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Lily BRS Neuro > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What is synaptic transmission?

A

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

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2
Q

What are the three stages of synaptic transmission?

A
  1. Biosynthesis, packaging and release of neurotransmitter
  2. Receptor action
  3. Inactivation of neurotransmitter
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3
Q

What are some types of neurotransmitters?

A

Amino acids (glutamate, GABA)

Amines (noradrenaline, dopamine)

Neuropeptides ( opioid peptides)

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4
Q

What happens during the activation of a synapse?

A

An action potential causes depolarisation of the axon terminal
(Sodium in, potassium out)

Activates voltace gated calcium channels, calcium influx into terminal

This causes the exocytotic release of neurotransmitter from their vesicles into the synaptic cleft

NT diffuses across the synaptic cleft

The NT binds to receptors on the post synaptic membrane

The neurotransmitter did then Inactivated (May be by reuptake, or enzyme degradation etc)

Then sodium potassium pump then returns everything to normal resting state

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5
Q

How are neurotransmitters released?

A

Calcium dependant and requires rapid transduction

Also ATP requiring

Calcium channels open

Influx of clacium

Docking (vesicle fusion to presynaptic membrane)

Priming

Vesicle fusion

Vesicle exocytosis

Transmitter release

The vesicles then bud off and are reformed by endocytosis and can be recycled

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6
Q

How do rapid release rates occur?

A

Pumps pump NT into the vesicles (4000-10000 molecules of NT per vesicle)

Influx of calcium causes vesicles to dock, and prime to release NT

Special proteins on the vesicle and presynaptic membrane that enable fusion and exocytosis - vesicular proteins (SNARE proteins)

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7
Q

What are vesicular proteins so important?

A

a) they play a vital role in the release of neurotransmitters
b) they are targets for neurotoxins:

Alpha latrotoxin - (from black widow spider) stimulates transmitter release to depletion. Which leads to muscular paralysis

Zn2+ -dependant endopeptidases, these inhibit transmitter release. Eg. Tetanus toxin which causes spasms and paralysis (prevents release of GABA and glycine). And Eg. Botulinum toxin which causes flaccid paralysis (cleaves peptide bonds of vesicular proteins) (used in Botox)

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8
Q

How is neurotransmitter action defined by receptor kinetics?

A

Ion channel linked receptors:

FAST responses (msecs)

Mediates all fast excitatory and inhibitory transmission

G-protein-coupled receptors:

SLOW responses (secs/mins)

Effectors May be enzymes (adenyl cyclase…) or channels (ca2+ or K+)

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9
Q

What are some examples of ion channel linked receptors?

A

Glutamate, use sodium ions

Gamma-aminobutyric acid (GABA) , normally uses chloride ion channels and are Inhibitory

In neuromuscular junctions: acetylcholine at nicotinic receptors (use sodium ions)

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10
Q

What are some examples of G protein coupled receptors?

A

Acetylcholine and muscarinic receptors (eg in heart)

Dopamine

Noradrenaline

Serotonin

And neuropeptides

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11
Q

How do ion channel linked receptors have different distinct functional properties?

A

They are formed of 5 subunits

There can be many different combinations of these

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12
Q

What are the differences between glutamate and GABA ion channel linked receptors?

A

Glutamate:

Na+ channel, leads to depolarisation, excitatory

GABA:

Cl- channel, leads to hyperpolarisation, inhibitory

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13
Q

What is an excitatory postsynaptic potential?

A

EPSP

Once reads in membrane potential from resting (-65 mV) which then returns over about 5ms back to resting

Eg in glutamate ion channel linked receptors

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14
Q

What is an inhibitory postsynaptic potential?

A

IPSP

Decrease in postsynaptic membrane potential from resting potential (-65 mV) and then back to resting in about 5ms

Eg by GABA ion channel linked receptors

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15
Q

What are the two main types of glutamate receptors?

A

AMPA receptors - majority of FAST excitatory synapses, rapid onset, offset and desensitisation
Permeable to sodium ions

NDMA receptors - slow component of excitatory transmission, serve as coincidence detectors which underlie learning mechanisms
Permeable to sodium and calcium ions. Lots in the hippocampus

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16
Q

How does an excitatory glutamate synapse work?

A
  1. Glutamate is synthesised from glucose in the TCA cycle and transamination, then loaded into vesicles
  2. Glutamate reversibly binds to ion channel linked postsynaptic receptors
  3. Glutamate is regulated by reuptake into the presynaptic membrane. It is also reuptaken into glial cells bt EAATs (excitatory amino acid transporters)
  4. Glutamate is enzymatically modified by glutamine synthetase to glutamine in glial cells. This glutamine can then be taken up by presynaptic nerve terminals to make more glutamate
17
Q

What does excess glutamate lead to?

A

Abnormal cell firing leads to seizures associated with excess glutamate in the synapse

This can be seen on an EEG (electroencephalogram) which measures electrical activity in the brain. It will look like more spikes than usual

Causes convulsions

18
Q

What is epilepsy?

A

One of the most common neurological conditions affecting 50 million people worldwide

Characterised by recurrent seizures due to abnormal neuronal excitability

25-30% of people are refractory to treatment (don’t really respond)

A new generation of drugs targeting the GABA synapse have proved beneficial

19
Q

What happens in an inhibitory GABA synapse?

A
  1. GABA is synthesised by decarboxylation of glutamate by glutamic acid decarboxylase (GAD). GABA is loded Into vesicles
  2. GABA reversibly binds to post synaptic receptors (linked to ion channels). This opens chloride channels allowing an influx of chloride ions
  3. This hyperpolarises the postsynaptic cell
  4. There is then rapid uptake of GABA by GABA transporters into the presynaptic cell
  5. GABA enzymatically modified by GABA- transaminase to succinic semialdehyde in glial cells (and maybe GABA nerve terminals)
20
Q

What is the structure of a GABA receptors and what are the therapeutic consequences of this?

A

Pentameric organisation

Provides pharmacologically important binding domains

Drugs that facilitate GABA transmission (and therefore inhibit the nervous system) may be used to treat epilepsy, these include:

Barbiturates, steroids, benzodiazepines

They are anti epileptic, anxiolytic, sedative, muscle relaxants

Lily BRS Neuro (8 decks)

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