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Flashcards in The Biological Basis of Psychological Abnormality Deck (41)
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1
Q

What are synapses?

A
  • Connection between two neurons
  • One cell changes its voltage and passes onto the next cell, happens at the synapse
  • The connections and means of communication between nerve cells.
  • Each neuron can have thousands of different synapses (connections) with other neurons.
    Communication through axons
2
Q

How do synapses communicate?

A
  • Synaptic communication mediated by the physical movement of chemicals (neurotransmitters). Movement of chemical causes changes in voltage
    Cleft = 0.00002 mm across. Happens on a tiny scale, really small gap
3
Q

What are the 6 stages of synaptic transmission?

A
  1. AP of presynaptic neuron, information (action potential, change in voltage) is coming down from the axon of the presynaptic neuron. Packages of neurotransmitters in the presynaptic neuron
  2. Transmitter release into synaptic cleft, after a large voltage change
  3. Transmitter binds to receptor
  4. Transmitter dissociates from receptor, end of chemical reaction
  5. Transmitter reuptake by transporters
  6. Transmitter recycling, ready for the next action potential
4
Q

What are the synaptic components?

A

· Presynaptic receptors, e.g. regulate transmitter release
· Postsynaptic receptors: ionotropic and metabotropic receptors, the two types of receptors
· Transporters, i.e. transmitter reuptake sites
· Enzymes that metabolize transmitters
· Second messenger systems
· All can affect the input-output relationship of neurons

5
Q

What are receptors?

A

· Work on a ‘lock-and-key’ principle. One neurotransmitter fits a certain kind of receptor.
Each neurotransmitter has its own receptor to bind to

6
Q

Examples of neurotransmitters?

A

· Monoamines – acetylcholine, serotonin (5-HT)
· Amino acids – GABA, glutamate, and others
· Catecholamines – still monoamines, dopamine, adrenalin/epinephrine, noradrenalin/norepinephrine
· Neuropeptides – Enkephalin – Endorphins – Substance P – Others (50+)
· Also neuromodulators: Mostly peptides
The main groups of neurotransmitters

7
Q

What are multiple receptor subtypes?

A

· Multiple receptor subtypes… different kinds of receptors
· Ionotropic (receptors) ion channels – voltage change by ions released in the gaps between neurons
· Metabotropic or 2nd messenger gated ion channels, more indirect, binds with the receptor and opens another ion channel

8
Q

What changes can happen at synapses?

A

· Synapses are capable of changing
· Underlie learning, memory formation and many disorders - Hebbian plasticity, long-term potentiation (LTP), long-term depression (LTD), etc.
· Change in receptor numbers, change in amount of transmitter release, etc.
· Change in structure of synapse
Change in efficacy of second messenger systems

9
Q

How do genes play a role in brain function?

A

· Play a large role in brain function.
· Code for receptors, enzymes, NTs, etc.
· Role can vary over time. Some influences may be apparent from birth, others may only manifest themselves later.
Environmental factors can determine whether a gene becomes “switched on” or not.

10
Q

How is induction used on animal models?

A

· Inducing mental health problems
· Genetic studies, e.g. gene “knockouts”
· Pharmacological studies – give them drugs and see how it affects their behaviour
Lesion studies. – removing parts of the brain and see how it changes behaviour

11
Q

How do you measure animal models?

A

· Behavioural monitoring
· Neural recordings – how single neuron firing patterns change
· Anatomical techniques, e.g. cell counts
Neurochemistry.

12
Q

How are human studies used in investigating brain function?

A

· Genetics – through twin studies
· Post-mortem studies – after someone has died, looked at the organisation of neurons in their brain
· Structural MRI (large scale abnormalities)
· Functional MRI (brain function)
· PET (changes in NT systems)
Problem: Most people with mental disorders will be taking medications that alter brain function – hard to see if differences are due to medication or mental health issues

13
Q

What are MZ and DZ twins?

A
· MZ stand for: monozygotic
· Means: identical
· Share 100% of genes
· DZ stands for: dizygotic
· Means: non-identical
Share 50% of genes
14
Q

· For a diagnosis of a major depression:

A

At least 5 of the following symptoms and at least one of the symptoms should be either (1) depressed mood or (2) loss of interest or pleasure.

15
Q

What are the common symptoms of depression?

A

· These symptoms must be present during the same 2 week period
· Depressed mood, nearly every day during most of the day
· Marked diminished interest or pleasure in almost all activities
· Significant weight loss (when not dieting), weight gain, or a change in appetite
· Insomnia or hypersomnia (excess sleep)
· Psychomotor agitation or psychomotor retardation – lack of movements
· Fatigue or loss of energy
· Feelings of worthlessness or inappropriate guilt
· Impaired ability to concentrate or indecisiveness
· Recurrent thoughts of death, recurrent suicidal
Depression is common: 1 in 8-10

16
Q

What are the subtypes of depression?

A

· Unipolar depression: Depression that alternates with “normal” emotional states. (10% of men, 20% of women suffer.)
Bipolar depression: Fluctuation between depressive periods and episodes of euphoric, positive mood/mania. (Equal numbers of men and women – less common than unipolar.)

17
Q

What do twin studies show about depression?

A

· Chance that if one twin has it, what’s the chance the other twin will have it
· Unipolar concordance: MZ = 40%, DZ = 15%
· Bipolar concordance: MZ = 70%, DZ = 15%
· Adoption studies show higher rates of depression in biological than adoptive parents.
Linkage studies have failed to identify a single gene for depression. Many genes contribute to a susceptibility, and environmental factors can trigger depression.

18
Q

What are Monoamine Oxidase Inhibitors?

A

· 1950s: Iproniazid (first MAOI) – first used
· 1960s: Reserpine (catecholamine depletion) - has an effect on catecholamines
· Normally serotonin is broken down by MAOI – stop the enzyme from breaking them down
· MAOI have side effects – control muscle, digestion (bad)
Led to Catecholamine theory of Depression (Schildkraut, 1965)

19
Q

What are Tricyclic Antidepressants?

A

· 1950s: Tofranil
· Tricyclic Antidepressants
Similar effect to MAOIs (catecholamine agonist) but different action.

20
Q

What are Catecholamines?

A

· Catecholamines: NA and Dopamine
· Reduced levels in the brains/bodies of depressed patients? No.
· Ignores another important NT – 5-HT (serotonin)
Therefore – more broadly – Monoamine theory of depression

21
Q

What are Selective Serotonin Reuptake Inhibitors?

A

· SSRIs are most modern drug treatment for depression: Prozac, sertraline, citalopram
· Works by stopping the reuptake of serotonin
Little effect on NA

22
Q

What are the main anti-depressants and how do they work?

A

· MAOIs – Affect mononamines. Highly effective. Nasty side effects. Only used in most resistant cases.
· TADs – Affect monoamines. Also highly effective. Some side effects. Suicide risk.
· SSRIs – Affect 5-HT (not NA or DA). Safe, and relatively few side effects.
· So, NA/DA or 5-HT important? Both?
· Low 5-HT disrupts functioning of NA/DA system = Depression
Correction of 5-HT system = correction of NA/DA system = symptom alleviation

23
Q

How is depression imaged?

A

· Increased activity in neural systems supporting emotion processing, e.g. amygdala and medial prefrontal cortex
Decreased activity in neural systems supporting regulation of emotion, e.g. dorsolateral prefrontal cortex

24
Q

How is bipolar treated?

A

· Standard antidepressants have little effect.
· 1940s: Discovery of Lithium’s effect in Bipolar. – an element
· Without Lithium – cycle every 14 months on average, with Lithium – every nine years. Extends your cycle rather than stopping it
Detailed mechanism unknown – neurotrophic and neurotransmitter systems affected.

25
Q

What is the definition of schizophrenia?

A

DSM-V definition: Two or more of the following for at least a one-month (or longer) period of time, and at least one of them must be 1, 2, or 3:

26
Q

What are the common symptoms of schziophrenia?

A

· Delusions – false beliefs
· Hallucinations
· Disorganized speech – can’t talk clearly
· Grossly disorganized or catatonic behaviour – not moving your limbs correctly, or not moving at all
· Negative symptoms, such as diminished emotional expression
· Some signs of the disorder must last for a continuous period of at least 6 months. This six-month period must include at least one month of symptoms (or less if treated). At least one of the symptoms needs to be a positive symptom (i.e., delusions, hallucinations, disorganized speech).
Not split personality of multiple personality

27
Q

What are positive symptoms of schziophrenia

A
· Behaviour you didn’t have 
· Hallucinations (auditory) 
· Delusions of grandeur, persecution etc. 
· Disordered thought processes 
Bizarre behaviours
28
Q

What are negative symptoms of schizophrenia

A
· Behaviour that you used to have 
· Social withdrawal 
· Flat affect (blunted emotional response) 
· Anhedonia Reduced motivation 
· Poor focus on tasks 
Catatonia
29
Q

Do genes play a role in schizophrenia?

A

Family studies
· The closer the biological relatedness, the greater chance that the relative will also be schizophrenic (Gottesman 1991)
A number of genes implicated in schizophrenia:
· Neuregluin 1: participates in glutamate, GABA and ACh receptor regulation
· COMT: catecholamines
G72: glutamatergic activity

30
Q

Twin studies and schzioprenia

A

· Concordance: MZ = 50%, DZ = 17%
· The symptomatic twin (identical twins, the one who has schizophrenia) frequently weighs less at birth (differential development in the womb)
· More physiological distress (affected twin has experienced different environmental factors)
The twins act differently, receiving different parental responses (e.g. affected twin is often more sensitive and tearful)

31
Q

Brain abnormalities in schzioprehnia?

A

· Ventricular abnormalities – e.g. larger ventricles (larger gaps in the centre of the brain filled with fluid)
· Enlargement not related to length of illness or duration of hospitalization
· Grey Matter loss: Thompson et al. (2001) Mapping adolescent brain change reveals dynamic wave of accelerated gray matter loss in very early-onset schizophrenia. Schizophrenia manifests in adolescence. Early onset, small amount of grey matter then spreads to other areas of the brain as time goes on
Cellular disarray of the hippocampus in chronic schizophrenia. The most impaired individuals show the greatest disorganization (Conrad 1991)

32
Q

Functional abnormalities in schizophrenia

A

· The hypofrontality hypothesis: Less activity in frontal lobes in schizophrenics.
· Decreased activity in right middle frontal gyrus (BA 9) during a context processing task in patients with schizophrenia.
Holmes et al. (2005) Schizophrenia research 76: 199-206

33
Q

The dopamine hypothesis

A

· Large doses of amphetamine (a strong DA agonist) can cause psychosis, with similar symptoms to schizophrenia.
· Treatment of Parkinson’s disease (associated with reduced dopamine) with L-dopa (a precursor to dopamine) may induce psychotic symptoms.
· Dopamine receptor antagonists such as chlorpromazine are effective anti-schizophrenic drugs. E.g. these “neuroleptic” drugs bind to dopamine D2 receptors, some of which are associated with projections from the mesolimbic dopamine system.
Some studies have found an increase in dopamine receptors (especially D2) in schizophrenic persons, including those no longer taking neuroleptic drugs.

34
Q

Is the dopamine hypothesis too simplistic?

A

· Some patients show no improvement when treated with DA antagonists.
· Atypical neuroleptics (i.e. clozapine) affect many receptor types, e.g. serotonin as well as D2 receptors. More effective at relieving negative symptoms than typical neuroleptics.
· Clozapine can also increase dopamine activity in the frontal cortex.
Studies on D2 receptor levels in schizophrenics are inconsistent.

35
Q

Glutamate hypothesis

A

· NMDA receptor - postsynaptic glutamate receptor.
· NMDA receptor antagonists, e.g. phencyclidine, ketamine, produce phenomena resembling both -ve and +ve symptoms.
· Glutamate receptor agonist LY2140023 reported to
· improve +ve and -ve symptoms in schizophrenia Patil et al. (2007)
Probably not just one NT system involved.

36
Q

Synthesis of schizophrenia

A

· Genetic influences lead to “brain abnormalities”
· Developmental influences/birth complications may exaggerate such abnormalities
· The emergence of schizophrenia is dependent on whether the “damaged” brain is exposed to environmental stressors
Rosso et al. 2000

37
Q

What are the 7 main groups of anxiety?

A
· DSM-V has seven major groups of anxiety disorders: 
· Panic Disorder
· Social Phobia/Anxiety
· Agorophobia
· Specifc phobias
· Generalised Anxiety Disorder 
· Separation anxiety disorder 
Selective mutism
38
Q

Is anxiety good?

A

· Fear is an important emotion as it protects us from dangerous situations.
· Anxiety is less focussed on an immediate external threat – more anticipatory.
· Promotes caution, and apprehension, while curbing excessive or careless behaviour.
Becomes a clinical problem when it occurs for no particular reason, or is excessively intense or long- lasting.

39
Q

What is panic disorder?

A

· Overwhelming anxiety, feeling of being about to die, general SNS activation – fight or flight response
· Causes:
· Psychological factors (general stress, life
· transitions etc.)
· Stimulants (caffeine, SSRIs)
· Metabolic hypothesis of panic – triggers for panic are lactate (acid formed in the muscles), carbon dioxide (not getting enough air)
Amygdala abnormalities

40
Q

Panic and the amygdala

A

· Amygdala is a crucially important link in the brain’s fear system. – appeared in our early evolution
· Ziemann et al (2009): Amygdala is a chemosensor that reacts to changes in the body’s pH produced by high levels of CO2
· Inhaling CO2 produces fear responses in mice, same responses produced
by reducing pH of the amygdala with microinjections.
Hayano et al. (2009): Volume of amygdala is related to anxiety in PD

41
Q

How is anxiety treated?

A

· Benzodiazepines – potent class of anxiolytics.
· Includes diazepam (Valium) – one of the most prescribed drugs ever.
· They act selectively on GABA receptors, which mediate inhibitory synaptic transmission, potentiating the effect of GABA – i.e. increasing inhibitory effects.
However, anti-depressants such as SSRIs can also be effective.