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PHAR0002 > Pharmacology Of The Brain (Lecture 16) > Flashcards

Pharmacology Of The Brain (Lecture 16) Flashcards

1
Q

Why is it hard to target output pathways for specific functions?

A

They only use ACh / noradrenaline - therefore have no FUNCTIONAL SPECIFICITY

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2
Q

Why do neurotransmitters have such a big modulatory effect?

A

NTs are synthesised and released from specific types of neurones (e.g. serotonergic neurones)
The neurones can project widely and release the same molecule in different areas
The same NT molecule can have different effects depending on the type of receptor-function specific pathway

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3
Q

Why are objective outcome measures difficult in neuropharmacology?

A

Subjective

E.g. with a drug aiming to change mood (e.g. antidepressants) the outcome is subjective

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4
Q

Why are neurotransmitter pathways effective targets for therapeutic modulation?

A

Disease states are typically caused by excessive / deficient signalling within a particular transmitter pathway (receptor sub-type is often important)
Therapeutic modulation targets this abnormal transmitter signalling

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5
Q

Why are neurotransmitter pathways better targets for therapeutic intervention than output pathways?

A

Information processing circuits within the brain (neurotransmitter pathways) offer more targets for modulation of function / behaviour with greater specificity than output targets

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6
Q

Which type of receptors produce slower & more sustained effects?

A

GPCRs

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7
Q

What type of receptor produces faster effects?

A

Ion channels

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8
Q

What is the use of nicotine and what transmitter pathway does it affect?

A

Recreational use
nicotinic ACh receptors

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9
Q

What is the use of heroin and what transmitter pathway does it affect?

A

Recreational / analgesic (pain relief)

Agonist of opioid peptides

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10
Q

What is the use of Fluoxetine and what transmitter pathway does it affect?

A

Antidepressant

Serotonin - acts as a selective serotonin re-uptake inhibitor

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11
Q

What is the use of Diazepam / Valium (type of benzodiazepine) and what transmitter pathway does it affect?

A

Anxiolytic (treats anxiety)

GABA - acts as a positive allosteric modulator of the GABA-a receptor

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12
Q

What is the use of cocaine and what transmitter pathway does it affect?

A

Recreational

Dopamine - inhibits dopamine re-uptake transporter

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13
Q

What type of receptor does LSD target, and what is the effect?

A

LSD is a 5-HT2A receptor agonist

Upregulates the function of 5-HT2A receptors, causing potent psychoactive effects

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14
Q

What type of receptor do antipsychotic drugs target?

A

Antipsychotic drugs are antagonists of the 5-HT2A receptor

*psychosis / schizophrenia are characterised by the hyperactive state of psychoactive functions

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15
Q

What is the motor output?

A

Signals to muscles to coordinate movement / behaviour
Signals via acetylcholine

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16
Q

What is the major challenge of neuropharmacology?

A

FUNCTIONAL SPECIFICITY

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17
Q

What is the function of the 5-HT2c serotonin receptor, and where is it mostly expressed?

A

Appetite

Mostly expressed in the brain stem

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18
Q

Describe the action of AUTORECEPTORS

A

Only respond to transmitters released from the cell of which they are embedded

Act as a regulatory mechanism - once NT reaches a certain level, it binds to autoreceptors which send an inhibitory signal and stop the release of NT

Usually terminate release - negative feedback mechanism

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19
Q

Describe the action of Heteroreceptors

A

Respond to NTs released from adjacent neurones

Usually increase release

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20
Q

What is the autonomic output and what does it signal via?

A

Signals unconscious, bodily, physiological processes (heart rate, blood pressure, digestion, etc.)

Signals via ACh & noradrenaline

21
Q

What is interoception?

A

Reception of internal stimuli

22
Q

What is exteroreception?

A

The reception of external stimuli

23
Q

What is a good target in the brain which increases specificity?

A

Neurotransmitter pathways

24
Q

What does the 5-HT2A serotonin receptor affect?

A

Cognitive function - cognition, perception, attention, memory

Highly expressed in the cortex

25
Q

What does a mix of receptor subtypes allow for?

A

Mixed effects from the same neurotransmitter
They can be excitatory / inhibitory
They can be fast (i.e. msecs) / slow (secs / mins)

26
Q

What determines the type of effect (excitatory / inhibitory) of NTs?

A

Their receptors

27
Q

What are the 7 stages of synaptic transmission of NTs?

A
  1. NTs synthesised & stored in vesicles
  2. AP arrives at presynaptic terminal
  3. Causing voltage-gated Ca2+ ion channels to open
  4. Influx of Ca2+ stimulates secretory vesicles containing NT to move to and fuse with the presynaptic membrane
  5. NT released by exocytosis
  6. NT diffuses across synaptic cleft and binds to postsynaptic receptors (causing them to open / close)
  7. Excitatory / inhibitory postsynaptic potential is generated
  8. NT removed by re-uptake channels (into neurone / glia) or by enzymatic degradation
28
Q

What are the 4 opportunities for pharmacological modulation of synaptic transmission?

A
  1. Synthesis - inc / inhibit
  2. Release - potentiate (inc / sustain) or inhibit
  3. Effects - target postsynaptic receptors
  4. Removal - block / inc re-uptake
29
Q

What are the 4 neuro-modulatory transmitters?

A
  1. Adrenaline
  2. Noradrenaline
  3. Serotonin (5-HT)
  4. Dopamine

(all have mixed effects)

30
Q

What are the 3 types of opioids?

A
  1. Endorphins
  2. Enkephalins
  3. Dynorphins
31
Q

What are the 3 types of neuropeptides and their effects?

A
  1. Opioid - inhibitory
  2. GLP-1 - mixed effects
  3. Substance P - excitatory
32
Q

What are the 2 types of receptor?

A
  1. Autoreceptors
  2. Heteroreceptors
33
Q

What are the 2 types of receptor targeted by NTs?

A
  1. Ionotrophic - ligand-gated ion channels
  2. Metabotrophic - GCPRs
34
Q

What are the 2 types of output?

A

Motor
Autonomic

35
Q

What are the 2 types of NT used in outputs?

A

ACh & noradrenaline

36
Q

What are the 2 major excitatory & inhibitory NTs?

A

Glutamate - excitatory
GABA - inhibitory

Work predominantly by ion channel receptors
Most neurones in the brain are glutamatergic / gabaergic

37
Q

What are the (5) criteria for being a ‘true’ NT?

A
  1. Present in the presynaptic terminal
  2. Stored in vesicles
  3. Dependant on Ca2+ for release
  4. Target postsynaptic receptors - have a postsynaptic effect
  5. Mechanisms exist for the termination of their effect (negative feedback)
38
Q

What are neuromodulators?

A

Messenger released from a neurone that affects the transmission of signals between neurones - modifies synaptic communication

They may not be ‘true’ NTs

Their action is always slow

39
Q

What are 3 other examples of NTs and their effects?

A
  1. Nitric oxide (gas) - mixed effects
  2. Adenosine - inhibitory effects
  3. Lipids (endocannabinoids, bile acids) - mixed effects (formed from the lipid membrane of neurones themselves)
40
Q

Pharmacological modulation of the release of NTs targets what receptors?

A

Presynaptic

41
Q

Pharmacological intervention of the effects of NTs targets what receptors?

A

Postsynaptic

42
Q

How many neurones & connections are there in the human brain?

A

Approx…

100 billion neurones
1 quadrillion (1x10^15) connections

43
Q

How can receptors be used to achieve some specificity for drugs (therapeutic intervention)?

A

Targeting a receptor allows us to pharmacologically modulate a NT pathway

44
Q

How can the same NT have different effects (inhibitory / excitatory)?

A

Same NT can act on different receptors
Receptors determine excitatory / inhibitory effect

45
Q

Are NTs agonists or antagonists?

A

Always agonists

46
Q

What are the 2 types of output from the brain, and what do they signal via?

A
  1. Motor output - signals via ACh
    - movement / behaviour
  2. Autonomic output - signals via ACh & noradrenaline
    - physiological processes (e.g. HR, BP, digestion)
47
Q

What is the major EXCITATORY NT?

A

Glutamate

48
Q

What is the major INHIBITORY NT?

A

GABA

PHAR0002 (20 decks)

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