ entry and more vesicle release -> bigger postsynaptic response

58
Q

Describe reciprocal inhibition

A

Present in neurons controlling antagonistic muscles

59
Q

What is recurrent inhibition?

A
  • Where neurons inhibit themselves in a negative feedback fashion
60
Q

What are reciprocal excitations?

A

Mechanism for maintaining long-lasting neuronal activities such as eye movements, posture and locomotion

PN3313 (9 decks)

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