Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drug Action In The CNS > Part 2 > Flashcards

Part 2 Flashcards

1
Q

What are the treatments for:

  1. Schizophrenia?
  2. Parkinson’s?
  3. Epilepsy?
  4. Alzheimer’s disease?
A
  1. Antipsychotics
  2. Dopaminergic drugs
  3. Anticonvulsants - dampen down excitation from excessive glutamate
  4. Current and novel treatments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can agonists of dopamine receptors do?

A

Induce psychotic symptoms in people with normal dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What agonist treatment can be given for Parkinsons?

A

D1 receptor agonists - D1 receptors stimulate movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What balances control and seizures in the CNS?

What factors influence excitation and inhibition?

A

The balance between excitatory glutamate and inhibitory GABA balances EPSPs and IPSPs

Factors that influence EPSPs:

  • Na+ influx
  • Ca2+ currents
  • paroxysmal depolarisation

Factors that influence IPSPs:

  • K+ efflux
  • Cl- influx
  • pumps
  • low pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What goes wrong in epilepsy?

How does treatment work?

A

Balance between excitation and inhibition is more towards excitation because of excess glutamate
Treatment aims to restore the balance between factors influencing EPSPs and those influencing IPSPs

This can be at many points

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What four main categories do current anticonvulsants fall into?

A
  1. Drugs that inhibit sodium channels
  2. Drugs that inhibit calcium channels (neurotransmitter release)
  3. Drugs that enhance GABA mediated inhibition
  4. Drugs that inhibit glutamate receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do drugs that inhibit sodium channels work?

A

Enhance sodium channel inactivation - less sodium into the cells = less APs generated
Antiepileptic drugs that target sodium channels prevent the return of these channels to the active state by stabilising them in the inactive state

Dosage is very important to get the right balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do drugs that inhibit calcium channels work?

A

Antiepileptic drugs inhibit T-type calcium channels which reduces current as these high voltage channels are involved in neurotransmitter release
These drugs are particularly useful for controlling absence seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is GABA:

  • synthesised?
  • stored?
  • released?
  • receptors?
A

Synthesis is mediated by glutamic acid decarboxylase

GABA is packaged into presynaptic vesicles by a transporter (VGAT)

In response to an action potential at the neurone terminal, presynaptic calcium channels open and calcium influx causes GABA to be released and to act on GABAa, b and c receptors and their subtypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is GABA action on receptors terminated?

A
  1. Reuptake - neurons and glia take up GABA via GABA transporters (GATs). Four GATs have been identified each with a characteristic distribution in the CNS
  2. Some GABA is broken down by the widely distributed mitochondrial enzyme GABA-transaminase (GABA-T) metabolises GABA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What drugs can be used on GABA pathways?

A

These drugs aim to enhance GABA mediation inhibition

  1. GABA receptor agonists
  2. GABA reuptake inhibitors
  3. GABA transaminase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the two categories of glutamate receptors?

  • how do the AMPA and kainate receptors work?
  • how does the NMDA receptor work?
A

Ionotropic and Metabotropic

Ionotropic: AMPA, Kainate and NMDA

AMPA and Kainate - used for very fast glutamate transmission. Receptor binding opens a channel though the receptor allowing sodium and small amounts of calcium to enter

NMDA - receptor opens slightly later. Channel in the receptor opens to allow large amounts of calcium to enter and sodium ions. This channel is blocked by magnesium in the resting states and opens once some depolarisation has occurred due to AMPA or Kainate receptors

Glycine site facilitates the opening of the NMDA receptor channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where do CNS stimulants/drugs of abuse mainly act?

A

Mainly dopaminergic activating the mesolimbic pathway

Pathways from the VTA in midbrain to the limbic region associated with reward, motivation, affect and memory
Includes the ventral striatum, amygdala, hippocampus and medial prefrontal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does cocaine work?

A

Dopamine transporter inhibitor

  • more DA left in the synapse
  • intensifies and prolongs the stimulation of postsynaptic dopamine receptors in the brains pleasure centre
  • acts in the mesolimbic pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How methamphetamine work?

A
  1. Blocks dopamine transporter
  2. Has an effect in increasing release

Overall more dopamine activating receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does nicotine work?

A

Acts on presynaptic nicotinic autoreceptors

Nicotine activating these increases the release of dopamine into the synapse

17
Q

What neurotransmitter is lost in Alzheimer’s disease?

A

Loss of acetylcholine in certain pathways that are important in controlling memory and cognition

18
Q

What medications can Alzheimer’s benefit from?

A

Cholinesterase inhibitors - increase amount of ACh in the synapse

They do not prevent the disease from progressing but may help people to function at a slightly higher level
Better in early or mild disease because ineffective once the ACh neurones are lost
- no effect after a couple of years as it is neurodegenerative

19
Q

What are potential novel treatments for Alzheimer’s?

What do they aim to do?

A

Novel treatments aim to prevent progression of the neurodegeneration

The pathology of Alzheimer;s is related to amyloid so treatments targeting amyloid and preventing the plaques forming are potential novel treatment

20
Q

How is amyloid precursor peptide processed?

A

2 pathways:
1. Alpha-secretase pathway - enzyme ADAM10 produces SAPPa and leads to neurogenic and neurotrophic factors

  1. Beta-secretase pathway (proamyloidogenic) - BACE1 forms SAPPbeta which is then cleaved by y-secretary to form amyloid beta peptide which forms the pathogenic plaques seen in alzheimers
21
Q

What novel approaches are there for Alzheimer’s?

A
  1. Secretase modulators - decrease amyloid beta production
    Inhibitors of the enzymes such as BACE1 enzyme
    Hard to get these drugs in the brain
  2. Anti-aggregants - prevent amyloid beta aggregation
  3. Immunotherapies - clear amyloid beta deposition

Note - not that much evidence for amyloid in late onset Alzheimer’s which is the majority of cases

22
Q

How is amyloid toxic to the brain?

A

Amyloid builds up causing synaptic loss and damage

Tau protein also becomes hyperphosphorylated and kills neurones

Drug Action In The CNS (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions