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PSYC 383, Psychopharmacology > Chapter 3, Chemical Signalling by Neurotransmitters and Hormones > Flashcards

Chapter 3, Chemical Signalling by Neurotransmitters and Hormones Flashcards

1
Q

Drug Action

A

Specific molecular changes produced when a drug binds to a particular target site or receptor

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2
Q

Drug Effects

A

Alterations in physiological or psychological functions
* Therapeutic effects vs. side effects
* Specific drug effects vs. non-specific drug effects

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3
Q

Neurotransmission

A
  • Drugs do not create a unique or novel effect… they merely modulate neuronal function by enhancing or inhibiting the actions of a specific neurotransmitter

Drugs can affect any stage
of neurotransmission!

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4
Q

Receptor Specificity

A
  • Binding affinity depends on the strength and number of noncovalent bonds between the drug and its target
  • Drugs with high affinity will occupy more receptors at any given concentration than drugs with a low affinity
  • Different drugs can bind the same target site, but with varying binding affinities
  • E.g., Competition between naloxone and fentanyl
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5
Q

Receptors

A

Proteins on cell surfaces or within cells

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6
Q

Ligand

A

Molecule that binds to a receptor with some selectivity
* Receptors have specificity for ligands, due to their molecular shape
* ”Lock and key” mechanism

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7
Q

Types of Receptors

A

A. Extracellular receptor *
B. Intracellular receptor

  • Recall: ionotropic vs. metabotropic receptors
  • Example: Nicotinic receptors vs. muscarinic receptors
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8
Q

Receptor Action

A
  • Ligand–receptor binding is temporary
  • Ligand binding causes change in receptor shape that initiates a series of events in the cell, ultimately causing a Biobehavioral effect
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9
Q

Receptor Specificity and the Agonists v. Antagonists

A
  • Agonists have the highest affinity and produce significant biological effects
  • Antagonists have lower affinity and little or no efficacy
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10
Q

Specificity with Agonists

A
  • Full agonists
  • Partial agonists have intermediate efficacy
  • Inverse agonists initiate a biological action that is opposite to that produced by an agonist
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11
Q

Specificity with Antagonists

A
  • Competitive antagonists: Drugs that compete with agonists to bind receptors but do not initiate intracellular effects, reducing the effect of the agonist
  • Noncompetitive antagonists bind to the receptor at a site other than the agonist binding site
  • Physiological antagonism: Two drugs interact and reduce the
    effectiveness of both
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12
Q

Receptor Binding Sites

A
  • The GABAA receptor has multiple binding sites, which means
    drugs can interact to have enhanced effects on GABA
  • Allosteric modulators only modify the effects of an agonist;
    they have no effects when given alone
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13
Q

Summary for Agonists and Antagonists

A
  • Agonists bind to receptors to produce a functional response.
  • Agonists can be full, partial, or inverse agonists
  • Antagonists block or reverse the effects of agonists.
  • Antagonists can be competitive or noncompetitive
  • Physiological antagonists bind to different sites
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14
Q

Receptor Subtypes

A
  • All neurotransmitters have a number of receptors that they can act on
  • Receptors may have different characteristics
  • Receptors can be distributed in different tissues
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15
Q

Receptor Action

A
  • Receptors have a life cycle and may be modified in a number and/or sensitivity with long-term receptor action
  • Changes in receptor number take days-weeks, while changes in receptor sensitivity can be much faster
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16
Q

Dose-Response Relationships

A
  • The drug effect will depend on receptor occupancy
  • We assume that increased drug doses will result in increased receptor occupancy, thus causing an increased response
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17
Q

Dose-Response Curves

A
  • To determine the effect of a drug, we have to study several doses and measure the change in response
  • The relationship between dose and response is called the dose-response curve (DRC)
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18
Q

Features of the dose-response curve

A
  1. Potency: Describes the amount of the drug required to produce a given effect.
  2. Efficacy: Describes the extent to which a drug can produce a desired effect.
  3. Slope: Describes how a change in a drug’s dose relates to a change in the drug’s effect.
  4. Variability: Individual differences in response to a given drug dose.
  • Dose-response curves are based on averages
  • Individual variation in response to drug effectiveness could be
    caused by a number of things
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19
Q

Potency

A

Potency refers to how well drug molecules attach to their sites of action (receptors)
* More potent drugs usually bind more tightly than less potent drugs

20
Q

Efficacy

A

Efficacy refers to the maximum possible effect of a drug, regardless of further increases in dose
* Most drugs are not used at doses that elicit their maximal effect because of toxicity an other unwanted side effects

21
Q

Agonists in the Dose-Response Curve

A
  • Full agonists
  • Partial agonists have intermediate efficacy
  • Inverse agonists initiate a biological action that is opposite to that produced by an agonist
22
Q

Important terms in the dose-response curve

A
  • Maximum effect (Emax)
  • Threshold dose
  • Effective dose (ED50)
  • Toxic dose (TD50 )
    (not shown)

Describe drugs X, Y, and Z in terms of their relative potency and efficacy
* NB: When comparing drugs, maximal efficacy is usually a more important criterion to consider than potency

23
Q

Effective Dose (ED)

A
  • Comparing ED50 of different drugs shows differences in
    potency
  • For the same effect you need: 2mg hydromorphone, 10mg morphine, more than
    100mg codeine
24
Q

The optimum condition for a drug

A

Drugs have both desirable effects and adverse side effects
* The optimum condition is to have a drug that is effective at a low dose
with no toxicity except at very high doses

25
Q

Therapeutic Index Formula

A
  • Therapeutic index (TI) = TD50 / ED50
  • The greater the TI, the safer the drug
  • The lower the ED50, the greater the potency, but the lower the TI, the lower the safety
  • LD = lethal dose (seldom used)
  • If two drugs produce a therapeutic effect that is desirable, the better drug (all things being equal) would be the one with the larger TI
26
Q

The attributes of the ideal drug

A
  • easy to administer,
  • fully absorbed,
  • spontaneously eliminated,
  • highly selective and
  • specific, and
  • of high affinity,
  • potency, and
  • efficacy
  • useful duration of action,
  • high therapeutic index (no adverse effects), and
  • no interactions…

However, there are no examples of
synthetic or natural drugs that satisfy all these criteria ”

27
Q

Combining drugs and competitive drugs

A
  • Competitive antagonists may be used to replace an excess of agonist
  • E.g. Naloxone is a competitive antagonist of morphine
  • Note change in curve placement with pretreatment
28
Q

Combining drugs and noncompetitive drugs

A

Noncompetitive antagonists are less effective at protecting against an excess of agonist
* Note the change in the shape of the curve

29
Q

Physiological antagonism in combining drugs

A

Two drugs may interact and reduce the effectiveness of both

30
Q

Additive effects of combining drugs

A

two drugs may interact and enhance the effectiveness of both

31
Q

Potentiation of combining drugs

A

two drugs may interact and enhance the effectiveness of both to produce effects greater than the sum of their individual effects

32
Q

Repeated drug use

A
  • Recall: The effect of a drug is proportional to its concentration
    at its site of action, increasing with increasing dose.
  • A reduced drug response can manifest due to tolerance
33
Q

Tolerance

A

diminished response to a drug after repeated exposure
* acute tolerance
* cross tolerance

34
Q

Types of tolerance

A
  1. Metabolic (drug disposition) tolerance
  2. Pharmacodynamic tolerance
  3. Behavioural (learned) tolerance
35
Q

Metabolic tolerance

A
  • AKA drug disposition tolerance or pharmacokinetic tolerance
  • Drugs increase their own rate of metabolism by liver microsomal enzyme induction
36
Q

Pharmacodynamic tolerance

A
  • Neural function changes to adapt to continued presence of the drug by up- or down-regulation
37
Q

Behavioural tolerance

A
  • Occurs in the same environment in which the drug was administered
  • Behavioural (learned) tolerance may involve
  • Pavlovian, or classical conditioning: the drug-taking procedure and/or the environment may elicit a conditioned response. It involves an individual learning to maneuver efficiently while intoxicated. Or tasks learned under the influence of a psychoactive drug may then be performed better in the drugged state
38
Q

Drugs and developing tolerance

A
  • Some drugs can cause all three kinds of tolerance, other drugs can have a tolerance to some of their effects but not others, and still other drugs do not cause tolerance at all
39
Q

Physical dependence

A

A physiological state in which the body adapts to the chronic presence of a drug
* Withdrawal symptoms appear if the drug is abruptly stopped

40
Q

Sensitization

A
  • reverse tolerance
  • Cross-sensitization
  • Unlike tolerance, sensitization is
    not easily reversible
41
Q

Dependence and sensitization

A

A drug may cause either or both dependence and sensitization
*Example: Chronic exposure to psychostimulants can lead to tolerance, but sensitization or reverse tolerance, is also seen…

42
Q

Pharmacogenetics

A
  • Pharmacogenetics: Study of the genetic basis for variability in drug response among individuals.
  • Goal: Identify genetic factors that confer susceptibility to specific side effects, or predict a therapeutic response.
  • Pharmacoepigenetics takes into account the role of epigenetic modifications that can alter gene function and arise from environmental and behavioral factors
43
Q

Personalized Medicine

A

Adjusting drug dose based on genotype
* Predicting how patients will respond to a medication before treatment begins would avoid the current costly and time-consuming method of trial and error

44
Q

Affinity in agonists and antagonists

A
  • Agonists have the highest affinity and produce significant biological effects
  • Antagonists have lower affinity and low efficacy
45
Q

potency and efficiency in graphs

A

potency is right to left
efficiency is down to up

46
Q

competitive and noncompetitive antagonism in graphs

A

competitive is different starting points
non-competitive has the same starting points

47
Q

Semi-log plot

A
  • The semi-log plot is the preferred method for plotting dose-response relationships because it becomes easier to accurately determine the EC50 value (the concentration which produces 50% of the maximum response)

PSYC 383, Psychopharmacology (8 decks)

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