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Pharmacology > Pharmacology of CNS drugs > Flashcards

Pharmacology of CNS drugs Flashcards

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1
Q

What are the two main types of ion channels in nerve cells?

A

Voltage-gated channels and ligand-gated channels.

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2
Q

What determines the gating of voltage-gated channels?

A

Changes in membrane potential (voltage across the neuron’s membrane).

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3
Q

What determines the gating of ligand-gated channels?

A

Binding of a neurotransmitter (ligand) to the receptor.

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4
Q

What are voltage-gated sodium channels responsible for in nerve cells?

A

Generating fast action potentials that transmit signals along the axon.

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5
Q

Where are voltage-gated sodium channels mainly found?

A

In the initial segment and axon of neurons.

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6
Q

What is the role of certain potassium channels activated by depolarization?

A

To slow further depolarization and limit action potential firing — they act like a brake.

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7
Q

What are ligand-gated channels also called?

A

Ionotropic receptors.

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8
Q

How do ionotropic receptors work?

A

Neurotransmitter binding directly opens the ion channel, allowing ions to flow.

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9
Q

How fast are ionotropic receptor responses?

A

Very fast — typically a few milliseconds to tens of milliseconds.

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10
Q

Are ionotropic channels sensitive to membrane voltage?

A

No, they are insensitive or only weakly sensitive to membrane potential.

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11
Q

What type of neural pathways rely on ionotropic receptors?

A

Hierarchical pathways in the CNS, responsible for fast synaptic transmission.

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12
Q

What is another name for metabotropic receptors?

A

G protein-coupled receptors (GPCRs).

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13
Q

What happens when a neurotransmitter binds to a metabotropic receptor?

A

A G protein is activated, which then modulates ion channels through second messengers

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14
Q

Do metabotropic receptors directly open ion channels?

A

No, they affect ion channels indirectly through G protein signaling.

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15
Q

How long do metabotropic receptor effects last?

A

From tens of seconds to minutes — much longer than ionotropic receptors.

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16
Q

What are membrane-delimited pathways?

A

G proteins interact directly with ion channels in the same membrane region.

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17
Q

What effect does G protein binding have on calcium channels?

A

It inhibits them — reducing neurotransmitter release (presynaptic inhibition).

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18
Q

What effect does G protein binding have on potassium channels (postsynaptic)?

A

It activates them, causing slow postsynaptic inhibition.

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19
Q

What do second messenger pathways involve?

A

G protein activation leads to production of chemicals like cAMP that affect distant parts of the cell.

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20
Q

What is a classic example of a second messenger pathway?

A

β-adrenoceptors activate adenylyl cyclase, which generates cAM

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21
Q

How do second messenger effects differ from membrane-delimited ones?

A

They can spread over larger areas of the cell, not just local membrane regions.

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22
Q

Which receptor type has faster effects: ionotropic or metabotropic?

A

Ionotropic.

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23
Q

Which receptor type causes longer-lasting effects?

A

Metabotropic.

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24
Q

Which receptor type directly gates ion channels?

A

Ionotropic.

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25
Which receptor type uses G proteins and second messengers?
Metabotropic.
26
Which receptor type is more common in diffuse neuronal systems in the CNS? Metabotropic receptors.
Metabotropic receptors.
27
What type of synapse is most common in the CNS?
Chemical synapse.
28
Are electrical synapses common in the CNS?
No, they're rare and mostly help synchronize neurons but aren't major drug targets.
29
What triggers synaptic transmission in a chemical synapse?
An action potential arriving at the presynaptic terminal.
30
What happens when the action potential reaches the presynaptic terminal?
Voltage-sensitive calcium channels open.
31
What enters the presynaptic terminal when calcium channels open?
Calcium ions (Ca²⁺).
32
What does increased calcium in the presynaptic terminal cause?
Fusion of synaptic vesicles with the membrane and release of neurotransmitters.
33
Where are neurotransmitters released?
Into the synaptic cleft.
34
What happens after neurotransmitters are released into the synaptic cleft?
They bind to receptors on the postsynaptic membrane.
35
What effect does transmitter binding have on the postsynaptic cell?
It changes the membrane's ion permeability (conductance).
36
How long is the synaptic delay between presynaptic action potential and postsynaptic response?
Approximately 0.5 milliseconds.
37
What causes most of the synaptic delay?
The time it takes for calcium channels to open and trigger neurotransmitter release.
38
What is the typical resting membrane potential of a neuron?
Around –70 mV.
39
What happens during an excitatory postsynaptic potential (EPSP)?
The membrane depolarizes due to increased cation (like Na⁺) permeability.
40
What kind of receptor mediates EPSPs?
Ionotropic receptors.
41
What causes the size of an EPSP to increase?
Stimulating more presynaptic fibers (stronger input).
42
When does an EPSP trigger an action potential?
When the depolarization reaches threshold.
43
What happens during an inhibitory postsynaptic potential (IPSP)?
The membrane hyperpolarizes due to chloride (Cl⁻) channel opening.
44
Why is the IPSP hyperpolarization small?
Because the chloride equilibrium potential is close to the resting membrane potential (~–65 mV).
45
What is the "shunting" effect of IPSPs?
They make the membrane leaky, reducing the effect of incoming EPSPs.
46
Can a normally effective EPSP fail during an IPSP?
Yes, because the IPSP shunts the current away and prevents threshold from being reached.
47
What is presynaptic inhibition?
Reduction of neurotransmitter release from a presynaptic terminal.
48
What kind of synapse causes presynaptic inhibition in the spinal cord?
Axoaxonic synapse.
49
What do axoaxonic synapses do?
They reduce neurotransmitter release by the primary presynaptic terminal.
50
Are axoaxonic synapses common in the brain?
No, they’re mainly in the spinal cord
51
How does presynaptic inhibition occur in the brain if axoaxonic synapses are rare?
Through neurotransmitter spillover that activates presynaptic receptors on nearby terminals.
52
Do presynaptic inhibitory receptors exist throughout the brain?
Yes, they are found on almost all presynaptic terminals.
53
What is the main way drugs act in the CNS?
By modifying steps in chemical synaptic transmission.
54
What are the two main categories of drug actions at the synapse?
Presynaptic and postsynaptic.
55
What do presynaptic drugs affect?
Synthesis, storage, metabolism, and release of neurotransmitters.
56
How does reserpine affect neurotransmitters?
It depletes monoamine transmitters by interfering with their storage in synaptic vesicles.
57
What happens when transmitter catabolism is blocked?
It increases the amount of transmitter available and can enhance release.
58
What does amphetamine do at synapses?
It increases the release of catecholamines (e.g. dopamine, norepinephrine) from adrenergic synapses.
59
What does capsaicin do to neurons?
It causes the release of substance P from sensory neurons.
60
What does tetanus toxin do at synapses?
It blocks the release of neurotransmitters.
61
How is neurotransmitter action usually terminated?
By reuptake into the nerve terminal or nearby glial cells, or by enzymatic degradation.
62
How does cocaine affect neurotransmitter levels?
It blocks the reuptake of catecholamines, increasing their effect.
63
How is acetylcholine inactivated?
By enzymatic degradation, not reuptake.
64
What do anticholinesterase drugs do? .
They block the breakdown of acetylcholine, prolonging its effect
65
Do peptide neurotransmitters have reuptake mechanisms?
No, and the role of enzymatic degradation is still unclear.
66
Where do postsynaptic drugs act?
At the neurotransmitter receptors or downstream signaling pathways.
67
What is an example of a neurotransmitter agonist drug?
Opioids, which mimic the action of enkephalins.
68
What is an example of a receptor antagonist?
Strychnine, which blocks glycine receptors.
69
How does strychnine cause convulsions?
By blocking inhibitory glycine receptors, leading to excess excitation.
70
Can drugs act directly on ion channels? .
Yes, for example, barbiturates can block excitatory ionotropic receptor channels
71
What type of receptors do methylxanthines affect?
They influence second messenger systems (e.g., cAMP) by blocking its metabolism.
72
What is retrograde signaling?
When the postsynaptic neuron sends signals back to the presynaptic terminal.
73
What are endocannabinoids?
Retrograde messengers released from postsynaptic neurons that bind to presynaptic receptors to reduce neurotransmitter release.
74
What gas is proposed as a retrograde messenger?
Nitric oxide (NO), though its role in the CNS is not fully understood.
75
Why is CNS drug selectivity possible?
Because different transmitters are used by different neurons, often organized into specific systems.
76
What allows for targeted drug effects in the CNS?
Segregation of neurotransmitters into distinct neuronal systems.
77
Why is this segregation important in medicine?
It enables the treatment of specific CNS disorders with drugs that target only certain pathways.
78
What is the main reason neuropharmacologists want to identify neurotransmitters in CNS pathways?
Because drug selectivity relies on different pathways using different neurotransmitters.
79
Why is identifying neurotransmitters more difficult in the CNS than in the peripheral nervous system?
Because of the greater complexity and overlapping pathways in the CNS.
80
What is the first criterion for identifying a neurotransmitter?
Localization — the chemical must be present in the presynaptic terminal.
81
What techniques are used to study localization of a neurotransmitter?
Biochemical analysis of regional concentrations and immunocytochemical methods for enzymes and peptides.
82
What is the second criterion for identifying a neurotransmitter?
Release — the substance must be released from the neuron in a calcium-dependent way.
83
How can scientists test for neurotransmitter release in a brain region?
By collecting extracellular fluid (in vivo) or stimulating brain slices (in vitro) and measuring released substances.
84
Why must neurotransmitter release be calcium-dependent?
Because normal synaptic transmission requires calcium influx for vesicle fusion and transmitter release.
85
What is the third criterion for identifying a neurotransmitter?
Synaptic mimicry — applying the substance should mimic the effect of the naturally released transmitter.
86
What technique is used to apply neurotransmitters directly to neurons?
Micro-iontophoresis, which allows precise and localized drug delivery.
87
How do scientists confirm the effect of a suspected transmitter is receptor-specific?
By using a selective antagonist to block the effect and seeing if it also blocks the natural synaptic response
88
Why is pharmacologic antagonism a powerful tool in neurotransmitter identification?
Because blocking the receptor response can confirm the involvement of that specific transmitter.
89
What does micro-iontophoresis help assess in neurotransmitter studies?
Whether a suspected transmitter mimics natural synaptic effects when applied locally
90
What must happen for a chemical to be officially identified as a neurotransmitter in the CNS?
It must meet all three criteria: proper localization, calcium-dependent release, and synaptic mimicry.

Pharmacology (4 decks)

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