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The Patient Year 3 Semester 2 > Drug Action in the CNS > Flashcards

Drug Action in the CNS Flashcards

1
Q

What are Dendrites?

A

Receives input from other neurons - where the receptors are. Receptor may cause change in electrical signal, which is how signals travel down the axon.

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2
Q

What is the Axon?

A

Main conduction unit - carries information in the form of electrical signal known as the action potential.
The length varies between neurons. Local processing neurons have short axons

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3
Q

What is the Axon Terminal?

A

The output region, release of neurotransmitter. Where the signals are passed between the neurons.

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4
Q

What are Synapses?

A

Spaces between neurons, therefore have ‘neurotransmitters’ – these are released from synaptic terminals and activate receptors to create a conformational change to allow a passage of signal.

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5
Q

What is the main type of Synaptic Transmission?

A

Synaptic transmission can be electrical or chemical.
Electrical synapses are very rare in the adult brain.
Most synapses in the brain are chemical.

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6
Q

What is the Synaptic Cleft?

A

At the chemical synapse, the pre- and postsynaptic elements are separated by a gap, called the ‘synaptic cleft’.

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7
Q

What type of signal conversion is needed to diffuse across a synapse?

A

The message needs to be converted to a chemical signal to diffuse across a synapse – then converted back to electrical.

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8
Q

What is Grey Matter?

A

Clumps of cell bodies, dendrites and axon terminals of neurons (where all the synapses are).

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9
Q

What is White Matter?

A

Axons covered in the myelin sheath which connect different parts of grey matter to each other.

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10
Q

What is Acetylcholine?

A

(ACh) released at neuromuscular junction to cause contraction.

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11
Q

What is an Action Potential?

A

An action potential occurs when a neuron sends information down an axon, away from the cell body.

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12
Q

What is the Neuron Resting Potential?

A

-70mV

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13
Q

What are the 5 steps of an Action Potential?

A

Stimulus, Depolarisation, Repolarisation, Hyperpolarisation, Resting State

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14
Q

What is the Stimulus?

A

Starts the rapid change in voltage. Sufficient current must be administered to the cell in order to raise the voltage above the threshold voltage to start membrane depolarisation.

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15
Q

What is Depolarisation?

A

Caused by a rapid rise in membrane potential opening of sodium channels in the cellular membrane, resulting in a large influx of sodium ions down the chemical and electrochemical gradient (causes the neuron to become more positive).

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16
Q

What is Repolarisation?

A

Results from rapid sodium channel inactivation as well as a large efflux of potassium ions resulting from activated potassium channels.

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17
Q

What is Hyperpolarisation?

A

A lowered membrane potential caused by the efflux of potassium ions and closing of the potassium channels.

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18
Q

What is the resting state?

A

When membrane potential returns to the resting voltage that occurred before the stimulus occurred.

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19
Q

What happens at a Synapse?

A

1) Pre-synaptic Terminal - signal arrives at the membrane causing an opening of voltage gated calcium channels.
2) Ca2+ comes into the cell and causes binding of pre-synaptic vesicles to the membrane and by exocytosis
3)diffuse out of the membrane into the Synaptic Cleft, diffusing across the cleft activating receptors on post-synaptic terminal, causes the binding of transmitter to receptor, causing conformational shift.
4)This is an excitatory signal being passed from the ‘Pre’ to the ‘Post’.
These signals can also be inhibitory.

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20
Q

What is ChAT?

A

Acetyltransferase (ChAT) - Specific to cholinergic neurons and present in neuronal terminal in excess (i.e enzyme is not saturated)
Excess - so if you have enough pre-cursors you can continuously make the transfer.

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21
Q

What does ChAT do?

A

Transfers acetate ion from acetyl-CoA to choline

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22
Q

Acetylcholine Synthesis, Storage, Release, Inactivation/Reuptake?

A

Synthesis - ChAT
Storage - Most stored in vesicles in pre-synaptic terminal
Release - - Released into the synaptic cleft upon the arrival of an action potential and influx of Ca2+
Inactivation/Reuptake - most are broken down and taken back up by receptors

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23
Q

What are Nicotinic Receptors composed of?

A 
5 types of subunits:
- Alpha (1-10) 
- Beta (B2-B5) 
- Delta 
- Epsilon 
- Gamma 
These subunits are found in different combinations in different types of nicotinic AchRs
24
Q

What two groups are Nicotinic Receptors divided into?

A

Muscle and Neuronal
MUSCLE:
- In Neuromuscular Junction
- Structure; ααßεδ, Ligand gated ion channel
NEURONAL:
- In Autonomic Ganglia, and CNS
- Structure; Various αß subunits, Ligand Gated Ion Channel

25
Q

What happens to the Choline formed from ACh breakdown?

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.
Choline is taken up again and recycled to be put back into vesicles to be stored in the pre-synaptic terminal

26
Q

What are Autoreceptors?

A

Synthesis inhibiting, Release inhibiting.

27
Q

What is a Neuromucular Junction?

A

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

28
Q

What is release of Acetylcholine initiated by?

A

The arrival of an action potential propagating along the axon of the motor neuron.

29
Q

What does depolarisation of the nerve endings lead to?

A

The opening of presynaptic voltage-gated Ca2+ channels and transmitter release Ca2+ - dependent vesicle exocytosis

30
Q

What does an influx of Na+ cause?

A

Postsynaptic ligand-gated ion channels open and let Na+ ions into the muscle cell, this causes depolarisation.

31
Q

What does Ca2+ entry do?

A

AP then generated on the membrane of the skeletal muscle, allowing Ca2+ entry which leads to muscle contraction

32
Q

What is Myasthenia Gravis?

A

An autoimmune condition that affects the nerves and muscles.
the immune system produces antibodies (proteins) that block or damage muscle acetylcholine receptors, which prevents the muscle contracting.

33
Q

What are the effects of Myasthenia Gravis?

A

Prevents messages being passed from the nerve endings to the muscles, which results in the muscles not contracting (tightening) and becoming weak.

  • Wasting away of the nerves and muscles
  • Lose control over contraction of the muscles
  • Want acetylcholine to stay there longer to have a greater effect
34
Q

What does Myasthenia Gravis most commonly affect?

A

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

35
Q

What medication is used to treat Myasthenia Gravis?

A

Pyridostigmine can be prescribed for Myasthenia Gravis. They prevent the breakdown of acetylcholine.
These medicines tend to work best in cases of mild myasthenia gravis. They can improve muscle contractions and strength in the affected muscles.

36
Q

How is dopamine synthesised?

A

L-Tyrosine – (Tyrosine Hydroxylase) –> L-Dopa – (Dopa Decarboxylase (DDC) –> Dopamine

37
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.

38
Q

Dopamine Storage and Release?

A

Storage:
- Stored in synaptic vesicles in the axonal terminal
Release:
- Released into the synaptic cleft upon the arrival of an action potential and influx of Ca2+
Binds to postsynaptic receptors:
- D1 family (D1 and D5) [Excitatory]
- D2 family (D2/3/4) [Inhibitory]

39
Q

How is Dopamine inactivated?

A

It is metabolised by Enzymes:

  • Catechol-O-methyltransferase (COMT)
  • Monoamine oxidase (MAO)
40
Q

How is Dopamine re-uptake completed?

A
  • Catecholamine’s have highly specific active transport mechanisms to remove transmitter from synapse into presynaptic terminal
  • Dopamine Transporter; DAT
41
Q

What are the 4 main Dopamine Pathways?

A

1) Nigrostriatal Pathway
2) Mesolimbic Pathway
3) Mesocortical Pathway
4) Tuberinfundibular Pathway

42
Q

What is the Nigrostriatal Pathway?

A

Pathway that connects the Substantia Nigra with the Dorsal Striatum (Caudate and Putamen).
The Dorsal Sriatum involved with motor control.
Associative Striatum - learning, habituation, memory, attention, motivation, emotion and volition.

43
Q

What is the Mesolimbic Pathway?

A

Connects the Ventral Tegmental Area (VTA) in midbrain to limbic regions associated with reward, motivation, affect and memory.

44
Q

What is the Mesocortical Pathway?

A

VTA to frontal cortex, including dorsolateral prefrontal cortex (DLPFC).
Cognitive function, motivation and emotional response

45
Q

What is the Tuberoinfundibular Pathway?

A

Connects the Tuberal Region to median eminence (infundibular region at top of pituitary stalk).
DA acts to inhibit prolactin release from pituitary.

46
Q

What causes Schizophrenia?

A

Increase of dopamine in the associative stratum - Dopamine antagonist to compete and block receptors, tricks brain into thinking there are normal Dopamine D2 levels (D2 Receptor antagonist - antipsychotics.)
Side Effect - Prolactin release no longer inhibited so you get hyperprolactinemia.

47
Q

What happens to the motor circuit if you use a D2 receptor antagonist in Schizophrenia?

A

Nothing wrong with dopamine in the motor circuit in Schizophrenia - therefore by putting in a D2 receptor antagonist, the brain thinks there is not enough dopamine in the motor circuit, so this can cause Parkinson like side effects to do with movement.

48
Q

What does the Tuberoinfundibular pathway regulate?

A

Regulates the secretion of prolactin.

49
Q

What are Agonists?

A

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

50
Q

What are Partial Agonists?

A

An agonist which is unable to induce maximal activation of a receptor population, regardless of the amount of drug applied

51
Q

What are Antagonists?

A

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

52
Q

What are 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 and GABA.
Very rapid response (msecs to secs)

53
Q

What are Metabotropic Receptors?

A

Receptor protein in membrane is coupled to effector mechanism via G-protein.
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.
Slower responses (secs to mins to hours)

54
Q

What are Kinase-Linked Receptors?

A 
Endogenous agonists include hormones and growth factors .
Involved in regulation of growth, differentiation and responses to metabolic signals. 
Slower responses (mins to hours)
55
Q

What are Intracellular Receptors?

A

Used by lipid-soluble steroid hormones, affecting DNA transcription processes.
Responses long-lasting, remain long after agonist binding.
Very slow responses (hours to days)

56
Q

Drugs affecting Neurotransmission?

A

Schizophrenia:
- Antipsychotics – D2 receptor antagonists
- Novel treatments for cognitive deficits
Parkinson’s Disease:
- Dopaminergic drugs (precursors/agonists)
Alzheimer’s Disease:
- Acetylcholinesterase inhibitors
- NMDA receptor antagonist
Epilepsy:
- Anticonvulsants (GABA/Glutamate transmission)
Depression:
- Selective serotonin reuptake inhibitors (SSRIs)
CNS Stimulants:
- Cocaine, Amphetamines, Nicotine

57
Q

What is 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 Year 3 Semester 2 (5 decks)

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