Chapter 5
- Give a definition of psychopharmacology.
- the effect of the substances on the behaviour, cognition and affect. Including
their mechanisms in the brain.
- (See also Kenemans, paragraph 1.2) What is a dose-response-curve
(DRC)?
A graph in which the x- axis shows the increasing dose of a substance,
usually in units such as mg/kg. the effect of that dose is displayed as
values along the y- axis
- See Kenemans Fig. 5.2: Does the DRC for one particular substance
always look the same? What does it depend on? How about
differences between individuals?
No. it is different for each individual. It depends on a lot of things. For example
adults are generally much faster at impulse control than children, which is why
adults need a lower dose for the same effect.
- What type of responses in a DRC and the relationship between them
are especially relevant for medications?
Potency, efficacy and the therapeutic window.
- Wat is efficacy? Potency? Therapeutic window?
Efficacy; does it actually improve, does it work?
Potency; lowest dose at which there is a visible effect on the group.
Therapeutic window; the range between the desired and the undesirable effects
of a substance.
- Which considerations are relevant for the individual titration of the
optimal dose of a substance?
Beginning with prescribing a minimum dosage and see if it has any effect. And
than you track the desirable and undesirable effects reported by the patient.
According these reports you can increase the dosage.
- What is receptor interaction?
Two substances meet one another and therefor interact. This happens in the
protein complexes in the brain (receptors)
- What is the relationship between receptor interaction and statistical
interaction?
Statistical interaction; on substance’s effect on behaviour (PPI) changes under
the influence of another.
The hypothesis of a receptor interaction results in the prediction of a statistical
interaction
- What is the importance of a statistical interaction between a
pharmacological variable and a psychological variable?
To describe the biochemical and physiological effects of a substance.
,- With receptor interaction, what is affinity, en what is efficacy?
Affinity; how much does the substance bind to the receptor
Efficacy; the degree to which the bond between the neurotransmitter and the
receptor results in a synaptic effect, such as opening the channels.
- (See also Kenemans paragraph 4.4) In what respect do full and
partial agonists differ, in affinity or efficacy?
Full agonist; high affinity and high efficacy
Partial agonist; high affinity but a receptor- efficacy between that of a full agonist
and an antagonist
- (See also Kenemans paragraph 4.4) What is high with a pure
antagonist, affinity, efficacy or both?
Full agonist; high affinity and high efficacy
Partial agonist; high affinity but a receptor- efficacy between that of a full
agonist and an antagonist
- (See also Kenemans paragraph 4.4) What is an allosteric receptor?
Can you give an example?
allosteric receptor; when they bind to the relevant substance it does not
immediately lead to opening of ion channels. This requires other receptors on the
same receptor complex to bind to their own neurotransmitter. The degree to
which the allosteric receptor is activated determines the degree to which the
bond to the neurotransmitter proper results in a the opening of the ionchannel.
An example is GABAa- receptor.
- What does the mode of administration mean for the
pharmacokinetics?
The effect of the substance
- What is tolerance?
The desensitisation of receptors what leads to;
- More of the same substance needed
- The substance as such is needed for ‘normal’ functioning (nicotine). You need
the drug because your whole system is messed up.
- What is the relationship between tolerance and compensating
processes?
Tolerance leads to needing more of the substance for the same effect and you
need the substance for ‘normal’ functioning.
- What is the relationship between tolerance en desensitisation?
Desentisation; Repeated administration leads to reduced affinity, reduced
receptor-efficacy, fewer receptors (‘down’-regulation).
Desensititsation of receptors can lead to tolerance
- How do tolerance and desensitisation contribute to dependence?
, You need the substance for ‘normal’ functioning. And everytime you take the
substance you need more because your receptors are desensitized which leads to
a higher tolerance.
- Why is it plausible that besides desensitisation, sensitisation plays a
role in dependence?
After prolonged blocking of the receptors you can become hypersensitive (you
get more effect for the same input, opposite of tolerance) for the substance.
- How does sensitisation occur with pathologically or
pharmacologically induced inhibition of neurotransmission?
Sensitisation after inhibiting a neurotransmission system (e.g. dopamine)
happens because the brain tries to compensate—and when that inhibition is lifted
(or even reduced), the system can overshoot and become hyperresponsive (e.g.
supersensitive dopamine this can worsen psychosis when the drug is withdrawn).
This is the same with nicotine. The nicotine receptors become hypersensitive so if
someone stops smoking and then after a while smokes again he or she has an
exaggerating effect because the receptors are hypersensitive. This can cause a
relapse.
- What can you say about the contribution of (de)sensitisation to the
difference between effects of acute and chronic administration of a
substance?
After acute administration the receptors are at baseline sensitivity. But after
chronic administration (de) sensitisation plays a role what can result in tolerance
and cravings.
Chapter 6
- What do stimulants stimulate (in terms of body, brain,
behaviour)?
The sympathetic nervous system (sympathomimetic)
- With which receptor does caffeine interact, and what are the
consequences on synaptic processes?
It blocks the adenosine receptor, this leads to a reduced secretion of a
neurotransmitter to which the receptor is bound. It blocks dopamine,
acetylcholine,noradrenaline, glutamine or GABA (blocking GABA has a
stimulation effect). The accumulation of adenosine leads to an increasing
degree of sedation (reduced drowsiness etc)
- How potent and efficacious is caffeine?
it is potent, but not very efficacious
- What does adenosine normally do?
Increasing sedation; reducing drowsiness, sleepiness
- Will we always perform better due to caffeine (with sufficiently
high dose)? Give an example.
- Give a definition of psychopharmacology.
- the effect of the substances on the behaviour, cognition and affect. Including
their mechanisms in the brain.
- (See also Kenemans, paragraph 1.2) What is a dose-response-curve
(DRC)?
A graph in which the x- axis shows the increasing dose of a substance,
usually in units such as mg/kg. the effect of that dose is displayed as
values along the y- axis
- See Kenemans Fig. 5.2: Does the DRC for one particular substance
always look the same? What does it depend on? How about
differences between individuals?
No. it is different for each individual. It depends on a lot of things. For example
adults are generally much faster at impulse control than children, which is why
adults need a lower dose for the same effect.
- What type of responses in a DRC and the relationship between them
are especially relevant for medications?
Potency, efficacy and the therapeutic window.
- Wat is efficacy? Potency? Therapeutic window?
Efficacy; does it actually improve, does it work?
Potency; lowest dose at which there is a visible effect on the group.
Therapeutic window; the range between the desired and the undesirable effects
of a substance.
- Which considerations are relevant for the individual titration of the
optimal dose of a substance?
Beginning with prescribing a minimum dosage and see if it has any effect. And
than you track the desirable and undesirable effects reported by the patient.
According these reports you can increase the dosage.
- What is receptor interaction?
Two substances meet one another and therefor interact. This happens in the
protein complexes in the brain (receptors)
- What is the relationship between receptor interaction and statistical
interaction?
Statistical interaction; on substance’s effect on behaviour (PPI) changes under
the influence of another.
The hypothesis of a receptor interaction results in the prediction of a statistical
interaction
- What is the importance of a statistical interaction between a
pharmacological variable and a psychological variable?
To describe the biochemical and physiological effects of a substance.
,- With receptor interaction, what is affinity, en what is efficacy?
Affinity; how much does the substance bind to the receptor
Efficacy; the degree to which the bond between the neurotransmitter and the
receptor results in a synaptic effect, such as opening the channels.
- (See also Kenemans paragraph 4.4) In what respect do full and
partial agonists differ, in affinity or efficacy?
Full agonist; high affinity and high efficacy
Partial agonist; high affinity but a receptor- efficacy between that of a full agonist
and an antagonist
- (See also Kenemans paragraph 4.4) What is high with a pure
antagonist, affinity, efficacy or both?
Full agonist; high affinity and high efficacy
Partial agonist; high affinity but a receptor- efficacy between that of a full
agonist and an antagonist
- (See also Kenemans paragraph 4.4) What is an allosteric receptor?
Can you give an example?
allosteric receptor; when they bind to the relevant substance it does not
immediately lead to opening of ion channels. This requires other receptors on the
same receptor complex to bind to their own neurotransmitter. The degree to
which the allosteric receptor is activated determines the degree to which the
bond to the neurotransmitter proper results in a the opening of the ionchannel.
An example is GABAa- receptor.
- What does the mode of administration mean for the
pharmacokinetics?
The effect of the substance
- What is tolerance?
The desensitisation of receptors what leads to;
- More of the same substance needed
- The substance as such is needed for ‘normal’ functioning (nicotine). You need
the drug because your whole system is messed up.
- What is the relationship between tolerance and compensating
processes?
Tolerance leads to needing more of the substance for the same effect and you
need the substance for ‘normal’ functioning.
- What is the relationship between tolerance en desensitisation?
Desentisation; Repeated administration leads to reduced affinity, reduced
receptor-efficacy, fewer receptors (‘down’-regulation).
Desensititsation of receptors can lead to tolerance
- How do tolerance and desensitisation contribute to dependence?
, You need the substance for ‘normal’ functioning. And everytime you take the
substance you need more because your receptors are desensitized which leads to
a higher tolerance.
- Why is it plausible that besides desensitisation, sensitisation plays a
role in dependence?
After prolonged blocking of the receptors you can become hypersensitive (you
get more effect for the same input, opposite of tolerance) for the substance.
- How does sensitisation occur with pathologically or
pharmacologically induced inhibition of neurotransmission?
Sensitisation after inhibiting a neurotransmission system (e.g. dopamine)
happens because the brain tries to compensate—and when that inhibition is lifted
(or even reduced), the system can overshoot and become hyperresponsive (e.g.
supersensitive dopamine this can worsen psychosis when the drug is withdrawn).
This is the same with nicotine. The nicotine receptors become hypersensitive so if
someone stops smoking and then after a while smokes again he or she has an
exaggerating effect because the receptors are hypersensitive. This can cause a
relapse.
- What can you say about the contribution of (de)sensitisation to the
difference between effects of acute and chronic administration of a
substance?
After acute administration the receptors are at baseline sensitivity. But after
chronic administration (de) sensitisation plays a role what can result in tolerance
and cravings.
Chapter 6
- What do stimulants stimulate (in terms of body, brain,
behaviour)?
The sympathetic nervous system (sympathomimetic)
- With which receptor does caffeine interact, and what are the
consequences on synaptic processes?
It blocks the adenosine receptor, this leads to a reduced secretion of a
neurotransmitter to which the receptor is bound. It blocks dopamine,
acetylcholine,noradrenaline, glutamine or GABA (blocking GABA has a
stimulation effect). The accumulation of adenosine leads to an increasing
degree of sedation (reduced drowsiness etc)
- How potent and efficacious is caffeine?
it is potent, but not very efficacious
- What does adenosine normally do?
Increasing sedation; reducing drowsiness, sleepiness
- Will we always perform better due to caffeine (with sufficiently
high dose)? Give an example.
