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Neuroscience > Neurotransmission > Flashcards

Neurotransmission Flashcards

1
Q

List the types of neurotransmitters in the CNS

A

Amino acids (glutamate, GABA, glycine)

Gaseous molecules (NO, CO)

Miscellaneous (purines, endocannabinoids)

Monoamines: Catecholamines (noradrenaline, dopamine), Indoleamines (5-hydroxtryptamine/ 5-HT), Others (melatonin, histamine)

Acetylcholine

Peptides:
Hypothalamic releasing factors (eg. somatostatin), Tachykinins (eg. Substance P), Opioids (eg. enkephalins), Others (eg. CCK, NPY, orexin)

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2
Q

What are the types of monoamines?

A

Catecholamines (noradrenaline, dopamine), Indoleamines (5-hydroxtryptamine/ 5-HT), Others (melatonin, histamine)

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3
Q

What signalling predominates in the cortex?

A

Interlaminar glutamate or GABA neurons, Local circuit GABA, gaseous or peptide

Cortico-cortical glutamate neurons

Cortico-subcortical glutamate neurons

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4
Q

What signalling predominates in the brain stem?

A

Monoamine/ACh projecting to higher centers

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5
Q

What signalling predominates in the subcortical regions (cerebellum, striatum, thalamus and spinal cord)?

A

Local circuit neurons GABA and peptides

Projecting GABA and peptide neurons

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6
Q

What are the criteria to localize a neurotransmitter to a neuron?

A

Neuronal localization: the neurotransmitter must be localized in the neuron including; the transmitter candidate itself, biosynthetic/metabolic enzymes, reuptake mechanisms and appropriate receptors

Synaptic mimicry: must be proven to occur by a different exogenous transmitter or receptor agonist, compare responses.

Neurotransmitter versus neuromodulator: must be understood if it transmits or just modulates

Neuronal release: must be evidence of release from neuron (sample supernatant produced)

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7
Q

What is an EPSP and an IPSP?

A

Excitatory post synaptic potential (depolarization) and inhibitory post synaptic potential (hyperpolerization)

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8
Q

What is pre-synaptic inhibition?

A

Presynaptic inhibition is an inhibitory input to a neuron to make it less likely to fire an action potential

GABA receptors are activated, it causes a chloride influx, which hyperpolarizes the cell

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9
Q

What are excitatory amino acids?

A

Glutamate

aspartate

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10
Q

Where are glutamate neurotransmitters located?

A

Cortico-cortical and cortico-subcortical neurons

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11
Q

How is glutamate synthesised?

A

De novo synthesis from glucose and from glutamine supplied by glial cells.

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12
Q

What packages glutamate into vesicles?

A

Vesicular glutamate transporters (vGluTs)

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13
Q

What receptors does glutamate bind to?

A

Ionotropic (ligand-gated ion channels) AMPA, NMDA, Kainate
(evoke fast EPSPs)

Metabotropic (G-protein coupled receptors) (mGlu1-8)

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14
Q

What does the NMDA receptor allow through?

A

Na+, Ca2+

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15
Q

What is the action of ketamine?

A

NMDA blocking drug

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16
Q

How is glutamate cleared from the synapse?

A

Excitatory amino acid transporters (EAATs) on neighbouring glial cells (EAAT1 and EAAT2).

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17
Q

What happens to glutamate within the glial cell?

A

Glutamate is converted to glutamine by glutamine synthetase

Glutamine is subsequently released by System N transporters and taken up by neurons through System A sodium-coupled amino acid transporters to complete the glutamate–glutamine cycle.

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18
Q

What are the functions of glutamate?

A

Memory: long term potentiation (LTP) is mediated by glutamate.

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19
Q

Describe excitotoxicity

A

Ischemia (hypoxia/hypoglycemia) leads to excess release of glutamate overstimulation of NMDA receptors - excessive Ca2+ entry into neurons - cell death.

NMDA receptor antagonists reduce cell death

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20
Q

What are the inhibitory amino acids?

A

GABA and glycine

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21
Q

What neurons release GABA/glycine?

A

Cortical interneurons, sub-cortical neurons (eg. basal ganglia).

Glycine in spinal cord interneurons

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22
Q

How is GABA synthesised?

A

From glutamate (Glu) by glutamate decarboxylase (GAD)

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23
Q

What are the GABA receptors?

A

GABAa receptor (Cl- channel) (Ionotropic GABAA receptors evoke fast inhibitory postsynaptic potentials (IPSPs))

GABAb (Gi-protein coupled)

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24
Q

Describe the GABAa channel

A

Ligand-gated ion channel (Cl-)

Pentameric structure

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25
Q

What role do GABAa blocking drugs have?

A

Channel blocking agents are convulsant agents.

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26
Q

How is GABA neurotransmission terminated?

A

Uptake of GABA by GABA transporter 2/3 (GAT 2/3) into astrocytes

27
Q

What happens to GABA in astrocytes?

A

GABA transaminase (GABAT) converts it into succinic semialdehyde (SSA).

SSA is then oxidized by SSADH to succinate and serves as a substrate within the tricarboxylic acid (TCA) cycle.

28
Q

What is the role of GABA?

A

Movement control: GABA is a major transmitter in the basal ganglia.

29
Q

What disease affecting movement is due to loss of GABAergic neurons?

A

Huntington’s disease due to loss of GABA-containing long projection neurones (striatopallidal) leads to uncontrolled movement.

30
Q

What do many anti-epileptic drugs target?

A

Anticonvulsants increase GABA transmission by facilitating GABAA receptor function (eg. benzodiazepines, barbiturates)

Inhibiting GABA metabolism (valproate) or uptake (tiagabine).

31
Q

Where are CNS ACh receptors located?

A

ACh neurons located in basal forebrain, septum and striatum.

32
Q

What are the ACh receptor subtypes?

A

Muscarinic (metabotropic)

Nicotinic (ionotropic)

33
Q

What are the CNS functions of acetylcholine?

A

Movement control: muscarinic antagonists (benzatropine) helpful in relief of tremor in Parkinson’s disease.

Reward and motivation: addiction to nicotine related to ACh interaction with midbrain dopamine (mesolimbic) pathways.

Memory: lesion of cholinergic pathways and muscarinic antagonists induce amnesia.

34
Q

What are peptide neurotransmitters stored in?

A

Dense cored vesicle, released by exocytosis

35
Q

What are tachykinins?

A

Substance P and the Neurokinins

36
Q

What are tachykinin receptors?

A

Slow excitatory responses via G-protein coupled receptors (NK1-3).

37
Q

Where is substance P localised to?

A

Primary sensory afferents (pain pathways), medulla (vomiting centre) and limbic system (anxiety pathways).

38
Q

What is the role of substance P?

A

Emesis, pain processes, and behavioural response to anxiety & stress.

39
Q

What are the opioid receptors?

A

µ, d, k: inhibitory, G-protein coupled.

CNS effects mainly mediated by inhibitory µ receptors.

40
Q

Role of opioid receptors

A

Pain transmission: opiate analgesics (eg. morphine) act on µ receptors in the spinal cord to relieve pain (also limbic system & brainstem).

Reward and motivation: morphine euphoria & addiction linked to opioid interaction with midbrain dopamine (mesolimbic) pathways.

41
Q

Chemistry of monoamine transmitters?

A

Contain one amino group connected to an aromatic ring by a two-carbon chain.

42
Q

Where do dopamine neurons innervate mainly?

A

Basal ganglia (striatum)

43
Q

Where is there a large amount of dopaminergic neurons?

A

Substantia nigra compacta

Locus coeruleus (NA)

Reticular formation

Nucleus raphe (5HT)

44
Q

Describe the firing of monoamine neurons, what does this mean?

A

Fire spontaneously and rhythmically, this provides a constant level of tone at the neuronal target - making modulation especially important.

45
Q

Function of monoamine neurons

A

Global arousal pathways (5HT)

Reward and behaviour (dopamine)

46
Q

How is noradrenalin transported from cytosol to vesicle?

A

Vesicular monoamine transporter (VMAT)

47
Q

How is noradrenaline removed from the synapse?

A

UT1 mechanism via NET transporter into cytosol, broken down by MAO or repackaged.

UT2 into postsynapse, digested by COMT

48
Q

Therapeutic uses of drugs targeting noradrenaline synapses

A

Anxiety: b-adrenoceptor antagonists (propranolol) are anxiolytic

Attention hyperactivity deficit disorder: Noradrenaline-releasing agents (ritalin and amphetamine) are therapeutically useful in ADHD

Depression: Noradrenaline reuptake inhibitors (reboxetine) and MAO inhibitors (phenelzine) are antidepressant.

49
Q

How is dopamine transported from the cytosol into synaptic vesicles?

A

Vesicular monoamine transporter, VMAT2

50
Q

What are the dopamine receptors?

A

Postsynaptic dopamine receptors, located on dendrites (the postsynaptic neuron), or presynaptic autoreceptors ( D2 and presynaptic D3 receptors),

51
Q

Therapeutic uses of drugs targeting dopamine synapses

A

Parkinsons disease: L-DOPA, dopamine agonists (ropinerole), COMT inhibitors (tolcapone) are used in the treatment of Parkinson’s disease.

Schizophrenia: Dopamine receptor antagonists (haloperidol) are antipsychotic.

Addiction: Partial dopamine receptor agonists (buproprion) help manage relapse to tobacco smoking.

Bipolar depression: Dopamine receptor antagonists (haloperidol) are anti-manic agent

52
Q

Describe the serotonin receptors

A

Except for the 5-HT3 receptor, a ligand-gated ion channel, all other 5-HT receptors are G-protein-coupled receptors

53
Q

Therapeutic uses of drugs targeting 5-HT synapses

A

Depression: Selective 5-HT (serotonin) reuptake inhibitors (fluoxetine) are antidepressant

Schizophrenia: Non-selective 5-HT2 receptor antagonists (risperidone) are antipsychotic.

Migraine: 5-HT1B/D agonists (sumatriptan)

Nausea and vomiting: 5-HT3 receptor antagonists (ondansetron) are antiemetic

54
Q

What is the underlying cause of epilepsy?

A

Excessive and abnormal neuronal activity in the cortex of the brain.

55
Q

What can a hyperexcitable state arise from (epilepsy)?

A

Increased excitatory synaptic neurotransmission,

Decreased inhibitory neurotransmission,

An alteration in voltage-gated ion channels,

An alteration of intra- or extra-cellular ion concentrations in favour of membrane depolarization.

56
Q

How can epilepsy be treated by antagonising excitable neurotransmission?

A

NMDA, AMPA, Kainate antagonists

57
Q

How can epilepsy be treated with agonising inhibitory neurotransmission?

A

GABAa agonists,

Barbiturates and benzodiazepines act by positive modulation

Vigabatrin acts by inhibiting GABA metabolism

Tiagabine, an inhibitor of the high-affinity GABA transporter GAT1.

58
Q

How can epilepsy be treated through modulation of voltage gated sodium and calcium channels?

A

Sodium channel-blocking AEDs, phenytoin, carbamazepine and lamotrigine. Inhibit high-frequency repetitive spike firing during seizure spread

Gabapentin binds to calcium channel subunits Might inhibit calcium currents, resulting in reduced excitatory neurotransmission.

Ethosuximide inhibits T-type calcium channels

59
Q

The receptor involved in hippocampal long term potentiation

A

NMDA

60
Q

Which neurotransmitter is released from retinal photoreceptors?

A

Glutamate

61
Q

A neuropeptide involved in suppressing nociceptive transmission

A

Neuropeptide Y

62
Q

NMDA receptors

A

Excitatory/ionotropic/Bind glutamate/require depolarisation to remove Mg2+ before channel can open/important in LTP

63
Q

Neurotransmitter released from granule cells in the cerebellum is

A

Glutamate

Neuroscience (19 decks)

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