LECTURE 1- INTRODUCTION TO PSYCHOPHARMACOLOGY

Question 1

what is psychopharmacology the study of?

Answer 1

it is the study of the effects of drugs on cognition, mood and behaviour (ie their psychoactive properties)

Question 2

how can drugs have psychoactive properties?

Answer 2

drugs can only have psychoactive properties if they interact with existing endogenous neurochemical processes in the brain

Question 3

what are the 2 types of psychopharmacological research?

Answer 3

• drugs can be used as ‘probes’ to study functions of endogenous neurotransmitter systems (NTs)
• investigation of drug effects ca also lead to development of treatments for medical/psychological conditions (Alzheimers, skits,depression ect)

Question 4

what are the two themes?

Answer 4

research is difficult
- evidence needs interpretating, critically

we only know what we happen to have found out so far
- methods aren’t perfect, and many discoveries come about by chance

Question 5

methodology for studying drug effects

Answer 5

as with most science, we need to compare with the effects in a control condition

Question 6

what is a confound?

Answer 6

a confound is a potential alternative cause of what appears to be a drug effect

Question 7

what are some examples of how confounds can be controlled for?

Answer 7

natural recovery
- control by: comparison with no-treatment group

expectation of drug effect
- control by: comparison with placebo condition (eg, sugar pill) and ensure “blinding” conditions

expectation can still occur with placebo controls if side-effects (or other drug effects) lead to correct guessing of participants condition (“unbinding”)
-control by: comparison with an active placebo condition (eg., another drug with similar noticeable effects)

Question 8

what are the types of drug study

Answer 8

• randomised controlled trials- RCTs
• open-label trials
• “blinding” of conditions
• between-subjects design
• within-subjects

Question 9

randomised controlled trials

Answer 9

these trials involve a control condition (eg placebo, but could be eg current best treatment) and random assignment of participants to groups

Question 10

open-label trials

Answer 10

studies without blinding are referred to as being open-label. (there may still be a comparison with a control group eg placebo)

Question 11

“blinding” of conditions

Answer 11

• blind= participant unaware of group assignment
• double blind= participant and researcher unaware of group assignment

= “unblinding” can occur when effects are detectable

Question 12

between subjects design

Answer 12

= the comparison is between participants: drug group versus control group

Question 13

within subjects designs:

Answer 13

= the comparison is between conditions for the same participants: drug condition when receiving drug versus control condition when receiving eg placebo
= for instance, a crossover design (eg., “AB/BA” : drug-then-control / control-then-drug. A “washout period” may occur between treatments.)

Question 14

measures of drug effects include:

Answer 14

• changes in subjective experience (‘phenomenology’) and mood (self-report alertness, happiness, anxiety ect)
• changes in physiological activity (fMRI, EEG, ect)
• changes in task performance (simple and choice RT tasks, vigilance tasks, memory, problem solving, ect)
• changes in behaviour (social co-operation, aggression, hyperactivity, ect)
• NB subjective measures (eg ratings by self or researcher) can be susceptible to bias or expectancy- hence double-blind technique

Question 15

neurocognitive models

Answer 15

• aim to explain the relationships between specific neurotransmitters systems, cognitive processes and subjective experiences
• the model could be of a type of drug effect (stimulant, edative, psychedelic, ect)
• or it could be of a neuropsychiatric conditions (adhd, depression, skits, ect)

Question 16

what are 3 basic neurophysiological processes?

Answer 16

• neurons and synapses
• neurotransmitters and receptors
• agonistic and antagonistic effects of drugs

Question 17

the neuron (nerve cell) and synapse

Answer 17

• dendrites receive chemical signals (neurotransmitters, NTs) from other neurons
• the cell body (soma) includes the nucleus, which controls cells activity
• the axon allows an electrical signal (action potential) to travel to axon terminal
• enzymes control synthesis of neurotransmitters, which are stored in vesicles and released from the axon terminal
• the signal is transmitted between neurons at the synapse

Question 18

generation of action potential

Answer 18

• multiple excitatory and inhibitory signals (‘post- synaptic potentials’; PSPs) are integrated (combined) to determine whether an action potential is generated
• axon hillock: action potentials are triggered here if sufficient depolarisation (+relative to -)
• excitatory signals increase likelihood of receiving neuron producing action potential
• inhibitory signals decrease likelihood of receiving neuron producing action potential

Question 19

endogenous processes involving neurotransmitters (NTs)

Answer 19

1) synthesised by enzymes and packaged in vesicles
2) released then bind with postsynaptic receptors
3) deactivated presynaptic reuptake or broken down by enzymes

Question 20

effects of (NTs) at the post- synaptic cell

Answer 20

• 3-D shape of NT molecule has to fit receptor (like a key in a lock) to be able to produce an effect
• NTs influence the opening and closing of post-synaptic ion channels. this allows electrically charged ions to move in or out of the post-synaptic cell, making it more or less likely to ‘fire’ (produce an action potential)
• some NTs have less direct effects eg modulating the effect of other NTs on ion channels, or leading to other synaptic changes (eg for learning)
• the effect of a NT depends on receptor type. NTs therefore have different effects at different receptors

Question 21

NT deactivation

Answer 21

• NT detaches from receptor and is then:
• transported back into the presynaptic neuron (reuptake)
  or
  -broken down by enzymes in the synaptic cleft (products of enzymatic breakdown may then be recycled)

Question 22

how drugs work

Answer 22

• psychoactive drugs interact with NT systems
• drugs can influence NT synthesis, storage, release, receptor interactions, and/or deactivation
• drugs can have agonistic effects, where they mimic or enhance the effects of a NT
• drugs can have antagonistic effects, where they block or reduce the effects of a NT

Question 23

some ways in which drugs interfere with endogenous processes

Answer 23

1) synthesised by enzymes and packaged in vesicles
2) released then bind with postsynaptic receptors
3) deactivated: presynaptic reuptake or broken down by enzymes

Question 24

what are the two major neurotransmitters

Answer 24

glutamate and GABA work in opposition to each other to maintain the right balance between inhibition and excitation. both are found throughout the brain
- glutamate (glutamic acid) is the main excitatory NT, released by 50% of neurons. it is a precursor for GABA
- GABA (gamma-amino-butyric) is the main inhibitory NT, released by 40% of neurons. it is synthesised from glutamate

Question 25

what are a few examples of GABA agonists

Answer 25

• benzodiazepines (BZDs), barbiturates and alcohol

Question 26

what do these drugs do?

Answer 26

enhance the inhibitory effects of GABA and are:
- anxiolytic (reduces anxiety)
- sedative (reduce arousal/ increase relaxation)
- hypnotic (promotes sleep)

Question 27

BZDs

Answer 27

(diazepam, temazepam, lorazepam, ect) are commonly prescribed for anxiety and are also used as pre-anaesthetic relaxants in surgery

Question 28

barbiturates

Answer 28

are more potent GABA agonits- mainly used as general anaesthetics, to induce coma (eg after brain injury) and to treat epilepsy

Question 29

what are a couple examples of GABA antagonists?

Answer 29

flumazenil and picrotoxin

Question 30

flumazenil

Answer 30

blocks BZD site on GABA receptor; reverses BZD sedation (eg after medical operation); antidote for BZD overdose

Question 31

picrotoxin

Answer 31

stimulant (increases arousal); convulsant (induces epileptic seizures at high doses); antidote for barbiturate overdose

Question 32

glutamate agonists and antagonists

Answer 32

• glutamate agonists (eg ibotenic acid, found in poisonous mushrooms) are excitoxic- ie can kill nerve cells through over excitation
• ketamine= NMDA receptor antagonist; blocks excitatory effects of glutamate, used medically as sedative and anaesthetic
• NB glutamate has various receptor sub-types. the NMDA receptor (named after N-methyl-D-aspartate, an agonist for this receptor):
• is important in initiating the long-term synaptic changes necessary for learning and memory
• is also implicated in drug addiction, skits and epilepsy