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The Patient Y3 Semester 2 > Drug action in the CNS > Flashcards

Drug action in the CNS Flashcards

1
Q

Briefly describe the structure of a neuron:

A

Dendrites, cell body, axon terminal

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2
Q

Describe the cell body function:

A

Nucleus, stores DNA and rough ER, which builds protein and mitochondria.

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3
Q

Describe the dendrites:

A

(receive information) the input region, receives input from other neurons.

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4
Q

Describe the axon:

A

Axon: main conduction unit, carries information in the form of electrical signal known as the action potential

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5
Q

Describe the axon terminals:

A

the output region, release of neurotransmitter. Conformational change, triggers release of other AP.

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6
Q

What are neurons?

A

Neurons communicate with one another at synapses

presynaptic cell –> synapse –> post synaptic cell

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7
Q

Is transmission electrical or chemical?

A

Synaptic transmission can be electrical or chemical.

Electrical synapses are very rare in the adult brain.

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8
Q

At the chemical synapse the pre- and postsynaptic elements are separated by a gap, called the _____ _____ .

A

synaptic cleft

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9
Q

When does an action potential occur?

A

An action potential occurs when a neuron sends information down an axon.

Neurons can alter their resting membrane potential to act as a signalling mechanism.

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10
Q

How does do action potentials initiate NT release?

A

At the presynaptic terminal the action potential opens Ca2+ channels and initiates neurotransmitter release.

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11
Q

Describe how an action potential affects ion channels:

A
  • Neruone Resting membrane potential: -70mV
  • Sodium is positive and moves in via electrochemical gradient therefore neuron becomes more positive
  • Sodium reaches its threshold (+30) so closes
  • K+ channel open and K+ moves out (repolarization) bringing neuron back down to negative mV
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12
Q

Examples of neurotransmitters:

A
  • Acetylcholine

- Dopamine

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13
Q

Describe the anatomy of the synapse:

A

Gap between pre synaptic terminal and post synaptic terminal where NT diffuses.

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14
Q

How is information passed from neuron to neuron?

A
  • Electrical signal arrives at pre synaptic terminal
  • Causes an opening of voltage gated calcium channels
  • Calcium enters cell and causes binding of the pre synaptic vesicles to the membrane then exocytosis occurs into the synaptic cleft
  • Then diffuses across the cleft
    Activate recepetos – conformational change and Enters post synaptic cleft via diffusion
  • Na+ moves in, = depolarization generating AP (excitatory signal)
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15
Q

What are the two types of signal?

A

Excitatory signal and inhibitory signal

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16
Q

What is an inhibitory signal?

A

= inhibiting different parts of pathway

Example: Cl- coming into cell (if chloride channels activated to open) cell goes more negative and wouldn’t get AP
GABA major inhibitory transmitter

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17
Q

What are the 2 dopamine receptors?

A

D1 excitatory, D2 inhibitory) – these receptors can be on different neurons

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18
Q

Describe acetycholine synthesis:

A
  • Acetyl coenzyme A + choline (choline acetyltransferase) = Acetycholine
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19
Q

What is ChAT?

A

Choline acetyltransferase. ChAT is specific to cholinergic neurons and present in neuronal terminal in excess (i.e. enzyme is not saturated). If you have enough precursors you can continue making the transmitter.

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20
Q

Acetylcholine storage:

A

Stored in synaptic vesicles in the axonal terminal

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21
Q

Acetylcholine release:

A

Released into the synaptic cleft upon the arrival of an action potential and influx of Ca2+.

Binds to postsynaptic receptors:
Muscarinic (M1 – M5) & Nicotinic (generally excitatory)

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22
Q

Nicotinic receptors are composed of five types of subunits. Name the 5 types:

A
  • Alpha (1-10)
  • Beta (β2- β5)
  • Delta
  • Epsilon &
  • Gamma

These subunits are found in different combinations in different types of nicotinic AChRs

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23
Q

Nicotinic Receptors are split into two types, what are the two types:

A

Muscle and neuronal

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24
Q

Location of muscle nicotinic receptors:

A

Neuromuscular junction

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25
Q

Location of neuronal nicotinic receptors:

A

Autonomic ganglia, CNS

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26
Q

Structure of muscle nicotinic receptors:

A
  • ααβεδ

- Ligand gated ion channel

27
Q

Structure of neuronal nicotinic receptors:

A
  • Various αβ subunits

- Ligand gated ion channel

28
Q

ACETYLCHOLINE – INACTIVATION/REUPTAKE

A

40-50% of the Choline formed from ACh breakdown is taken up into presynaptic terminal by active, high affinity transporter specific to cholinergic cells

29
Q

The basal forebrain contains two groups of cholinergic neurons:

A

(1) Medial Septal group and

(2) the Nucleus Basalis group

30
Q

Describe the NMJ:

A

NMJ is a chemical synapse between a motor neurone and skeletal muscle fibre. Communication between these two cells is carried out by Acetylcholine

31
Q

What initiates the release of Acetylcholine?

A

Release of Acetylcholine is initiated by the arrival of an action potential propagating along the axon of the motor neuron

32
Q

What leads to opening of presynaptic voltage-gated Ca2+ channels and transmitter release Ca2+ -dependent vesicle exocytosis?

A

Depolarisation of the nerve endings

33
Q

What ion channels open and let Na+ ions more into the muscle cell to cause depolarisation and what does this generate?

A

Postsynaptic ligand-gated ion channels.

This generates an action potential on the membrane of the skeletal muscle cell, this allows Ca2+ entry. Ca2+ entry into the muscle cell leads to muscle contraction

34
Q

Action of acetylcholine is terminated by:

A

AChE

35
Q

Describe myasthenia gravis:

A
  • Anautoimmune condition that affects the nerves and muscles
  • InMyasthenia Gravis theimmune system produces antibodies (proteins) that block or damagemuscle acetylcholine receptors, whichprevents the muscles contracting
  • This prevents messages being passed from the nerve endings to the muscles, which results in the muscles not contracting (tightening) and becoming weak
36
Q

Symptoms of myasthenia gravis:

A

The eye and facial muscles and those that control swallowing are commonly affected

37
Q

Treatment of myasthenia gravis:

A

Medications such asPyridostigmine can be prescribed for Myasthenia Gravis. They prevent the breakdown of acetylcholine. Don’t target antibodies.

These medicines tend to work best in cases of mild myasthenia gravis. They can improve muscle contractions and strength in the affected muscles

38
Q

Synthesis of dopamine:

A 
- L Tyrosine 
(Tyrosine hydroxylase)
- L Dopa 
(Dopa decarboxylase DDC)
- Dopamine
39
Q

What is the rate determining step in dopamine synthesis:

A

Tyrosine hydroxylase is the rate-determining step as it is normally saturated by substrate.

40
Q

Where is dopamine stored?

A

Stored in synaptic vesicles in the axonal terminal.

41
Q

Describe the release of dopamine?

A

Released into the synaptic cleft upon the arrival of an action potential and influx of Ca2+

42
Q

What receptors does dopamine bind to ?

A

Binds to postsynaptic receptors:

  • D1 family (D1 & D5) [Excitatory]
  • D2 family (D2/3/4) [Inhibitory]
43
Q

Dopamine inactivation:

A

Metabolism by Enzymes:

  • Catechol-O-methyltransferase (COMT)
  • Monoamine oxidase (MAO)
44
Q

Dopamine reuptake process:

A

Catecholamines have highly specific active transport mechanisms to remove transmitter from synapse into presynaptic terminal

Dopamine Transporter - DAT

45
Q

Name the 4 dopamine neuron projections:

A

1) Nigrostriatal pathway
2) Mesolimbic pathway (meso = mid)
3) Mesocortical pathway
4) Tuberoinfindibular pathway

46
Q

Nigrostriatal pathway:

A
  • Substantia nigra
  • Dorsal striatum - (motor), Parkinson’s disease
  • Associative striatum - learning, habituation, memory, attention, emotion, motivation,
47
Q

Mesolimbic pathway (meso = mid)

A
  • Ventral tegmental area in midbrain to limbic regions associated with reward, motivation, affect and memory.
  • Include ventral striatum, amygdala, hippocampus and medial prefrontal cortex.
48
Q

Mesocortical pathway

A
  • VTA to frontal cortex, including dorsolateral prefrontal vortex
  • Cognitive function, motivation and emotional response
49
Q

Tuberoinfindibular pathway

A
  • Tuberal region to median eminence (infundibular region at top of pituitary stalk)
  • DA acts to inhibit prolactin release from pituitary
50
Q

Cause of schizophrenia:

A

– increase of dopamine in associative striatum that leads to psychosis – therefore block receptor (D2 antagonist) to treat. SE’s - increase of prolactin release. Dopamine in motor (dorsal striatum) = bad as the dopamine anatagonist is blocking the receptor so isn’t being released therefore bofy responds by releasing more = reduced motor control.

51
Q

What are agonists?

A

Substances which stimulate the receptors and mimic the natural ligand (e.g. neurotransmitter, hormone)

52
Q

What are antagonists:

A

Substances that block the receptor and prevents/stop the effect of the natural ligands

53
Q

Partial Agonist

A

A partial agonist is an agonist which is unable to induce maximal activation of a receptor population, regardless of the amount of drug applied.

= partial activation

54
Q

Most hormones and neurotransmitters produce an effect by interacting with specific sites on cell membranes (Receptors).
There are several families of receptors, using common mechanisms, these families include:

A

Ionotropic Receptors
Metabotropic Receptors
Kinase-linked Receptors
Intracellular Receptors

55
Q

Ionotropic Receptors:

A
  • Receptor is part of ligand-gated ion channel protein and activation results in ion conductance changes
  • These receptors are opened by the transmitter to allow the passage of Na+ (excitatory) or K+/Cl– ions (inhibitory) and are involved in fast transmission (msecs)
  • Examples include some receptors for Acetylcholine, Glutamate & GABA
56
Q

Metabotropic Receptors:

A
  • Receptor protein in membrane is coupled to effector mechanism via G-proteins
  • In this signalling mechanism, agonist molecule combines with receptor proteins in the membrane
  • The resulting conformational change causes activation of a membrane-associated enzymes via G-protein
  • The cellular effect is usually much slower than that associated with ionotropic receptors. E.g. Dopamine receptors
57
Q

Summary of the speed of receptors: (fastest to slowest)

A

Ionotropic, metabotropic, kinase linked, intracellular

58
Q

Drugs for schizophrenia:

A
  • Antipsychotics – D2 receptor antagonists

- Novel treatments for cognitive deficits

59
Q

Drugs for Parkinson’s disease:

A

Dopaminergic drugs (precursors/agonists)

60
Q

Drugs for Alzheimer’s disease:

A
  • Acetylcholinesterase inhibitors

- NMDA receptor antagonist (glutamate)

61
Q

Drugs for epilepsy:

A

Anticonvulsants (GABA/Glutamate transmission)

62
Q

Drugs for depression

A

Selective serotonin reuptake inhibitors (SSRIs)

63
Q

CNS stimulant drugs:

A

Cocaine, amphetamines, nicotine

64
Q

Parkinson’s Disease:

A
  • Loss of dopamine neurons in the Nigrostriatal pathway
  • Diminished in the striatum (~20% of control)
  • The precursor of dopamine, L-dopa, is an effective treatment of the symptoms
  • Also use agonists at dopamine receptors

The Patient Y3 Semester 2 (21 decks)

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