Psychoactive drugs Flashcards
1
Q
What effects do psychoactive drugs cause?
A
They cause profound changes in perception, mood and behaviour
2
Q
What are some other terms used to describe psychoactive drugs?
A
Psychotomimetic
Psychotropic
Psychoactive
(these all cause mind alterations and hallucinations)
3
Q
Where do many hallucinogens occur from?
A
many are naturally occuring
4
Q
Name 2 naturally occuring hallucinogens?
A
Ayahuasca
Peyote
5
Q
Tell me about Ayahuasca (caapi)
obtained from?
Its active constiuent?
What recpetors does it have an effect on?
A
- Obtained from vines
- The active constituent is harmaline
- Gives an hallucinogenic effect
- The harmala alkaloid are psychoactive in humans
- interact with 5-HT signalling in the brain and is a acetylcholinesterase inhibitor
6
Q
Tell me about peyote
Why is it used?
What is it obtained from?
Whats the active constituent?
What receptors does it interact with?
A
- Peyote is used by native Americans in religious ceremonies
- This is a cactus.
- The active constituent is Mescaline
- This is a hallucinogenic alkaloid
- Binds to and activates the serotonin 5-HT2C receptors
- Also stimulates the dopamine receptors, but it’s unclear whether it possesses dopamine receptor agonist properties or initiates the release of dopamine).
7
Q
Compare the following hallucinogens with their dose, duration of action and therefore potency?
Psilocybin
Mesacaline
Lysergic acid diethylamide (LSD)
Which ones are natural and which ones are synthetic?
A
Potency (least to most)
Mesacaline > Psilocybin > LSD
8
Q
When was LSD first synthesised and why was it created?
A
Why was it synthesised? 10th century there were roughly 40,000 victims in France of ergotism and they suffered from gangrene. It was due to the rye from their rye bread.
9
Q
What is LSD a derivative of?
A
Naturally occuring ergot alkaloids
This is a fungus that grows on rye and less commonly wheat e.g., compound ergotamine is an examples of an ergot alkaloid
10
Q
What type of effects do ergot alkaloids cause?
In the past, due to the effects of the ergot’s what did they try and use them for?
A
Peripheral Vasocontriction
The derivatives were sought which could be used to control post-partum bleeding
11
Q
When was LSD first synthesised and who did this?
A
In 1943, Albert Hoffman, working for Sandoz, was the first to synthesise LSD and the first to ingest it
12
Q
What type of effects was recorded to have been experienced by LSD?
Explain a bit about each of these effects
A
- Somatic (mild autonomic changes of mydriasis- pupil dilation, tachycardia, tachypnoea- fast breathing, hyperthermia- high body temperature, hypertonia- too much muscle tone so the limbs are hard to move and hyperglycaemia- high glucose levels)
- Perceptual (5HT2A receptors plays a crucial role in changes in perception and thought)
- Psychological (stimulates serotonin-2A or 5HT2A receptor which is involved in mood and cognition)
- Synaesthesia is the mixing of the senses (LSD bring about this)
13
Q
What two hallucinogens is there a cross tolerance between?
What does this mean?
What does this suggest?
A
There is a cross tolerance between Mescaline and LSD
Cross-tolerance can be defined as a specific type of drug tolerance that is formed through continued use of another drug with similar effects
·This suggests that both psychotomimetic act at the same class of receptor site
14
Q
The structure of LSD, mescaline and 5-HT are all what type of structures?
A
These structures are similar as are all indoleamine like structures
Indolamines are a classification of monoamine neurotransmitter, along with catecholamines and ethylamine derivatives.
15
Q
Why does tolerance come about in the brain?
A
Brain undergoes neuroadaptation and downgrades the pathways that mediates the effects of the drug. The brain tries to rebalance the signalling network in the body. Hence how tolerance comes about
16
Q
What did early in vitro pharmacological studies show about LSD interactions?
A
Showed that LSD interacts with 5-HT receptors in the peripheral vasculature
17
Q
What does LSD act as in the periphery?
A
It acts as a 5-HT2 receptor antagonist
18
Q
What receptors mediate the effect of LSD on the vasculature smooth muscle?
A
5HT2 receptors
19
Q
What does LSD decrease the levels of?
A
LSD decreases the levels of 5-HT metabolites when adminstered to rate
20
Q
Explain neurotransmitter turnover and what this means
Explain this process involving LSD
A
Neurotransmitter turnover:
In the brain theres 5-HT synases that release 5-HT which acts on post synaptic neurons. Post-synaptic receptors of 5-HT and pre-synaptic autoreceptors of 5-HT which regulate signalling through this network. 5-HT can bind to the autoreceptors and inhibit further 5-HT release. A negative feedback mechanism.
With an antagonist like LSD, it can act at the pre- and post- synaptic 5-HT2 receptors. Which leads to more 5-HT release metabolites CSF plasma urine. However, LSD was found to decrease the level of metabolites hence LSD is a 5-HT2 receptor agonist.
In the brain LSD acts as a 5-HT receptor agonist/ partial agonist
21
Q
Where does LSD act in the brain?
What does it effect?
A
22
Q
How does LSD alter perception
Think about what neurons it has an effect on
A
- Look at reticular activating system as this deals with the input of the modality specificity input
- LSD decreases the firing rate of raphe neurones (5-HT1A receptor)
- In the raphe cell body has local projections (dendrites) which can release 5-HT (dendritic release)- usually released at nerve ending of axonal projection. The dendritic release can act on the 5-HT1A receptors. If LSD is applied, the firing rate of these neurons is decreased as it acts on the 5-HT1A receptors.
- Another proof that LSD is an agonist at 5-HT receptors
- Raphe neurons send extensive projection to the forebrain
23
Q
Even though LSD and Mescaline are shown to have cross tolerance which suggests they act on the same neurotransmitter pathways, how is the effect on perception different between these two hallucinogens?
A
…but investigation of further classes of hallucinogens showed that they did not all exert this effect (e.g., mescaline).
This firing effect was not done by mescaline; and other effects that LSD caused on 5-HT receptors.
24
Q
Tell me about the results and experiments done on rats when scientists lesion the raphe nucleus of rats
A
Lesioning the raphe nucleus in rats: they can still discriminate between saline and LSD. Suggests that Raphe nuclei is involved with LSD but not the hallucinogenic properties of the drug
The below technique is used to know when rats are hallucinating:
25
What effect does LSD have on the **locus coerueus neurones**?
LSD increases the activity in these neurons
26
What is the role of the Locus coeruleus neurones?
The locus coeruleus (LC), a small brainstem nucleus, is the primary source of the neuromodulator norepinephrine (NE) in the brain.
27
Tell me the effect that LSD has on the neurones in the **cortex**?
It increases the activity
28
The noradrenergic pathway in the CNS
Noradrenergic neurons project bilaterally (send signals to both sides of the brain) from the locus ceruleus along distinct pathways to many locations, including the cerebral cortex, limbic system, and the spinal cord, forming a neurotransmitter system
29
What is the receptor that LSD interacts with? Where is this receptor present?
**5HT2A receptors** (GPCR) are present in **temporal and prefrontal cortex**, and **thalamus** (remember the thalamus processes somatosensory inputs and receives afferents from the locus coeruleus)
LSD Increases firing rate of LC neurons
30
What is LSD described as being?
An extremely potent hallucinogen
31
What does LSDs structure and effect on 5-HT turnover in the brain suggest?
What does it inhibit?
Its structure and its effect on 5-HT turnover suggests it acts as a **potent agonist of brain 5-HT receptors**
Its distortion of sensory perception indicates an effect in pathways that process sensory information
Interest has focused on noradrenergic (LC) input to the thalamus and cortex
LSD has a direct **inhibitory** effect on the **Raphe nucleii**
32
Does LSD exert its effect through 5HT2A receptors?
33
A table showing the comparioson of human doses of selected hallucingoens with their potency using drug discrimination tests in LSD-trained rats
34
A plot of the inverse of the equilibrium dissociation constant against the inverse of the ED50
35
What receptors does LSD act on?
Where are these receptors expressed?
LSD acts on **5HT2A receptors**
These receptors are highly expressed in cortex: on **pyramidal neurones**
36
What layer of the pyramidal neurons in the cortex does LSD increase?
LSD increases activity of layer V pyramidal neurones in cortex
37
What have imaging studies of LSD and humans shown?
Imaging studies indicate increased cortical activity in humans
If LSD given to a rat and you electrophysiological recordings from the cortex show an increase in epsc
Administration of LSD causes widespread uncoordinated activity in the cortical networks. Entropic activity so becomes disordered.
38
What is the **Default mode network**?
**Default mode network-** network of cortical circuits that becomes more active when an individual is less connected to their surroundings
39
Summary of potential sites of action for LSD
40
Give an example of another psychomimetic drug
Tell me about its class
What effects does it cause when taken
**Phencyclidine (PCP)**- angel dust
* is a ‘dissociative’ anaesthetic
* same class as Ketamine (class B)
* causes a catatonic-like state without muscle relaxation
* withdrawn from clinical use in 1965 due to ‘emergence phenomenon’- vivid hallucinogenic result
41
Tell me some obervations of PCP in a controlled study done in 1959 by Luby et al., when administered a sub-anaesthetic dose in clinic
* Altered body image "my arms and legs feel distant”
* Feeling of isolation
* Cognitive disorganization
* Drowsiness and apathy
* Negativism and/or hostility
* Euphoria and inebriation
* Hypnagogic (dreamlike) states
Exacerbated symptoms of psychotic patients
PCP intoxication associated with drug-induced hallucinations
42
What has radioligand binding studies shown about PCP ?
It interacts with 2 main classes of receptor...
1. **Sigma opiate receptor** (GPCR)- modulates NAdr release
2. PCP is a non-competitive antagonist of the NMDA (**glutamate receptor**)
43
Tell me about the NMDA channel
NMDA is a ligand gates ion channel. Gets its name from the agonist that selectively interacts with it. And it binds glutamate and is excitatory. PCP blocks the channel.
44
What is the VTA region of the brain?
The ventral tegmental area, or VTA, is in the midbrain, situated adjacent to the substantia nigra.
Although it contains several different types of neurons, it is primarily characterized by its **dopaminergic neurons**, which project from the VTA throughout the brain
45
When PCP is given to a rat, what changes are seen in VTA activity?
If PCP is given to a rat, then there is an **increase in VTA activity seen**
46
Cortical structures give an inhibitory response to sub-cortical structures, tell me about the NT involved...
Pathways to the cortex use glutamate as the NT.
Glutamate is released from the cortex and (binds to a neuron?) which releases GABA (the inhibitory NT)- look up pathway
47
What hallucinogenic drugs have been used in animal studies for schzophrenia?
LSD and PCP
48
is LSD toxic or addictive?
no
49
Name some drugs which act on catecholamine transmission
**Cocaine**
**Amphetamine**
**MDMA**
50
Tell me **Cocaines** effect on catecholamine transmission
* act at catecholamine synapses
* after release they are taken back up via high affinity uptake transporters where the NT can be packaged into vesicles for release again
* cocaine blocks the high affinity transporters for the catecholamines
51
Structure of cocaine
52
What was **amphetamine** first synthesised from?
ephedrine
53
What type of compound is amphetamine and what does it mean on the physiolgical effects its causes?
amphetamine is an **‘indirect sympathomimetic’**- it stimulates the release of catecholamines
sympathomimetic amine- if administered to an individual it mimics the effects of the sympathetic NS e.g., high BP
54
Tell me some of the actions amphetamine can cause if taken
* appetite suppressant
* causes euphoria
* raises blood pressure
* uses for: weight control, narcolepsy, and attention deficit disorder
* can also cause psychosis
55
Tell me the effects of amphetamine on catecholamine NT?
elevation of catecholamine NT, rather than blocking high uptake transporter (which cocaine does), it induces a phenomenon called reduced transport.
Dopamine is released (the catecholamine), so elevates the levels of catecholamines at the synapse.
It is calcium independent unlike typical NT release
56
Amphetamine structure
57
Tell me the effects of **MDMA (3,4-methylenedioxy-N-methyamphetamine), ‘ecstasy’**
* Enhanced sense of well-being
* Increased extroversion
* Emotional warmth
* Empathy towards others
* Enhanced sensory perception
58
Tell me the health effects of taking MDMA
Health effects: OD, high blood pressure (hypertension), faintness, panic attacks, jaw clenching, lack of appetite, depersonalisation, nausea etc. and in severe cases a loss of consciousness, seizures, and hyperthermia
59
Structure of MDMA
60
Tell me some pharmacology to do with MDMA...
What is it structurally related to?
natural or synthetic?
Effect?
Inhibits?
* Structurally related to amphetamines
* Main difference is the presence of the methylenedioxy group (-O-CH2-O-) attached to the aromatic ring on MDMA. This attachment also makes it resemble mescaline
* Synthetic substance
* Indirect serotonergic agonist, increasing the amount of serotonin released into the synapse
* Enhances the release of dopamine and noradrenaline
* Inhibit monoamine uptake
* Delay metabolism by inhibiting monoamine oxidase
61
Tell me about MDMAs toxicity
Toxicity: damage to Raphe neurons, can induce long term toxicity which can be severe
62
What is **Mephedrone**?
**Mephedrone-** novel psychoactive substances. Law to regulate distribution and use in 2016
Mephedrone (4-methylmethcathinone) is a stimulant drug, which means it speeds up the messages traveling between the brain and body. 1. Mephedrone is classed among New Psychoactive Substances (NPS), a range of drugs that have been designed to produce effects similar to those of established illicit drugs.
63
**So far...**
* Hallucinogens- and how this may inform understanding of psychoses
now. ...
* Cocaine- and how this may inform understanding of addictive behaviours
64
What is the definition of addiction?
" Persistent disorder of brain function in which compulsive drug use occurs despite serious negative consequences for the afflicted individual"
65
With addiction, an individual can suffer what consequences,
**physical and psychological** (still biological) **dependence** can occur
**Physical**: autonomic NS hyperactivity
**Phycological:** Cocaine can induce euphoria, withdraw associated with alcohol abuse
66
What does tolerance build up due to?
Tolerance builds up due to the neurones maladapting to the drug which means a high dosage is required for the same effect
67
What are the four features of addiction?
**Compulsion to take the drug**
**"withdrawl" syndrome**
**Tolerance**
**Withdrawal relief**
68
Tell me about "withdrawl" syndrome?
**"withdrawal" syndrome** (opposite effects to those experienced in presence of drug)
i.e., alcohol withdraw which can be life threatening.
Adaptation is **down regulation of inhibitory signalling** in the brain.
Interacts with **GABAA** receptors.
Alcohol acts on these receptors. Continued alcohol use leads to the down regulation of those receptors.
When drinking excessive amounts, the inhibitory signalling is compromised.
Issue is seizures are caused by increased excitatory signalling in the brain due to the inhibitory ones (GABAA) being compromised
69
Tell me about **Tolerance**
**Tolerance** (decreased response to repeated administration)- as brain adapts to presence of drug. Homeostatic mechanism which tries to rebalance signalling
70
Tell me about **withdrawl relief**
**Withdrawal relief** i.e., if alcohol abuser stops drinking, it can lead to hyperactivity, anxiety and in extreme cases seizure.
Then when drink again these symptoms are relieved.
71
Where do psychotomimtic drugs with abuse potential act?
They have common actions on the **limbic system** of the brain
72
What structures are meant as the limbic system?
Those in red are the key areas of the limbic system and the ones in black can sometimes be incorporated
73
What neurons does the VTA harbour
What other areas of the brain does it have an effect on?
The Ventral tegmental area harbours **dopaminergic neurons**
There are projects from the VTA which go to the **nucleus accumbens** which is therefore then implicated in addiction also
74
The selection of behaviours approproate for survival is achieved how?
selection of behaviours appropriate for survival is achieved by **‘reward’ and ‘punishment’ systems**
reward will promote pleasure systems e.g., eating
punishment is avoiding things that are toxic to you
75
How are the reward and punishment systems implicated in addiction?
these systems are fundamental to motivation and avoidance
inappropriate activation of these systems underlies addictive behaviour
76
A psychological framework for reward and addiction is the 'reward' circuit. Can you explain this circuit and how drugs can affect the flow?
* positive feedback loop
* drugs (blue arrow) act on reinforcing system to perpetuate behaviour that is long term detrimental to an individual. This is a direct interaction
77
What pathways are involved in 'reward and motivation'?
explain using an experimental example
Evidence provided from animal behavioural experiments conducted by James Old (1954)
Rats implanted with stimulating electrodes in the reticular formation
when rat enters shaded area, a stimulus is delivered to the electrode
Old observed that in some experiments the animals repeatedly returned to the shaded area
in these animals the electrodes were placed in the medial forebrain bundle
**Summary: experimental evidence of a reward pathways**
* Olds and Milner 1954
* implanted electrodes
* delivered stimulus every time rat entered part of cage
* rat kept ‘coming back for more’
* = Rewarding stimulus
* The behaviour is called **REINFORCEMENT**
78
Tell me about the **operant chamber** experiment performed on rate
What did it tell us about the pathways involved in addiction?
allows a rat to self-deliver either a stimulus or drug by pressing a lever
these studies showed that rats would self-administer a stimulus if the electrode was placed in the medial forebrain bundle i.e., reinforcement
this contains a mixture of axons, but the dopamine containing neurones seem to be crucial for reinforcement, evidence?
noradrenergic, serotinergic and dopaminergic present so how do you know which one?... (**dopaminergic system is acted on**)
* spiroperidol (DA antagonist blocks reinforcement)
* 6-OH-DA lesions block reinforcement
rats will also self-administer cocaine or amphetamine
the rats would do this until exhausted or experiences toxic effects of drug administration
79
What pathways are in the medial forebrain bundle and where do they originate?
**Dopamine, noradrenaline, and 5-HT** (in the medial forebrain bundle)
these pathways originate in the **midbrain/ medulla**
80
Where do the Dopamine, noradrenaline, and 5-HT project?
When are they implicated?
**project anteriorly** to innervate areas throughout the brain
are implicated in **mood and behaviour**
81
Therefore, based on the implications on the Dopamine, noradrenaline, and 5-HT pathways, what does the 'reinforcement system' involve?
Therefore the ‘reinforcing system’ seems to involve **dopamine axons** in the medial forebrain bundle: **these axons project to the nucleus accumbens**
82
What is the medial forebrain bundle?
The medial forebrain bundle (MFB), is a neural pathway containing fibers from the basal olfactory regions, the periamygdaloid region and the septal nuclei, as well as fibers from brainstem regions, including the ventral tegmental area and nigrostriatal pathway.
83
What pathway does the MFB have?
Dopamine pathway
84
Do you think PCP (Phencyclidine) would be addictive?
Yes, as has an impact on the brain’s chemical composition
85
What does cocaine bind to?
COCAINE binds with **high affinity** to monoamine, including **dopamine transporters (DAT- presynaptic transporter)**
86
Is there evidence for the involvement of specific transporters in the reinforcing properties of cocaine?
DAT transporter is blocked by cocaine which increases the levels of dopamine in the synapse (as it cannot be removed via the transporters as they are blocked) and therefore leads to increased locomotor activity
87
Tell me about the role of the DAT using the experiment with mice **"knock-outs"** of DAT
These are germ-line KO. So hard to interpret in adult mouse
Mice with DA transporter knockout have **chronically elevated synaptic dopamine**
cocaine administered to these animals produces **no change in base-line DA** (also no increase in locomotor activity)
nonetheless these animals will self-administer cocaine... therefore there may be another ‘reinforcing stimulus’ other than DA
this is a controversial topic
88
Tell me about the role of the DAT with cocaine in the mutant **'knock-in"** in mice
Cocaine in the mutant DAT knock-in mice **did not:**
* elevate extracellular dopamine
or
* increase locomotion
i. e., the knock-in mice are apparently insensitive to the neuropharmacological actions of cocaine as predicted
what happens to rewarding effects of cocaine?
89
What tests can be done to assess the reinforcing properties of cocaine?
90
**so far...**
**So far…**
* **Hallucinogens- and how this may inform understanding of psychoses**
* **Cocaine- is highly addictive. In animal models this is manifest by the reinforcing actions of cocaine. Reinforcement (reward) is dependent on an increase in dopamine signalling in the VTA/ nucleus accumbens pathway.**
* **now...**
* **Alcohol and alcohol use disorder**
91
Are there common mechanisms for reinforcement/ addiction for other addictive drugs?
**Pathways**
92
What are the different pathways involved in addiction?
Evidence for common involvement of **limbic system**
Evidence for common involvement of dopamine signalling especially the **VTA projection to the nucleus accumbens**
**NEUROTRANSMITTERS**
Evidence for involvement of **dopamine** in the action of cocaine (direct)
93
Dopamine appears to be a common factor in drugs which have abuse potential,
Tell me about this NT in regards to ethanol and opiate addiction
**Ethanol increases DA release** in the **nucleus accumbens**
DA receptor antagonists block ethanol self-administration in animal models
**Opiates** (e.g., morphine, heroine) also **increase dopaminergic transmission** in the limbic system
94
Where do addictive drugs increase the release of dopamine?
What is this common for?
Addictive drugs increase the release of dopamine in the nucleus accumbens
This seems to be common for all addictive drugs: nicotine, ethanol, opiates (heroin), cocaine, amphetamine
Therefore an interaction of addictive drugs with the reward pathway
95
What NT has an increased release with addictive drugs?
dopamine
96
Evidence for altered dopamine signalling in addiction
97
A common pathway for addiction?
Common adaptations in the limbic circuitry following chronic drug exposure
98
What are the long-term changes associated with addiction?
animal studies suggest changes in gene expression:
increased DA --\> increased cAMP --\> CREB --\> immediate early gene expression
this may alter levels of receptor expression e.g., changes in dopamine receptors (similar mechanism for opiates)
99
Give an example of an immediate early gene?
NOTE: Immediate early genes (IEGs) are genes which are activated transiently and rapidly in response to a wide variety of cellular stimuli.
c-fos
C-fos is a proto-oncogene that is expressed within some neurons following depolarization.
100
Why are some individuals more susceptible than others to addiction?
**ALDH2**- aldehyde dehydrogenase 2, a protein coding gene, disease associated with this includes alcohol sensitivity, polymorphisms are assoicated with a risk of drug addiction (this enzyme converts alcohol --\> aldehyde --\> acetic acid)
**D2-** dopamine receptor 2, commonly been linked to alcohol addiction, also associated with other addictive behaviours
**OPRM1-** opioid recepotr mu 1, polymorphisms have been associated with alcohol use an dependence, and opioid addiction. This receptor is a GPCR, it inhibits adenylate cyclase and down regulates cAMP, inhibits the release of GABA
[see "Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction." 2006. Kreek et al.]
101
Tell me simply the main interactions of addictive drugs with the reward pathway
102
A more complex view...
103
But addiction is about more than just reward...
Explain the progression of the disease addiction
104
Studying alcohol dependence in a rat ‘model’
* msP alcohol preferring rats
* looked at a peptide called **corticotrophin releasing factors (CRF)**. Which is important for the physical response to stress. It’s a hypothalamic hormone which acts on the anterior pituitary which leads to the released of ACTH and then leads to an increased in cortisol levels.
* CRF --\> ANT PIT --\> ACTH --\> increase cortisol
* CRF is a neuro peptide and involved in stress responses. This is found in the amygdala
* study looked at levels of CRF in amygdala, and used In situ hybridisation, expression was shown to be higher in those which are alcohol dependent, very high levels of CRF in rats which were alcohol preferring. Shown higher levels of CRF in amygdala in those rats which chose or depended on alcohol
105
What are the two families in the dopamine receptors?
D1 and D2
106
What dopamine receptor does 18F- fluoromethylspiroperidol label in PET imaging studies on humans?
D2
107
Tell me about the changes in the levels of cAMP and adenylate cyclase as morphone is given and taken away...
As morphine is given: adenylate cyclase (a/c) increases over time as simultaneously the cAMP decreases. When morphine is withdrawn the enzyme a/c is overexpressed which leads to the over expression of cAMP
108
What circuit is reinforcement related to?
The amygdala circuit
109
Using the following evidence, explain the evidence for a compromised reward system in addicts
110
CRF antagonism suppresses stress-induced relapse-like behaviour in msP rats
111
**summary**
* **Psychotomimetic drugs exert their actions through distinct molecular effectors**
* **Subclasses of psychotomimetic drugs with addictive potential share the capability to cause neuroadaptive responses in the limbic circuitry of the brain**
* **Currently the evidence suggests that altered signalling in the 'reward' circuitry of the brain underpins the phenomena of drug addiction, especially in the dopaminergic pathway from the VTA to the nucleus accumbens**
* **(But it’s not just about dopamine and reward)**
112
**LO**
* **Provide an overview of neurotransmitter systems in the brain and their putative functional roles**
* **Use examples of psychotomimetic and psychotropic drugs to discuss the biochemical basis of mood and behaviour**
* **Describe the various techniques used to investigate CNS disorders and to assess their limitations**
* **Assess the hypotheses put forward to explain the neurochemical and neurophysiological bases for the following: schizophrenia, affective disorders, drug addiction and autism spectrum disorders.**
* **Describe the treatments used in these disorders, their efficacy, and side-effects**
* **Highlight recent advances in drug therapy that have arisen from a better understanding of the pharmacology of the brain**
