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Cell Biology > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

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1
Q

What could happen after a NT has had its effect on the target cell?

A

Re-uptake, enzymal inactivation and diffusion.

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2
Q

What are the 2 types of NT receptors?

A

Ionotropic and metabotropic.

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3
Q

What are the 3 types of NTs?

A

AAs, biogenic amides and peptides.

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4
Q

What are examples of AA NTs?

A

Glutamate, GABA and glycine.

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5
Q

What comprises the biogenic amines?

A

Catecholamines and indolamines.

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6
Q

What are examples of catecholamines?

A

Noradrenaline, adrenaline and dopamine.

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7
Q

What is an example of an indolamine?

A

Serotonin.

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8
Q

What are examples of peptide NTs?

A

Encephalin, endorphin and dynorphin.

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9
Q

What is the function of glutamate as a NT?

A

Primary excitatory NT in the CNS.

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10
Q

What is glutamate involved in?

A

Memory, learning and cell death.

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11
Q

What does GABA stand for?

A

Gamma- aminobutyric acid.

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12
Q

What is the function of GABA?

A

Principal inhibitory NT in the CNS.

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13
Q

How does GABA act?

A

Via chloride channels.

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14
Q

What is the function of glycine in the CNS?

A

Second most common inhibitory NT in the CNS.

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15
Q

What is the function of glycine outside the CNS?

A

Primary inhibitory NT in the spinal cord and brainstem.

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16
Q

What type of post-synaptic receptor does glutamate use?

A

Mostly via ionotropic receptors

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17
Q

What are the 3 types of ionotropic receptors that glutamate uses?

A

NMDA, Kainate and AMPA.

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18
Q

What ions do NMDA receptors allow the passage of?

A

Calcium ions.

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19
Q

Which ions do the Kainate receptors allow the passage of?

A

Sodium and potassium ions.

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20
Q

Which ions do the AMPA receptors allow the passage of?

A

Permeable to cations (positive).

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21
Q

Where does glutamate act?

A

Widespread in the CNS.

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22
Q

Where do glutamate neurons span in the CNS?

A

Hemispheres and descending to the brainstem or spinal cord.

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23
Q

What is synaptic plasticity?

A

Process by which synapses are strengthened or weakened by feedback mechanisms.

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24
Q

What is synaptic plasticity used for?

A

For storing long or short term memories.

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25
Q

What is excitotoxicity?

A

Excessive stimulation of NMDA receptors causes a large influx of calcium ions.

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26
Q

What can excitotoxicity result in?

A

Cell death.

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27
Q

What is dysfunction of glutamate NT linked to?

A

Karl Lashley’s visual aura in migraines.

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28
Q

What mental disorder is glutamate implicated in?

A

Cortical spreading depression (CSD).

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29
Q

Which brain disorder is glutamate dysfunction linked to?

A

Epilepsy.

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30
Q

How does glutamate dysfunction cause epilepsy?

A

Excess excitation causes a feedback loop, uncontrolled excitation causes over expanding in brain.

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31
Q

What can epilepsy begin as?

A

Partial seizures.

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32
Q

What happens if partial seizures become more uncontrolled?

A

They can become Grand Mal seizures.

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33
Q

What can epileptic seizures be treated with?

A

Phenytoin and Benzodiazepines.

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34
Q

How does phenytoin treat epilepsy?

A

Increases the refractory period between firings in voltage gated sodium channels.

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35
Q

How does benzodiazepines treat epilepsy?

A

Increase the action of GABA (inhibitory).

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36
Q

What is the mechanism of benzodiazepines on GABA channels?

A

When benzodiazepines are bound, GABA can open the channel more often.

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37
Q

Are benzodiazepines specific?

A

They only enhance the action of existing GABA molecules.

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38
Q

Where is GABA mainly found?

A

In the interneurons of the CNS.

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39
Q

Where is GABA also found?

A

In striatum and globus pallidus.

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40
Q

What does GABA act on?

A

Ligand gated chloride channels.

41
Q

What is GABA inactivated by?

A

Presynaptic reuptake.

42
Q

What does alcoholism cause?

A

A change in GABA transmission.

43
Q

What does withdrawal of alcohol from an alcoholic result in?

A

Convulsive movements and seizures.

44
Q

What can alcoholism be treated with?

A

Benzodiazepines and phenytoin.

45
Q

What is tetanus caused by?

A

Toxin from clostridium tetani.

46
Q

How does tetanus cause disease?

A

Inhibits release of glycine and shifts excitation-inhibition balance.

47
Q

What are the mild effects of tetanus?

A

They are restricted to muscles innervated by cranial nerves.

48
Q

What are the more serious effects of tetanus?

A

Epileptiform fits.

49
Q

What is tetanus treated with?

A

Anti-toxin and benzodiazepines.

50
Q

What is dopamine?

A

A NT and neuromodulator.

51
Q

What is dopamine involved in?

A

Pleasure, addiction and movement.

52
Q

Which system is noradrenalin involved in?

A

The sympathetic (fight or flight) NT.

53
Q

What is decreased potentiality of noradrenaline associated with?

A

Parkinson’s and ADHD.

54
Q

Where are all catecholamines synthesized?

A

In the bouton and inactivated by reuptake.

55
Q

What is adrenaline involved in?

A

The sympathetic system.

56
Q

Where is adrenaline produced?

A

A peripheral hormone from the adrenal medulla.

57
Q

What is the synthesis route order of catecholamines?

A

Tyrosine, DOPA, dopamine, noradrenaline and finally adrenaline.

58
Q

What are adrenoreceptors?

A

G-protein linked metabotropic receptors for noradrenaline.

59
Q

Which areas of the brain does noradrenaline work in?

A

Locus coeruleus and medulla/hypothalamus.

60
Q

For what processes is noradrenaline used in the locus coeruleus?

A

Sleep, wakefulness, alertness and attention.

61
Q

For what is noradrenaline controlling in the medulla?

A

Feeding behaviour.

62
Q

For what is noradrenaline controlling in the hypothalamus?

A

Blood pressure regulation.

63
Q

What are dopaminergic receptors?

A

G-protein linked metabotropic receptors.

64
Q

Where does dopamine work in the brain?

A

Nigrostriatal, mesolimbic and mesocortical and the tuberohypophyseal system.

65
Q

What is dopamine controlling in the nigrostriatal area in the brain?

A

Motor control.

66
Q

What is dopamine controlling in the mesolimbic and mesocortical areas of the brain?

A

Behavioural effects.

67
Q

What is dopamine controlling in the tuberohypophyseal system?

A

Endocrine control via the anterior pituitary.

68
Q

How is dopamine linked to Parkinson’s?

A

Symptoms due to depleted dopamine in the motor coordinated circuits.

69
Q

What are the symptoms of Parkinson’s linked to dopamine dysfunction?

A

Tremor, muscle rigidity and bradykinesia or akinesia.

70
Q

What does bradykinesia mean?

A

Slowness of movement.

71
Q

What does akinesia mean?

A

Loss of ability to move muscles voluntarily.

72
Q

How is dopamine dysfunction linked to Schizophrenia?

A

Over production of dopamine in the mesolimbic system.

73
Q

What is used to treat Schizophrenia?

A

Antipsychotics.

74
Q

How is addiction linked to dopamine?

A

Works through pleasure centres of the CNS located in the mesolimbic dopamine system.

75
Q

Where in the brain does serotonin work?

A

Locus coeruleus and the Raphe nuclei.

76
Q

What processes is serotonin involved in the locus coeruleus?

A

Sensory signals.

77
Q

What processes is serotonin involved in the raphe nuclei?

A

Sleep, wakefulness and mood.

78
Q

Which mental disorders are associated with serotonin?

A

Depression and OCD.

79
Q

How is depression and OCD treated?

A

With serotonin reuptake inhibitors such as Fluoxetine.

80
Q

What is Fluoxetine also known as?

A

Prozac

81
Q

How are the effects of MDMA caused?

A

By causing the release and preventing subsequent reuptake of serotonin.

82
Q

How is serotonin involved in some drugs of abuse?

A

Receptor agonists include LSD, psilocybin and mescaline.

83
Q

Where are peptide NTs made?

A

In the cell body and transported to the bouton.

84
Q

Which peptide NTs are implicated in schizophrenia?

A

Neuropeptide Y, neurotensin and cholecystokinin.

85
Q

What is substance P involved in?

A

Pain transmission.

86
Q

What are the effects of endorphins and encephalins on opioid receptors?

A

They act on opioid receptors as endogenous ligands.

87
Q

What are examples of opioids?

A

Morphine, codeine, pethidine, methadone and diamorphine.

88
Q

What do opioids do to opioid receptors?

A

Cause downregulation of opioid receptors in the CNS.

89
Q

What does downregulation of opioid receptors cause?

A

Opioid tolerance and increased tolerance.

90
Q

Where are opioid receptors also present?

A

In the limbic system and periaqueductal grey.

91
Q

What can reduce opioid withdrawal symptoms?

A

Naloxone as an opioid receptor antagonist.

92
Q

Where is acetylcholine found?

A

In the peripheral and CNS as well as neuromuscular junctions.

93
Q

Which areas of the brain are essential for formation of new memories and learning?

A

The hippocampus and cortex.

94
Q

In the CNS, where do neurons project into?

A

The hippocampus and cortex.

95
Q

Which disease is associated with dysfunction of ACh in the CNS?

A

Alzheimer’s disease.

96
Q

How does nicotine affect the body?

A

Acts on nicotonic acetylcholine receptors found in the CNS and PNS.

97
Q

What do anticholinesterases do?

A

Prevent the breakdown of ACh and prolong its activity.

98
Q

What are the therapeutic uses of anticholinesterases?

A

Donepezil in Alzheimer’s.

99
Q

What are the toxic uses of anticholinesterases?

A

Insecticides and nerve gases.

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