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Psychopharmacology
(psychoactive drugs)
1. Name ways to get a drug into your system
(sources of drug administration)
2. Rank those sources based on how fast
they reach blood & thus the brain
3. List the factors that determine the effect of
a drug on an individual. (In other words, what
makes a psychoactive drug be more effective in
one person than another)
Outline
• Pharmacokinetics
– Dose-response curve
• Pharmacodynamics
– Drugs vs. NTs
– Agonists vs. Antagonists
– Receptor types
• Tolerance
• Specific Neurotransmitter Systems (& drugs that affect them)
Pharmacokinetics
Pharmacodynamics
• Whatever the body does
to the drug
• Whatever the drug does
to the body
• how drugs are
– absorbed,
– distributed within the
body,
– metabolized, and
– excreted.
• Main effect: increasing or
decreasing the effect of
neurotransmitter X
• Side effects (unwanted
effects)
Pharmacokinetics
• Sources of administration:
oral, intranasal, inhalation, topic,
intravenous (i.v), sublingual,
intramuscular (i.m.) subcutaneous,
intraperitoneal
• Distribution:
– Lipids (fats) vs. non-lipids (proteins, ionized molecules)
• Metabolization: liver
• Excretion: kidneys
– Half-life: time it takes to eliminate half the drug from the
bloodstream. It is used to determine inter-dose interval
Ways to administer a drug (& time to reach blood)
Dose-response curve: Effect of a drug as a function of the
amount of the drug administered.
Therapeutic index: The ratio between the dose that
produces the desired effect in 50% of the animals and the dose
that produces toxic effects in 50% of the animals.
Pharmacodynamics
• A drug can do only two things, either:
– Increase the effect of neurotransmitter X (agonist)
– Decrease the effect of neurotransmitter X (antagonist)
Thus, in order to understand the action of a ‘drug X’, we need to
understand the neurochemical system it interacts with.
In other words, we need to understand how Neurotransmitter X
- is produced & released from the pre-synaptic neuron
- acts on the receptors of the post-synaptic neuron
- is removed from the synaptic cleft
Pre-synaptic
receptors
Post-synaptic
receptors
--
precursors
NT ‘x’
1. produce
2. pack
AP  Ca++ inflow
3. release
4. Bind
++
5. Post-synaptic
changes
(e.g., epsp)
6.A Recycle
6.B Destroy
Pre-synaptic
Neuron
(axon)
synaptic
cleft
Post-synaptic
neuron
(dendrite)
Copyright © Allyn & Bacon 2004
Receptors
• Receptors are specific for individual neurotransmitters
• More than one receptor for each neurotransmitter.
e.g., Acetylcholine (muscarinic & nicotinic receptors)
Ionotropic Receptors
(e.g., nicotinic)
Metabotropic Receptors
(e.g., muscarinic)
Agonists and Antagonists
• Agonist (Greek: Agon, meaning contest)
– Substance that facilitates post-synaptic effects
• Antagonist
– Substance that inhibits or blocks the postsynaptic effects
• Exogenous vs. Endogenous (drugs vs. neurotransmitters)
• Agonist vs. Antagonist: Both bind to a receptor. The agonist
activates it, the antagonist does not (antagonists block the receptor)
• Competitive vs. non-competitive: whether the drug works at the
same receptor as the NT or at a different receptor as the NT, but one
that modifies the NT’s action
1. Will an antagonist produce a rightward shift or a
leftward shift in the dose-response curve? (graph)
2. How would a competitive antagonist modify the curve?
(draw with a solid line)
3. How would a non-competitive antagonist modify the
curve (draw with a dotted line)
Tolerance
a decreased response due to frequent use.
• Metabolic tolerance: faster metabolism of the drug.This is
a pharmacokinetic mechanism (e.g., alcohol metabolization by
hepatic enzimes)
• Cellular-adaptive tolerance: down-regulation of receptors
(a pharmacodynamic mechanism)
Before drug
After Drug
Factors that determine the effect of a
drug on an individual
•
•
•
•
•
•
Age
Weight
Setting in which the drug is used
History of use (tolerance)
Level of proteins in blood
Time of day drug is consumed
• These effects are underlined by both pharmacokinetic
and pharmacodynamic modulations