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B > Neurotransmitters and Pharmacology > Flashcards

Neurotransmitters and Pharmacology Flashcards

1
Q

What are the adaptations and functions of the dendrites in neurones

A

Dendrites have spines which increase the surface area for the receipt of information from the other neurones etc. So the dendrites are information receptors

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2
Q

Function of soma/ cell body in the neurone

A

Integration of the signals received

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3
Q

Function of the axon

A

Rapid transfer of the action potential

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4
Q

Where are neurotransmitters release from

A

The synaptic terminal

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5
Q

Neurotransmission is restricted to specialised structures called …

A

Synapses

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6
Q

What are the three stages of synaptic transmission

A

1) Biosynthesis, packaging and release of neurotransmitter ( which is packed into vesicles )
2) Receptor action
3) Inactivation of neurotransmitters to allow for the system to work effectively

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7
Q

The three classes of neurotransmitter present

A

Amino acids
Amines
Neuropeptides

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8
Q

Amino acid neurotransmitter

A

Glutamate
Gamma-amimobutytic acid (GABA)
Glycine (Gly)

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9
Q

Amines neurotransmitter

A

Noradrenaline ( NA)

Dopamine (DA)

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10
Q

Neuropeptide neurotransmitters

A

Opioid peptides

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11
Q

Glutamate

A

Single most important amino acid in brain , normally excitatory transmitter

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12
Q

GABA

A

Most important inhibitory transmitter in brain

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13
Q

Glycine

A

Inhibitory neurotransmitter in spinal cord

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14
Q

Noradrenaline

A

Involved in sympathetic and parasympathetic nervous system

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15
Q

Opioid peptides

A

Endorphins etc

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16
Q

Step 1 of CNS synapse activation

A

AP

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17
Q

Step 2 of CNS synapse activation

A

Depolarisation of nerve terminal ( sodium and potassium ion channels start working etc )

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18
Q

Step 3 of CNS synapse activation

A

Voltage gated calcium channels open and calcium enters into presynaptic nerve terminal down the concentration gradient

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19
Q

Step 4 of activation of CNS synapse

A

Calcium ions stimulate the release of neurotransmitters into the synaptic cleft

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20
Q

Step 5 of activation of CNS synapse

A

Neurotransmitters bind to receptors on post synaptic neurone. In the case of an excitatory synapse, they cause sodium ions to go into cell and stimulate another AP

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21
Q

Step 6 of activation of a CNS synapse

A

Reputable of neurotransmitters into presynaptic nerve terminal where it is packaged into vesicles

Or broken down by enzymes

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22
Q

What enzyme works to break down ACh

A

Acetylcholine is broken down by acetylcholinesterase which sits in cleft and so inactivates it

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23
Q

Step 7 of activation of CNS synapse

A

Sodium potassium transported restores status before another AP arrives

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24
Q

What conc of calcium is needed to be reached inside the cell for the neurotransmitter to be released

A

200 microM , resting cellular calcium conc is less that 1 microM

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25
Q

Quanta

A

Packets of 4000-10000 molecules of neurotransmitters

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26
Q

Neurotransmitter release

A

Activation of transmitter release is calcium dependent and required RAPID transduction

Membrane depolarisation 
Calcium channels open 
Calcium influx
Vesicle fusion 
Vesicle exocytosis
Transmitter release
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27
Q

How do rapid release rates occur

A

Synaptic vesicles are filled with neurotransmitter and docked in the synaptic zone
Special proteins on the vesicle and presynaptic membrane enable fusion and exocytosis ( called vesicular proteins )

28
Q

What are proteins on the vesicles called

A

SNARE proteins like synapse in ,synaptobrein and SNAP25

They mediate the process of exocytosis and the release of the neurotransmitter

29
Q

Name some neurotoxins

A

Vesicular proteins are targets for neurotoxins

  • alpha latrotoxin
  • tetanus toxin
  • botulinum toxin
30
Q

Alpha tarotoxin

A

From black widow slide and stimulates the transmitter release until depletion and so none is left. It focuses on cholinergic terminal which releases ACh. Eventually you see muscular paralysis

31
Q

Examples of zinc dependent endopeptidases

A

Tetanus

Botulinum toxin

32
Q

What do zinc dependent endopeptidases do

A

Inhibit transmitter release

33
Q

Tetanus toxin ( Ctetani)

A

Causes spasms and paralysis - inhibits the release of 2 main neurotransmitters GABA and glycine which are inhibitory transmitter release

34
Q

Bolulinum toxin ( C botulinum)

A

Causes flaccid paralysis due to the complete muscle relaxation . It is a bichain molecule. First part of molecule binds to cholonergic NT terminal.

Second chain penetrates nerve terminal and interacts with vesicle protein so cleaves peptide bonds and inactivates vesicular protein and so NT cannot be released

35
Q

Botox

A

Causes relaxation of muscle and smoothing of brow to stop release of ACh

36
Q

What can botulism cause

A

Nasty form of food poisoning and can cause resp arrest and death

37
Q

Transmitter release requirements

A

Calcium dependent
Transmitter containing vesicles are to be docked on ore synaptic membrane
Protein complex formation between vesicle, membrane and cytoplasmic proteins to enable both vesicle docking and a rapid response to calcium ion entry leading to membrane fusion and exocytosis
ATP and vesicle recycling - pumps which fill vesicle with neurotransmitters are ATP requiring pumps

38
Q

Ion channel linked receptor

A

Mediate all fast excitatory and inhibitory transmission in CNS( msec)

39
Q

Excitatory ion channel linked receptor

A

Sodium ions

40
Q

Inhibitory ion channel linked receptor

A

Chloride ions

41
Q

Glutamate receptor

A

Glutamate binds and stimulates and opens the receptor allowing sodium ions to enter cell and stimulate an action potential

42
Q

G Protein coupled receptor

A

Slow response ( secs/mins/hrs)

43
Q

What is usually the effector in G protein coupled receptors

A

Enzymes ( adenyl cyclase, phosplipase C, cGMP-PDE) or channels ( calcium or potassium ) . When stimulated by agonist, Binds to G protein which then binds to AC ( enzyme)

This may stimulate / inhibit enzyme

44
Q

What does a G protein coupled receptor consist of

A

7 alpha helical transmembrane proteins

45
Q

Examples of Ion channel linked repceptors inCNS

A

Glutamate , GABA

46
Q

Example of ion channel linked receptor at neuromuscular junction

A

Acetylcholine at nicotine’s receptors ( links to sodium ions)

47
Q

Examples of G protein coupled receptors at the CNS and PNS

A

ACh atmuscarinic receptors ( heart - stimulates vagus nerve which decreases heart rate due to ACh) , dopamine, noradrenaline , serotonin ( 5 HT) , and neuropeptides ( enkephalinn)

48
Q

Nicotinic receptors are which kind of receptors

A

Ion channel linked

49
Q

Muscarinic receptors are which kind of receptor

A

G protein linked

50
Q

Influx of chloride ions lead to

A

Hyperpolarisation . IPSP produced

51
Q

Influx of sodium ions leads to

A

Depolarisation . EPSP produced

52
Q

Two types of glutamate receptors

A

AMPA and NMDA

53
Q

AMPA receptors

A

Majority of fats excitatory synapses,
Rapid onset, offset and desensitisation

Only sodium ions can enter

54
Q

NMDA receptor

A

Dosimeter and calcium ions can enter
Slow component of excitatory transmission
Serve as coincidence detectors which underlie learning mechanisms and memory processes

55
Q

What does coincidence receptor mean

A

Needs another incoming signal to stomata signal and glutamate

56
Q

Which part of the body has an increased density of NMDA receptor

A

Hippocampus ( involved in short term memory)

57
Q

Excitatory glutamate synapse process

A

1) glutamate synthesised from glucose via TCA cycle and transamination
2) glutamate reversibly binds to post synaptic receptors ( NMDA and AMPA ion channels )
3. Rapid uptake of glutamate by excitatory amino acid transporters - reuptake of inactivated gluamate
4. Glutamate is emzymatically modified by glutamine sythetase to glutamine in glial cells

58
Q

What happens to the glutamine in glial cells

A

Glutamine is released by glial cells and can then be taken up by presynaptic membranes to make glutamate, referred to as glutamate-glutamine cycle

59
Q

Seizures

A

Abnormal cell firing leads to seizures associated with excess glutamate in the synapse. Uncontrolled glutamate release leads to increased spiking on EEG , increased electrical activity in brain and the seizures and physical effects of convulsions

As glutamate decreases, glutamine increases and decreases . Excess glutamate is metabolised to glutamine

60
Q

What does refractory mean

A

Doesn’t respond to treatment

61
Q

Difference between seizures and epilepsy

A

Single seizure can be due to high temp etc but recurrent seizure are classed as epilepsy

62
Q

Inhibitory form of GABA synapse

A

1) GABA synthesised by de carboxylation of glutamate by glutamic acid decarboxylase ( GAD)
2) GABA reversible binds to post synaptic receptors ( linked to ion channels)
3) rapid reuptake of GABA by GABA transporters ( GATs)
4) GABA enzymatically modified by GABA transaminase ( GABA-T) to succinic semialdehyde ( glial cells and GABA nerve terminals )

63
Q

What happens to the succinic semialdehyde

A

Broken down to succinate which is put back into TCA cycle

64
Q

Epilepsy may be due to

A

GABA receptors not working well

65
Q

Structure of GABA receptor

A

Pentameric organisation provides pharmacologically imp binding domains

66
Q

Drugs facilitating GABA transmission are

A

Anti-epileptic- barbiturates and benzodiazepines
Anxiolytics
Sedative
Muscle relaxant

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