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Reuben's Neuroscience > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

What is the relay site for classic senses? (Touch, taste, smell, hearing, sight)

A

Thalamus

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2
Q

List sources (think of 6) of internal stimuli.

A 
o Pressure
o O2/CO2
o Temperature
o pH
o Also involved in homeostasis
o Show another afferent/efferent link
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3
Q

Describe an action of alpha adrenoceptors on the eye.

A

pupil constriction via vasoconstriction and constriction of the pupillary muscle

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4
Q

Describe an action of the beta adrenoceptors.

A

heart (↑HR), kidneys (↑renin), vasculature (↑vasodilatation)

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5
Q

What type of cholinergic receptors are involved in the CNS?

A

Muscarinic

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6
Q

What type of cholinergic receptors are involved in somatic control?

A

Nicotinic

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7
Q

What chemical is important for neurotransmitter vesicle?

A

Calcium

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8
Q

What is a legal use of amphetamine?

A

ADD/ADHD

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9
Q

What does amphetamine do?

A

It is an indirectly-acting sympathomimetic amine. In the synapse, it will enter the presynaptic neuron carried by amine transporters where it will dislodge NA from vesicles. NA will re-enter the synaptic cleft and increase excitation of the postsynaptic neuron.

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10
Q

What does cocaine do?

A

Cocaine blocks the reuptake channel for NA, increasing the amount in the synaptic cleft.

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11
Q

How does cocaine affect amphetamine?

A

Cocaine prevents the uptake of amphetamine

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12
Q

What features of drug will make it able to pass the BBB?

A

There must be lipophilic, not be extruded by p-glycoproteins and the ABC series of transporters. They might be able to utilise amino acid transporters (mimetics).
o Other examples include glucose and nucleoside mimetics
o There are also ion transport mechanisms that can be utilised
o Be aware of these active processes

Also:
- Small, uncharged

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13
Q

How many neurotransmitters have been discovered thus far (roughly)?

A

40

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14
Q

T/F: Similar neurotransmitter molecules can be affected by the same drug (at varying concentrations).

A

True

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15
Q

What are the catecholamines?

A

NA, adrenaline, dopamine

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16
Q

What are the ‘emergency hormones’?

A

NA and adrenaline

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17
Q

What differentiates the end products within vesicles in terms of neurotransmitters?

A

The selectivity and availability of enzymes

18
Q

What part of the brain is involved in motor coordination?

A

Substantia nigra in the basal ganglia

19
Q

T/F: The dopamine signalling pathway is quite diffuse.

A

False. It is localised.
o Substantia nigra in the basal ganglia are involved in motor coordination
o Some pathways run down to the tuberoinfundibular system and some run to the prefrontal cortex
o Regional location

20
Q

Where does the NA pathway run?

A

The noradrenaline pathway:
o Signals much more broadly to the cerebral cortex – wider distribution with overlap with DA
o More discrete pathways head into the cerebellum and into the brainstem
o There are also efferent pathways feeding back – prejunctional adrenoceptor activation inhibits these efferent pathways at the caudal raphe nuclei area of the brainstem, for example
o NA pathways feed into the area of mood and arousal and at the raphe for control of blood pressure

21
Q

What is Parkinson’s disease caused by?

A

Degeneration of dopaminergic pathways (signal up to the corpus striatum)

22
Q

What is the treatment for Parkinson’s disease?

A

Rx: L-DOPA + peripheral DDC inhibitor (allows for crossing the BBB)
• MAO-B inhibitors
• Dopamine receptor agonists
• Muscarinic receptor antagonists

23
Q

What is Huntington’s disease caused by?

A

GABA deficiency (deficiency in the inhibitory pathway to the motor cortex)

24
Q

What is the treatment for Huntington’s disease?

A

Rx: GABA agonist Baclofen (crosses the BBB)
Rx: Dopamine antagonists Chlorpromazine (antipsychotic)

25
Q

What are some side-effects of the treatment of Parkinson’s disease?

A

Side effects (from overstimulation of other brain areas):
• Schizophrenia-like delusions
• Disorientation
• Insomnia

26
Q

As a side effect of the treatment of Parkinson’s disease, what (generalise) causes schizophrenia?

A

Changes in dopamine rich areas e.g. frontal cortex, basal ganglia, temporal lobe

27
Q

What is a reason for the addictive properties of cocaine and amphetamines?

A

Cocaine and amphetamines have a greater selectivity for DA (dopamine) transmission, and DA is involved in the nucleus accumbens and ventral tegmental area which are the reinforcing parts of the brain

28
Q

What sort of stimulation (excitatory or inhibitory) does dopamine elicit?

A

BOTH!!

29
Q

T/F: The current level of neuroscience thinking suggests that interneurons link other neurons, modifying their activity.

A

False. Interneurons are no longer thought to exist in the CNS, but rather modulatory inputs from neuron next to the pathway play a role

30
Q

What is the basis of epilepsy?

A

Excessive discharge of action potentials.
Disturbed motor function from either of or a combination of too little inhibitory input (GABA) or too much excitatory input (glutamate)

31
Q

What are the treatments of epilepsy?

A

• Enhance inhibitory input (GABA)
o Benzodiazepines enhance GABA receptor activity
• Effective sedatives as well as muscle relaxants
• Work as allosteric modulators

• Reduce excitatory input (glutamate)
o A. Phenytoin – limits excitatory nerve activation
• Not useful for all types of seizures
o B. Ethosuximide – inhibit T-type Ca2+ channels
• T-type channels are abundant in the nervous system
o C. Felbemate – inhibit NMDA receptor
• Act in another subset of epilepsies
• NMDA is a critical neurotransmitter in the CNS, but not so much in the periphery
o These drugs also provide a level of analgesia as a side-effect

32
Q

What is the difference between analgesia and anaesthesia?

A

Analgesia targets pain/sensory pathways and their chemical mediators.
Local anaesthetics cause regionalised inhibition of pain/sensory pathways. They may also cause excitation by affecting other nerves in the region. They do no cause any loss of consciousness.
General anaesthetics depress cortical processing of the pain/sensory signal through excitation & perhaps chemical signalling. These anaesthetics do cause loss of consciousness and their effects are not regionalised.

33
Q

Describe the pain pathway and where analgesics and anaesthetics work.

A
  • Pain moves up periphery/sensory nerves to the dorsal horn of the spinal cord segment and is relayed up to the thalamus where messages are sent to the cortex to act to reduce the painful stimuli
  • Analgesics act on the peripheral nerve, the spinal cord segment and the thalamus
  • Local anaesthetic should only work on the peripheral nerves up to the point where they meet their relays in the spinal cord
  • General anaesthetics act on the thalamic and cortical regions
34
Q

Describe the overarching mechanism of action of local anaesthetic agents.

A

Reversibly block conduction of nerve impulses at the axonal membrane by binding selectively to sodium channels specifically at the transmembrane domain S6 in domain IV in the lower internal membrane.
They are weak bases differing in onset, duration & toxicity.

35
Q

Name some local anaesthetic agents.

A

• Aminoesters: procaine
o Shorter acting, hydrolysis by esterases
• Aminoamides: lignocaine (antiarrhythmic affecting sodium channels in the heart), bupivicaine, ropivicaine
o Longer acting, hepatic metabolism (by cytochrome p450s)
• Benzocaine (neither an ester or an amide)
• Also:
o Lethal toxins
• Tetrodotoxin (puffer fish)
• Saxitoxin (dinoflagellates)

36
Q

Why are local anaesthetic agents preferred over cold compress?

A

They do not damage nerves like the cold compress.

37
Q

Where do toxins bind to sodium channels?

A

To the extracellular domains as they are attracted to glycoproteins and sulfhydryl groups.

38
Q

Describe the actions of hydrophobic local anaesthetics.

A

These are fast and non-use dependent.
They simply diffuse into the ion channel blocking it and preventing action potentials by preventing threshold membrane potential to be reached.
Example: benzocaine

39
Q

Describe the actions of hydrophilic local anaesthetics.

A

These are slow and use-dependent.
They must lose their charge, cross the membrane, regain their charge and then enter the sodium channel from the cell side to elicit a response.
Examples: aminoesters (procaine), aminoamides (lignocaine, bupivicaine, ropivicaine)

40
Q

Sensory nerves, motor nerves, autonomic nerves: what is the order of sensitivity to local anaesthetics?

A

Sensory > ANS > motor

41
Q

What is the rationale behind OTC local anaesthetics?

A

Poor absorption over epithelium means that less will get into the systemic circulation.

42
Q

What are the stages of general anaesthesia?

A 
•	Stage I - amnesia and euphoria
•	Stage II – “Excitement”
o	Excitement
o	Delirium
o	Resistance to handling
•	Stage III – “Surgical anaesthesia”
o	Unconsciousness
o	Regular respiration
o	Decreasing eye movement
•	Stage IV – “Medullary depression”
o	Respiratory arrest
o	Cardiac depression and arrest

Reuben's Neuroscience (10 decks)

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