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Introduction to neuroscience - L1 > Lecture 9 - synapses & neurotransmitter > Flashcards

Lecture 9 - synapses & neurotransmitter Flashcards

1
Q

What should a neurotransmitter be?

A
  • be present in the presynaptic terminals
  • be released in response to stimulation
  • act on the postsynaptic neuron
  • blocking the neurotransmitter should prevent synaptic transmission
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2
Q

How do we experimentally determine if a molecule acts a neurotransmitter?

A
  • IS IT THERE? –> immunostaining
  • does the cell express enzymes to synthesise it, or immunostaining, in situ hybridisation
  • IS IT RELEASED? –> collect fluid around the neurons after stimulating them (this might be difficult) - remember Loewi’s 1921 experiment

DOES IT AFFECT THE POSTSYNAPTIC CELL? –> test if the molecule mimics the effect of stimulating the presynaptic cell

BLOCK THE NEUROTRANSMITTER? –> apply drugs; delete genes encoding enzymes/transports/receptors

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3
Q

What are 3 types of neurotransmitters?

A
  • amino acids
  • amines
  • peptides
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4
Q

Describe the features of amino acids & amines

A
  • small molecules (100-200 Da)
  • stored in synaptic vesicles
  • can bind to ligand-gated ion channels or G-protein coupled receptors
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5
Q

Describe the features of peptides

A
  • large molecules (1000-3000 Da)
  • stored in secretory granules
  • only bind to G-protein coupled receptors
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6
Q

How many kinds of neurotransmitters do neurons usually release?

A

one kind of neurotransmitter, but some can release more than one

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7
Q

What do peptide-releasing neurons also release?

A

a small molecule transmitter, called a ‘co-transmitter’

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8
Q

Describe different types of neurotransmitter receptors

A
  • Ligand-gated ion channels (ionotropic receptors) –> directly depolarise or hyperpolarisation and the post synaptic cell
  • G-protein- coupled receptors (metabotropic receptors) –> more complex effects (multiple possible second messengers, which allow amplification)
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9
Q

How does convergence & divergence allow flexibility?

A
  • each transmitter can activate multiple different receptors
  • each receptor can activate different downstream effectors
  • different transmitters or receptors can activate the same downstream effector
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10
Q

Describe the features of glutamate

A
  • most common excitatory transmitter in CNS
  • amino acid, therefore found in all neurones
  • 3 ionotropic glutamate receptor subtypes based on the drugs which act as selective agonists
  • action is terminated by selective uptake into the presynaptic terminals & glia
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11
Q

What are the 3 types of receptors affected by Glutamate?

A
  • AMPA
  • NMDA
  • Kainate
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12
Q

Describe features of Glutamate - AMPA receptors

A
  • AMPA receptors mediate fast excitatory transmission
  • Glutamate binding to AMPA receptors trigger Na+ & K+ currents resulting in an EPSP (excitatory post synaptic potential)
  • opening of the receptors is going to depolarise the cell, as the cell is already negative - leading to positive current flowing into the cell
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13
Q

Describe the features of a Glutamate - NMDA receptors

A
  • NMDA receptors often co-exist with AMPA receptors
  • NMDA receptors have a voltage-dependent Mg+ block
  • so, NMDA receptors only open when the neurons is already depolarised
  • NMDA receptors let Ca+ in –> leads to downstream signalling
  • NMDA receptors function as a coincidence detector: when a neuron is activated right after it was already activated
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14
Q

What else do glutamate activate?

A

metabotropic glutamate receptors (mGluRs)

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15
Q

Describe ionotropic receptors

A
  • 4 subunits forming a gated ion channel
  • Examples - AMPAR NMDAR
  • works by opening ion channel
  • FAST (msec)
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16
Q

Describe metabotropic receptors

A
  • G-protein coupled receptor
  • Examples - mGluR1, mGluR2
  • works by activating G-protein, which triggers downstream singalling cascade
  • SLOW (sec-min)
17
Q

What do mGluRs allow?

A

mGluRs allow glutamate to sometimes be inhibitory (e.g. in the retina)

18
Q

What is GABA (Y-amino butyric acid)?

A
  • not an amino acid used to synthesise protein
  • synthesised from glutamate by enzyme glutamic acid decarboxylase (glutamate without carboxyl group)
  • action is terminated by selective uptake into presynaptic & glia
19
Q

Is GABA normally an inhibitory neurotransmitter?

A

YES
- most common inhibitory transmitter in the CNS
- produces IPSPs (inhibitory postsynaptic potential) via GABA-gated chloride channels (GABAa receptors), if the membrane potential is above chloride’s Nerst potential

20
Q

What happens if there isn’t the right amount of inhibition via GABA?

A
  • too much –> coma or loss of consciousness
  • too little –> seizures
21
Q

Describe what occurs during the modulation of GABAa receptors

A
  • other chemicals can bind to the GABAa receptor and modulate the response to GABA binding
  • these chemicals have no effects without GABA binding (allosteric drug)
  • Benzodiazepines e.g. diazepam, used to treat anxiety
  • barbiturates are sedatives & anti-convulsants
  • neurosteriods are metabolites of steroid hormones e.g. progesterone (possible natural regulators)
22
Q

How does GABA act?

A

via metabotropic GABAab receptors

23
Q

Describe how GABA acts via metabotropic GABAb receptor

A
  • like the mGluRs, GABAb receptors are GPCPs
  • they act in diverse ways in different cells, but might:
  • open K+
  • close Ca2+ channels
  • trigger other second messengers like cAMP
  • often presynaptic or autoinhibitory
24
Q

What is glycine?

A
  • inhibits neurones via glycine-gated chloride channel (glycine receptor)
  • but it also binds to NMDA glutamate receptors
25
Q

What is dendritic integration?

A
  • each individual EPSP is not enough by itself to trigger an action potential (a few millivolts) - multiple EPSP (either from different parts of the neuron or in quick succession) to depolarise the cell enough to fire an action potential
  • when the postsynaptic neuron is depolarised, the voltage rises, but when the glutamate leaves, the postsynaptic neuron DOESNT FALL BACK DOWN STRAIGHT AWAY - few milliseconds in between - this create a window in which, if another EPSP arrives, it will raise cells voltage from a higher starting point (or baseline)
  • depolarisation at various parts of the dendritic tree (positive currents) - these currents diffuses and propagates passively till it reaches the part of the neuron with has a high concentration of voltage-gated sodium channels - usually the axon segment (axon pollick)

The axon pillock is where there may be enough voltage-gated sodium channels, that if a wave of depolarisation from the dendrites arrives, this will lead to a rise in membrane potential past the threshold, triggering the sodium channels

26
Q

Does it matter how excitatory & inhibitory synapses are arranged spatially?

A

YES
- an inhibitory synapse can block the propagation of an EPSP towards the soma
- GABAa receptors don’t always produce an IPSP, e.g. if Vm is near chloride’s Nernst potential
- in this can they act by SHUNTING INHIBITION
- opening chloride conductance decreases the membrane resistance –> current leaks out the membrane

  • location/geometry of the synapses are important - e.g. inhibitory synaose must be after excitatory synapse otherwise there would be no point of the inhibitory synapse
27
Q

Explain how inhibition often occurs pre-synaptically?

A
  • an action potential arises at the axon terminal, which opens voltage gated calcium channels - triggering synaptic release. HOWEVER, the release of GABA on the first neuron - activating GABAb receptors - triggering a downstream signalling cascade - e.g. deactivation of calcium channels - this will prevent the release of the presynaptic release of neurotransmitters
28
Q

What is inhibition for?

A
  • inhibitory neurons control/sculpt the activity of excitatory neurons
  • inhibitory neurons can gate signals and shut down pathways
29
Q

What is glutamate?

A

the major excitatory neurotransmitter

30
Q

What is GABA?

A

the major inhibitory neurotransmitter

Introduction to neuroscience - L1 (10 decks)

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