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NSB! > Chemicals in the brain > Flashcards

Chemicals in the brain Flashcards

1
Q

Specific amino acids are in high concentrations in the CNS acting as neurotransmitters. Are they always inhibitory and excitatory?

A
  • no
  • can inhibitory OR excitatory OR both
  • depends on the receptor
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2
Q

Neurotransmitters are created from amino acids, that are in high concentrations in the CNS. What effect do inhibitory and excitatory neurotransmitters have on the action potential?

A
  • inhibitory = hyperpolarise (no action potential)
  • excitatory = depolarise (increase action potential)
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3
Q

What is the main excitatory and inhibitory neurotransmitters in the CNS?

  1. excitatory = glutathione, inhibitory = glutamate
  2. excitatory = glutamate, inhibitory = GABA
  3. excitatory = dopamine, inhibitory = glutamate
  4. excitatory = GABA, inhibitory = dopamine

GABA = y-aminobutyric acid

A
  1. excitatory = glutamate

inhibitory = GABA

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4
Q

The main excitatory neurotransmitters in the CNS is glutamate. Glutamate possess both direct (the main way it causes depolarisation) and indirect effects (a mechanism coupled with direct effects) that cause depolarisation. What are the direct and indirect effects of this neurotransmitter on the action potential of the cell?

  1. direct = increased Na+ and Ca2+ enter cell, indirect = K+ cannot leave the cell
  2. direct = increased K+ and Ca2+ enter cell, indirect = Na+ cannot leave the cell
  3. direct = increased K+ and Mg+ enter cell, indirect = Na+ cannot leave the cell
  4. direct = increased Mg+ and Ca2+ enter cell, indirect = K+ cannot leave the cell
A
  1. direct = increased Na+ and Ca2+ enter cell, indirect = K+ cannot leave the cell
  • direct = increased Ca2+ and Na+ enter the cell
  • indirect = K+ is stopped from leaving the cell and increased Ca2+ enters the cell
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5
Q

The main inhibitory neurotransmitters in the CNS is y-aminobutyric acid (GABA). GABA possess both direct (the main way it causes hyperpolarisation) and indirect effects (a mechanism coupled with direct effects) that cause hyperpolarisation. What are the direct and indirect effects of this neurotransmitter on the action potential of the cell?

  1. direct = increased Ca2+ enters the cell, indirect = K+ cannot leave the cell
  2. direct = increased Cl- enters the cell, indirect = Ca2+ blocked from entering the cell
  3. direct = increased Cl- enters the cell, indirect = Na+ blocked from entering the cell
  4. direct = increased Po enters the cell, indirect = K+ cannot leave the cell
A
  1. direct = increased Cl- enters the cell, indirect = Ca2+ blocked from entering the cell
  • direct = increased Cl- enters the cell
  • indirect = Ca2+ is blocked from entering the cell as K+ leaves the cell instead
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6
Q

Where are the neurotransmitters GABA (inhibitory) and glutamate (excitatory) present in the CNS?

A
  • throughout, especially in the brain
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7
Q

Is the majority of glutamate be synthesised or consumed in the diet?

A
  • mostly consumed in the diet
  • little can be synthesised
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8
Q

Glutamate is transported in high concentrations into synaptic vessels before they are released at the pre synapse following an action potential. What is the name of the vesicular glutamate transports?

  1. microtubules
  2. post synaptic vesicles
  3. Vesicular Glutamate Transporter
  4. dynaine
A
  1. Vesicular Glutamate Transporter (VGLUTs)
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9
Q

What does glutamatergic mean?

A
  • receptor in CNS that bind with glutamate
  • present throughout the CNS
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10
Q

What are 3 main effects that glutamatergic synapses (glutamate specific receptors) are linked with in the brain?

  1. cerebral neurotoxicity, memory, addiction
  2. pain, cerebral neurotoxicity, amnesia
  3. pain, synaptogenesis, memory
  4. pain, cerebral neurotoxicity, memory
A
  1. pain, cerebral neurotoxicity, memory
    * pain is initially good to help protect ourselves, but can then become toxic
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11
Q

Glutamatergic transmission is 99.9% excitatory. What 2 classes of receptors bind with glutamate? (i.e. ligand gates ion, tyrosine kinase receptor etc..)

A
  • ionotropic (NMDA, AMPAr and Kainate)
  • metabotropic (ACPD)
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12
Q

Glutamatergic transmission is 99.9% excitatory. Glutamate can bind with both ionotropic (NMDA, AMPAr and Kainate) and metabotropic (ACPD) receptors. Are these receptors fast transmission and which receptors are the main receptors that facilitate this?

A
    • fast excitatory transmission
    • AMPA is fastest
    • NMDA is slower than AMPA
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13
Q

Glutamatergic transmission is 99.9% excitatory. Both ionotropic (NMDA, AMPAr and Kainate) and metabotropic (ACPD) receptors can bind with glutamate. Which receptors has a small amount of glutamatergic transmission and is mediated by a slower receptor?

A
    • metabotropic (lots of intracellular pathways)
    • specifically mGlu (Metabotropic Glutamate Receptor Groups)
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14
Q

NMDA and AMPA are fast glutamatergic transmission receptors. How many subunits does each one have?

  1. 2 subunits
  2. 3 subunits
  3. 4 subunits
  4. 5 subunits
A

4 subunits

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15
Q

NMDA and AMPA are fast glutamatergic transmission receptors. That have 4 subunits in each receptor. Which ions are AMPA and NMDA channels permeable to?

  1. AMPA = Na+ and K+, NMDA = all are Ca2+, Na+ and K+
  2. AMPA = Na+ and Ca2+, NMDA = all are Ca2+, Na+ and Cl-
  3. AMPA = Na+ and K+, NMDA = all are Ca2+
  4. AMPA = Na+, NMDA = all are Ca2+, Na+ and K+
A
  1. AMPA = Na+ and K+, NMDA = all are Ca2+, Na+ and K+
    * most AMPA are Na+ and K+
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16
Q

AMPA is a fast glutamatergic transmission receptor that have 4 subunits. What is the main ion this channel is not permeable to?

  1. Mg+
  2. Ca2
  3. Cl-
  4. Po
A
  1. Ca2+
17
Q

On the NMDA receptor there is a Mg2+ blockage, which inhibits the receptors ability to bind with glutamate and initiate an action potential. What must happen for the Mg2+ ion to be removed so that the NMDA receptor can open and contribute towards the action potential?

A
  • glutamate must bind with AMPA causing cell to depolaire
  • glutamate and glycine bind to NMDA
  • Mg2+ is removed and Ca2+ can then flow through the NMDA receptor
  • Mg2+ on the NMDA is a safety feature though
18
Q

When AMPA receptors bind with glutamate we initially feel pain, this a good thing to alert the body to pain. However, when we have chronic pain stimulus there is a large concentration of glutamate that binds with AMPA receptors and depolarises the cell causing for the Mg2+ blockage on the NMDA receptors (similar to a safety switch) to be removed. When glutamate and glycine then bind with NMDA there is an influx of Ca2+ (and Na+ and K+, mostly Ca2+) causing increased depolarisation. What is this called on the post synapse?

  1. sensitisation
  2. de-sensitisation
  3. wind up
  4. excitatory co-stimulation
A
  1. wind up (driven mainly by increased Ca2+)
    - mechanism for high ROS, kinases, gene transcription and increased glutamate receptors
    - can lead to altered synaptic morphology and cell death
19
Q

When AMPA receptors bind with glutamate when we initially feel pain, this a good thing to altert the body to pain. However, when we have chronic pain stimulus there is a large concentration of glutamate that binds with AMPA receptors and depolarises the cell causing for the Mg2+ blockage on the NMDA receptors to be removed. When glutamate and glycine then bind with NMDA there is an influx of Ca2+ (and Na+ and K+, mostly Ca2+) causing increased depolarisation. This is called wind up and can be excitotoxic, which is essentially where too much of the neurotransmitter and stimulation of the neuron causes damage. What has this been linked with?

  1. synaptogenesis
  2. cardiac arrest
  3. DVT
  4. neuronal pathology
A
  1. neuronal pathophysiology
    - neurodegenerative syndromes, alzheimer’s, stroke, epilepsy and hyperalgesia (increased sensitivity to pain)
20
Q

Once glutamate has been released from the pre synapse and the action potential has finished, what are the 3 main ways in which glutamate can be removed from the synaptic space?

A

1 - absorbed by astrocytes (glial cells) and put back in pre synpase

2 - re-absorbed by the pre synapse through endocystosis

3 - degraded by enzymes and recycled

21
Q

Once glutamate has been released from the pre synapse and the action potential has finished, it can be absorbed by astrocytes (glial cells) and put back in pre synpase or re-absorbed by the pre synapse through endocystosis and added back into pre synaptic vessels for glutamate. Why is it important to have more than one mechanism, especially the astrocytes?

A
  • this is a defence mechanism
  • insufficient glutamate means it cannot be continually excited
  • astrocyte uptake and recycling of glutamate is slow
22
Q

If there is excessive stimulation of NMDA and AMPA receptors by glutamate, this can lead to neuronal damage. What is this called?

A
  • excitotoxicity (causes cell death)
  • common in stroke and neurodegenerative diseases
23
Q

If there is excessive stimulation of NMDA and AMPA receptors by glutamate, this can lead to neuronal damage. This is called excitotoxicity and can lead to neuronal cell death and has been linked to strokes and neurodegenerative disease. What can be done to stop this?

  1. GABA antagonist
    • SAFE glutamate receptor antagonists
    • SAFE glutamate receptor agonists
    • dopamine antagonists
A
  1. SAFE glutamate receptor antagonists
24
Q

Why is a glutamate receptor antagonist a useful drug choice for anticonvulsants?

A
  • convulsions are due to over excitation of neurons
  • reduce the excitation and the convulsions will stop
  • perampanel (AMPA antagonist)
25
Q

Why is a glutamate receptor antagonist a useful drug choice for Amyotrophic lateral sclerosis (disease causing over stimulation of muscles, breathing etc)?

A
  • Riluzole essentially reduces depolarisation, so reduced muscle excitation
  • blocks Na+ gated channels acting as an NMDA antagonist
26
Q

GABA is the main inhibitor in the CNS. What affect does GABA have on anxiety, sleep and muscle tone?

A
    • anxiety = more GABA = less anxiety
    • sleep = more GABA = more sleep
    • muscle tone = more GABA = less muscle tone
27
Q

GABA is the main inhibitor in the CNS. It has a large effect on arousal, muscle tone, anxiety and sleep amongst others. However, if you take GABA agonist what might this have on muscle tone?

A
  • should decreases muscle tone
  • BUT, increase relaxed muscle tone and increase drowsiness
28
Q

What is y-aminobutyric acid (GABA) generally synthesised from?

  1. glutamate within GABAergic neurons
  2. dopamine within GABAergic neurons
  3. glutathione within GABAergic neurons
  4. L-DOPA within GABAergic neurons
A
  1. glutamate within GABAergic neurons
29
Q

y-aminobutyric acid (GABA) is synthesised and then transported to the pre synapse in vesicles. What vesicular GABA transporter is responsible for this?

  1. microtubules
  2. post synaptic vesicles
  3. Vesicular Glutamate Transporter
  4. GABA transporters
A
  1. GABA transporters (GAT)
30
Q

What are the 2 most important GABA receptors?

  1. GABAc = metabotropic and GABAB = metabotropic
  2. GABAA = iontropic and GABAB = iontropic
  3. GABAA = metabotropic and GABAB = iontropic
  4. GABAA = iontropic and GABAB = metabotropic
A
  1. GABAA = iontropic and GABAB = metabotropic
31
Q

GABAA (iontropic) and GABAB (metabotropic) are the 2 most important GABA receptors. Which is fast or slow transmission?

A
  • GABAA (iontropic) = FAST
  • GABAB (metabotropic (GCPR) = FAST
32
Q

GABAA (iontropic) is slow transmission and GABAB (metabotropic) is fast transmission. What neurons/channels is GABAA and GABAB associated with? (main effects)

A
  • GABAA = FAST allowing high Cl- concentrations to enter the cell (cell remain hyperpolarised)
  • GABAB = SLOW opening K+ channels, allowing K+ to leave the cell (cell remain hyperpolarised)
33
Q

GABAC receptors are also GABAergic transmission. What is the main ion they are permeable to?

    • Cl-
  2. K+
  3. Fluride
  4. Na+
A
  1. Cl-
34
Q

What is the main GABA receptor that most GABAergic receptors work through?

  1. GABAD
  2. GABAB
  3. GABAC
  4. GABAA
A
  1. GABAA
35
Q

Once GABA has been released from the pre synapse and the action potential has finished, it needs to be removed from the synaptic space. What glial cell is involved in this process?

  1. astrocyte
  2. oligodendrocyte
  3. microglia
  4. gliomas
A
  1. astrocytes
36
Q

Once GABA has been released from the pre synapse and the action potential has finished, what 2 methods ensure GABA is removed from the synaptic space?

A
  1. astrocyte uptake and recycle GABA which is slow through GAT 1, 2 and 3 transporters
  2. re-absorbed into pre-synapse through endocytosis (GAT-1 transporter) on GABAergic neurones
37
Q

Once GABA has been reabsorbed from the synaptic space via GAT1, 2 or 3 transporters. What must happen to it in order for it to be recycled?

A
  • GABA is converted to glutamate and then glutamine
  • glutamine is transported back into GABAergic neurones
  • glutamine is then converted to glutamate and then GABA
  • GABA is repackaged into GABA vesicles in pre synapse

NSB! (53 decks)

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