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Lecture notes psychopharmacology
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This contains extensive elaborations of the lectures of the course Psychopharmacology . Written in English (according to the language in which lectures have been given.
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UU Psychopharmacology 2024 - All studyquestions + answers!!
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Psychopharmacology overzicht neurotransmitters en hun werking
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Summary of psychopharmacology UU
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Lectures psychopharmacologyLecture 1 – introduction and overview
• Drug/pharmacon: an administered substance that influences physiological processes
o Sometimes also body’s own substances
o No pharmacon if it’s primarily a nutrient (metabolizes and other purposes)
• Psychoactive substances: influence processes in the brain and hence behaviour, cognition,
affect (emotions)
o Different purposes:
▪ Therapeutic: cure a disease or alleviate some symptoms
▪ Recreational purpose
• Pharmacology: studies the influence of substances on biological processes
• Psychopharmacology: focusses on substances that influence the brain, effects on behaviour,
cognition and affect
o Affects the brain
• You use in daily life lots of psychopharmacological influences
o Tea, coffee, energy, beer, smoke, recreational drugs
• Interest: clinical applications, often quite a bit of media attention for new psychoactive drugs
or certain adverse reactions that drugs may have
o How does this work? Why do theses substances do what they do?
o Some prescription drugs are used for recreational purpose (Ritalin —> ADHD)
• Interest: development of future applications
o Cannabinoid system for extinction of fear in the brain???
• Pharmacokinetics: how does a substance move through the body?
o How do you administer it?
o How is it absorbed? In fat? Does it reach the blood easily? Is it easily degraded in the
body?
o May be important for some medication.
• Pharmacodynamics: what does the substance do to the body once it’s in there?
o To what receptors does the substance bind? If it binds, what kind of effect does it
have there?
Neurotransmitters (basics etc.)
• Brain consists of all kinds of cells
• Neurons ‘talk’ to each other
• Neuron emits an action potential
o Synaps at the end of the axon can be activated, what happens there is a chemical that
interacts
• Neurotransmitters is released in the synaptic cleft
o In order to be released, it has to be synthesized (has to be present there, or
generated)
o Has to be released
• After release there is a form of degradation to end the action on the post-synaptic neuron
• Neurotransmitters work on neurons via receptors
o Complex protein chains
• What is the most typical receptor?
o Either presynaptic, postsynaptic or auto-receptor?
, o Postsynaptic! Effects of neurotransmission depend primarily on post-synaptic
receptor
• What is not a drug target to influence the functioning of neuron?
o Ether receptor activation, metabolite excretion, reuptake blockade, enzyme
modulation, all of the above are possible targets?
o Metabolite excretion! Metabolites are the parts in which a molecule is dissembled
before it is excreted, don’t have a psychoactive effect
• Neurotransmission: drugs activate a certain receptor
o Some kinds of receptor have control in ion-channels (changes in the membrane)
o Some receptors have an effect on the membrane potential, but indirectly through
another route
• Nerves are surrounded by membranes, and have an intercellular space
o Difference between within and outside the nerve cell divided by this membrane
o Potential difference between inside and outside (+/- 70 mV)
o Neurotransmitters act on neurons via receptors
o Effect: small change with respect to the resting potential (EPSP/IPSP) that can add up
to the threshold for an action potential
o EPSP: excitatory post-synaptic potentials
o IPSP: inhibitory post-synaptic potentials
• Inhibitory receptors increase the potential differences
• Excitatory receptors reduce the potential difference to zero, increases the chances of an AP
being generated
• Building blocks for neurotransmitters, some of them typically come from diets
• Tyrosine —> DOPA —> dopamine
o When the neurotransmitters have been synthesized they can enter little vessels which
allow the release of the NT into the synaptic cleft
• NT have an effect on a relatively low amount of neurons in the brain
o Norepinephrine, dopamine, serotonin (only a small proportion)
o Relatively specific targets
• Other NT’s are used by lots of different neurons in the brain
o Inhibitory neurotransmitter GABA, excitatory neurotransmitter glutamate
o Used in about 50% of the synapses
o Also: endocannabinoid is present in many synapses
• Neurotransmitters have been implicated receptors in many synapses
o GABA: alcohol, sedatives, anxiolytics
o GLU, NMDA: epilepsy, Huntington, aids, dementia, schizophrenia
o Typically a problem of specificity of drug targets
Specific neurotransmitters
• Neurotransmitters come from precursors: substances that are needed to construct the
neurotransmitter from
• Monoamines: precursor is tyrosine, essential amino acid (through food!)
o Catecholamine, DA, NE, E
▪ Tyrosine —> dopa —> dopamine —> norepinephrine —> epinephrine
o Serotonine (5-HT), precursors is tryptophan
• Amino acid: glutamate, GABA, precursor is glucose
• Acetylcholine (ACh): precursors is choline/lecithin
• Peptides: oxytocin, endorphins, precursor = many different amino acids
,Neurotransmission: types of receptors
• Post-synaptic/axo-dendritic: receptors that are activated by a combination of an axon and a
dendrite
• Presynaptic receptors, most important is the auto-receptor
o Sits quite close to the synaps, can detect neurotransmission or release of
neurotransmitter from its own axon terminal
o Typically has a feedback role in which, neurotransmitter release will be ended
• Heteroreceptor: receptor on presynaptic neuron that reacts to input from another neuron
o Modulates synaps from another neuron
• Auto-receptors on other locations on the neuron, e.d. Dendrite, soma or other parts
• Activation of all of the receptors can have different implication on modification of
neurotransmission
Types of neurotransmission
• Synaptic axo-dendritic receptor
• Retrograde transmission: case in cannabinoid system
o Post-synaptic neuron releases endo-cannabinoids that active receptors on the pre-
synaptic neuron and can also end neurotransmission
• Non-synaptic diffusion: not really transmission between pre-synaptic and post-synaptic cell,
but receptors on other parts of the receptor can be activated
• Neuromodulators: do not active receptors directly, but modify receptors that when
neurotransmitter binds, properties of receptors are different
o Benzodiazepine
• Neurohormones: released in the blood, not released in synaptic communication. Can also
activate receptors on distant sides
Specific/most important neurotransmitters in the brain
Afkorting Substance Receptors Functions
ACh Acetylcholine Muscarinic (M1-M5), Memory, sensory
nicotinic (Nn, Nm) processes, motor
coordination,
parasympathetic ANS
NE Norepinephrine Alpha1-2, Beta1-2-3 CNS sensory
processes, cerebellum,
sleep, mood, learning,
memory, arousal,
sympathetic ANS
DA Dopamine D1-D5 (families: D1, Motor coordination,
D2) reinforcement, smell,
mood, concentration,
hormone regulations
5-HT Serotonin 18, divided in families Emotion, mood,
5-HT1-5-HT8 appetite, sleep, pain,
hallucinations, reflexes
GLu Glutamate NMDA, quisqualate, LTP, memory,
kainate excitation in
central/peripheral NS
, GABA Gamma amino-butyric GABAa, GABAb Inhibition in CNS
acid
VAR Peptide E.g. hormone E.g. social behavior,
pain, etc.
• Different subtypes! For this course you don’t need to know all different types of all different
receptors
o Only the important different subtypes (mentioned explicitly)
Specific neurotransmitters (NT): where to? Ending NT activity
• Neurotransmission has to be ended in order for the post-synaptic neuron to stop being
activated
• Different neurotransmitters have different ways in how their transmission is being degraded
• Combinations of degradations (metabolism) in synaps and reuptake within the cell
• For example: ACh is degraded outside of the cell, metabolites (parts that its broken down into)
are taken back up in the cell to be reused
• 5-HT: reuptake within the cell, broken down inside the cell (intracellular degradations)
• Peptides: outside of cell
• ACH: extracellular degradation
• Catecholamine: NE & DA, neurotransmission mostly ended by reuptake in the cell. 5%
extracellular by COMT enzyme (catechol-O-methyltransferase) in PFC. Makes it interesting
target for psychiatric disorders
• Amino-acids GLU & GABA: can be transferred into each other, have a very similar structure.
Degradation inside the cell. Glu is precursor for GABA
• What is NOT a precursor for noradrenaline?
o Either tyrosine, tryptophan, dopamine
o Tryptophan! Precursor for serotonin
• From modulation of which neurotransmitter do you expect the most specifically localized
effects in the brain?
o Either glutamate, GABA, dopamine
o Dopamine!
Specific neurotransmitters: anatomical origin NE/5-HT tracks
• NE & 5-HT origins in midbrain & brainstem
o NE: cell bodies in locus coerulus, other parts in pons and brain stem
o 5-HT: cell nuclei in raphe nuclei
• Relatively few cells, but many influential projections to entire cortex
Points of engagement around the synapse
• Modulate presence of precursor or activity of enzyme that synthesize neurotransmitters
• Influence of uptake in and release from vesicles
• Modify post-synaptic receptors
o Blocking (neurotransmission no longer has an effect)
o Administer drug that activates receptor as if neurotransmitter has bound to it
o Different ways of doing it
o Can both be done on pre- and post-synaptic receptors
• Drugs sometimes target how neurotransmission is being ended
o Blocking reuptake, often used mechanism
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