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BRS > neurotransmitters and pharmacology > Flashcards

neurotransmitters and pharmacology Flashcards

1
Q
  • What is synaptic transmission?
A

Information transfer across the synapse requiring the release of neurotransmitters and their interaction with postsynaptic receptors

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2
Q
  • List 4 characteristics of synaptic transmission
A

Rapid timescale

Diversity 

Plasticity 

Learning and memory
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3
Q
  • List the basic structures of the neurone
A

Dendrites (contains spines on surface)

Soma (cell body)

Axon 

Synaptic terminal
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4
Q
  • What is the purpose of spines being present on the surface of dendrites?
  • What neuronal structure integrates all the information coming into a neurone?
A

Protein molecules that increase the SA for information reception

Soma (cell body)
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5
Q
  • What are the 3 steps that occur when a dendrite of one neurone receives an electrical impulse from another neurone?
A

Information reception at dendrites

Integration (occurs at the soma)

Rapid transfer (action potential) - impulse passed along axon towards the synaptic terminals
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6
Q
  • What does a synapse consist of?
A

Presynaptic nerve ending/terminal

Gap (synaptic cleft) ~ 20-100nm 

Postsynpatic regions (dendrite or cell soma)
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7
Q
  • What are the 3 stages of synaptic transmission?
A

Biosynthesis, packaging and release of neurotransmitter stored in vesicles

Receptor action - activation of post-synaptic receptors

Inactivation - NT is inactivated rapidly once it's activated its receptors on the post-synaptic terminal
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8
Q
  • List 3 types of molecules that can be neurotransmitters and include examples of each
A

Amino acids - glutamate, gamma-aminobutyric acid (GABA), glycine

Amines - noradrenaline and dopamine 

Neuropeptides - opioid peptides
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9
Q
  • What is the single-most important excitatory neurotransmitter in the brain?
  • What is the single-most important inhibitory neurotransmitter in the brain?
  • Where is glycine most active and is it excitatory or inhibitory?
A

Glutamate

GABA

Spinal cord and brainstem

Inhibitory
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10
Q
  • What happens when a CNS synapse is activated?
A

Arrival of action potential - spreads across pre-synaptic nerve terminal

Depolarisation of whole terminal (Na+ influx followed by a K+ efflux) 

Activates VGCC to open allowing Ca2+ to flow into presynaptic terminal (down its concentration gradient) 

Activates exocytotic release of neurotransmitter into synaptic cleft → diffuses across synaptic cleft and makes contact with receptors (in this case excitatory receptors) on post-synaptic terminal 

Depolarisation of post-synaptic terminal leading to generation of another action potential 

Inactivation of neurotransmitter as it is returned to the pre-synaptic terminal back into its vesicle where it can be reused

Sodium-potassium pump returns membrane potential to normal (separate from synapse pathway)
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11
Q
  • What are the methods by which the neurotransmitter can be returned to the pre-synaptic terminal after depolarising the post-synaptic terminal?
  • How fast is neurotransmission?
  • What is the source of neurotransmitter?
A

Re-uptake of neurotransmitter via a protein transport channel
Enzymatic degradation within the synaptic cleft (e.g. acetylcholine broken down by acetylcholinesterase)

Happens within a few ms 

Synaptic vesicles (4,000-10,000 molecules per SV)
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12
Q
  • Outline process of neurotransmitter release
A

Membrane depolarisation leading to the opening of Ca2+ channels

Ca2+ influx leading to docking of synaptic vesicles (SVs) onto the pre-synaptic membrane- by a protein complex forming between vesicle, membrane and cytoplasmic proteins 

They are primed and undergo fusion → they open and neurotransmitter is released via exocytosis into the synaptic cleft 

The empty vesicle buds off (budding) and recycles forming new vesicles that can be reused (endocytosis)
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13
Q
  • What 2 things does neurotransmitter (NT) release require?
  • What type of proteins on the vesicle and presynaptic membrane enable fusion and exocytosis?
  • What are vesicular proteins targets for?
A

Calcium influx and RAPID transduction (electromechanical transduction - links the Ca2+ influx with NT release)

SNARE proteins (vesicular proteins e.g. synapsin, synaptobrevin, snap25)

Neurotoxins (particularly those that interfere with the NT release process)
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14
Q
  • What does the neurotoxin alpha larotoxin (from black widow spider) do?
  • What do Zn2+ dependent endopeptidases do?
A

Stimulate NT release until depletion of NT → muscular paralysis

Inhibits transmitter release
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15
Q
  • What does tetanus toxin cause and what bacteria produces it?
A

Causes spasms and paralysis as it inhibits GABA and glycine (both inhibitory in CNS)

Produced by Clostridium tetani

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16
Q
  • What does botulinum toxin cause and how does it do this?

- What bacteria produces botulinum toxin?

A

Flaccid paralysis (due to complete muscle relaxation)
Cleaves peptide bonds of vesicular proteins leading to inactivation
so docking, fusion and release of NT can’t occur
One of the most powerful toxins

Clostridium botulinum → release botulinum toxin
17
Q
  • How can you measure the toxicity of a drug?
A

The minimum dosage required to kill a mouse

18
Q
  • List all the transmitter release requirements
A

Ca2+ dependent

Transmitter-containing vesicles docked on presynaptic membrane 

Protein complex formation between vesicle membrane and cytoplasmic proteins enabling vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis 

Vesicle recycling (ATP is required)
19
Q
  • What responses do ion channel-linked receptors mediate?

- What type of responses do G-protein coupled receptors mediate?

A

All FAST (msecs) excitatory and inhibitory transmission

SLOWer (secs/mins) than ion channel-linked receptors

20
Q
  • Give examples of responses where ion channel-linked receptors are used
  • Give examples of responses where G-protein coupled receptors are used
A

CNS - glutamate, GABA
NMJ - Acetylcholine at nicotinic receptors

CNS and PNSL: Acetylcholine at muscarinic receptors (on heart), dopamine, noradrenaline, serotonin (5HT) and neuropeptides (e.g endorphin and enkephalin)

21
Q
  • What does the opening of Na+ channels via a glutamate molecule do to the postsynaptic membrane potential?
  • What postsynaptic potential does an inhibitory NT receptor (e.g. GABA a) cause?
A

Increase for short time

Inhibitory postsynaptic potential (IPSP) caused by GABA A receptor → Cl- influx
Decrease in membrane potential
22
Q
  • Name the 2 main types of ion-channel linked glutamate receptors and what do they mediate?
A

AMPA - majority of FAST excitatory synapses. Rapid onset, offset and desensitisation. Only permeable to Na+

NMDA - SLOW component of excitatory transmission.
Serve as coincidence detectors which underlie learning mechanisms.
Permeable to both Na+ and Ca2+.
Hippocampus has a very high density of these receptors

23
Q
  • Outline the process that occurs at an excitatory glutamate synapse
A

Glutamate synthesised from glucose via TCA cycle and transamination. Loaded into vesicles and released into synaptic cleft via exocytosis

Glutamate reversibly binds postsynaptic receptors (AMPA and NMDA)

Inactivation of glutamate (re-uptake into presynaptic terminal) + can also be re-uptaken into surrounding glial cells.

Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)
24
Q
  • What happens when glutamate is in glial cells?
  • What does an EEG (electroencephalography) measure?
  • What can abnormal cell firing associated with excess glutamate lead to?
A

Glutamate is enzymatically modified by glutamine synthetase to glutamine, which can then be pumped back into the pre-synaptic terminal

Electrical activity in the brain 

Seizures 
Shown by spikes on an EEG
25
Q
  • Outline the process that occurs at an inhibitory GABA synapse
A

GABA synthesised in the pre-synaptic terminal by decarboxylation of glutamate by glutamic acid decarboxylase (GAD)

GABA reversibly binds to post-synaptic receptors (GABA a receptors) → opens chloride channels → influx of chloride ions into post-synaptic terminal leading to hyperpolarisation 

Inactivated by rapid uptake into pre-synaptic terminal by GABA transporters (GATs) 

OR GABA can be taken into glial cells where it is enzymatically modified by GABA-transaminase (GABA-T) to succinic semialdehyde
26
Q
  • Which drugs facilitate GABA transmission?
A

Barbiturates

Benzodiazepines 

Steroids 

Convulsants 

Zn 2+ 

Ethanol
27
Q
  • What properties do drugs facilitating GABA transmission have?
A

Antiepileptic

Anxiolytic 

Sedative 

Muscle relaxant
28
Q
  • How many subunits does the GABA A receptor have?

which drug binds to which receptor

A

5 (pentameric organisation)
provides pharmacologically important binding domains

benzodiazepines, zn2+, convulsant on GABA alpha
ethanol on another
barbiturates on another
steroids on another

BRS (41 decks)

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