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Clinical Neuroscience > Cellular Physiology of the Brain - Neurotransmission > Flashcards

Cellular Physiology of the Brain - Neurotransmission Flashcards

1
Q

What are the three chemical classes of neurotransmitters in the CNS?

A

Amino acids
Biogenic amines
Peptides

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2
Q

Examples of amino acid neurotransmitters in the CNS
Are they excitatory or inhibitory?

A

Glutamate - excitatory
GABA -inhibitory
Glycine - inhibitory

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3
Q

Examples of biogenic amines neurotransmitters in the CNS

A
  • Acetylcholine
  • Noradrenaline
  • Dopamine
  • Serotonin / 5-HT
  • Histamine
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4
Q

Examples of peptides neurotransmitters in the CNS

A
  • Dynorphin
  • Encephanlins
  • Somatostatin
  • Cholecystokinin
  • Neuropeptide Y
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5
Q

What is the main excitatory amino acid neurotransmitter?

A

Glutamate

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6
Q

What are the inhibitory amino acid neurotransmitters?

A

Glycine
GABA

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7
Q

Types of glutamate receptors
How do they exert their effects

A

Ionotropic: contain integral ion channel
- AMPA: permeable to Na + K
- Kainate: permeable to Na + K
- NMDA receptors: permeable to Na, K + Ca
.
Metabotropic: G protein coupled receptors
- mGluR1-7: via IP3/Ca or changes in cAMP

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8
Q

Types of ionotropic glutamate receptors
What are they permeable to?

A
  • AMPA: permeable to Na + K
  • Kainate: permeable to Na + K
  • NMDA receptors: permeable to Na, K + Ca
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9
Q

What does glutamate release cause?

A
  • depolarisation on post synaptic cell by acting on ligand gated ion channels
  • excitatory postsynaptic potential
  • causes APs
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10
Q

What do AMPA receptors mediate?

A

Initial fast depolarisation

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11
Q

What do NMDA need to allow ion flow?

A

Glutamate binding
Cell to be depolarised

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12
Q

What do NMDA receptors have an important role in?
How?

A

Learning + memory
- activation of NMDA receptors > up regulates AMPA receptors
- strong high frequency stimulation casues long term potentiation
- Ca2+ entry through NMDA receptors is important for LTP

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13
Q

What is long term potentiation?

A

Persistent strengthening of synapses leading to long lasting increase in signal transmission between neurones

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14
Q

What can cause exictotoxicity?

A

Too much Ca2+ entry through NMDA receptors
(Too much glutamate)

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15
Q

What is the main inhibitory transmitter in the brain?

A

GABA

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16
Q

What is the main inhibitory transmitter in the brainstem + spinal cord?

A

Glycine

17
Q

How do inhibitory amino acid transmitter work?

A
  • GABA + glycine have integral Cl- channels
  • opening of the channels + Cl- influx causes hyperpolarisation
  • inhibitory post synaptic potential
  • decreased firing of AP
18
Q

What drugs enhance the response to GABA?
What effects do they have?

A

Barbiturates
Benzodiazepines
Sedative + anxiolytic

19
Q

What is benzodiazepines used to treat?

A

Anxiety
Insomnia
Epilepsy

20
Q

What are barbiturates not used as much now?

A

Risk of fatal overdose
Addictive

21
Q

What receptors do ACh act on in the brain?

A

Nicotinic
Muscarinic

22
Q

What are cholinergic pathways in the CNS involved in?

A

Arousal
Learning
Memory
Motor control

23
Q

Key dopaminergic pathways in CNS
What are their functions?

A
  • nigrostriatal: motor control
  • neocortical + mesolimbic: mood, arousal + reward
24
Q

Degeneration of what pathway causes Parkinson’s disease?

A

Nigrostriatal

25
Q

Overactivity of what pathway may contribute to schizophrenia?

A

Mesolimbic

26
Q

Why can amphetamine use cause similar symptoms to schizophrenia?

A
  • Causes release of dopamine
  • Overactivity of dopamine can contribute to schizophrenia
27
Q

What is the nigrostriatal pathway between?
What is its function?
What is its clinical significance?

A
  • substantia nigra to striatum
  • motor control
  • degeneration causes Parkinson’s disease
28
Q

What is the mesolimbic pathway between?
What is its function?
What is its clinical significance?

A
  • midbrain to limbic system
  • mood, arousal, reward
  • Overactivity can contribute to schizophrenia
29
Q

What is the neocortical pathway between?
What is its function?

A
  • midbrain to cerebral cortex
  • mood, arousal + reward
30
Q

How can Parkinson’s disease be treated?

A

co-careldopa
- levodopa (dopamine precursor)
- converted to dopamine by DOPA decarboxylase
- given with carbidopa

31
Q

Why do you give carbidopa with L-DOPA in treatment of Parkinson’s disease?

A
  • you want levodopa to be converted to dopamine in the brain not the periphery
  • high levels in periphery can effect heart, GI + urinary systems
  • cardbidopa does not cross BBB + inhibits conversion in periphery
32
Q

Outline noradrenergenic pathways in CNS

A
  • cell bodies of NA containing neurone within brainstem locus coeruleus
  • diffuse release throughout cortex, hypothalamus + cerebellum
  • involved in behavioural arousal
33
Q

Where does most noradrenaline come from?

A

Locus coeruleus in brainstem

34
Q

What is a low level of NA related to?

A

Depression

35
Q

When are locus coeruleus neurones inactive?

A

During sleep

36
Q

Functions of serotonin

A

Sleep/wakefullness
Mood

37
Q

What is used for the treatment of depression or anxiety?

A

Serotonin selective reuptake inhibitors SSRIs

38
Q

Where is serotonin released from?

A

Raphe nuceli of brainstem

39
Q

What transmitters are involved in pain transmission?

A

Dynorphin
Encephalins

Clinical Neuroscience (20 decks)

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