The Biological Bases of Anxiety, Depression and Schizophrenia
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- Created by: Yasmetron
- Created on: 07-03-23 16:45
define synapses
the connections and means of communications between nerve cells. Each neuron can have thousands of different synapses with other neurons. Synaptic communication mediated by the physical movement of chemicals (neurotransmitters).
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what happens at synaptic transmission?
An AP reaches a pre-synaptic terminal.
NT is released from vesicles inside the pre-synaptic terminal into the synaptic cleft. NT diffuses across the gap and binds to receptors on the post-synaptic terminal. The NT binding depolarises the post-synaptic te
NT is released from vesicles inside the pre-synaptic terminal into the synaptic cleft. NT diffuses across the gap and binds to receptors on the post-synaptic terminal. The NT binding depolarises the post-synaptic te
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Why are receptors special?
Receptors work on a lock and key principle. One neurotransmitter fits a certain kind of receptors.
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Give some examples of neurotransmitters
• Amines – acetylcholine
• Monoamines
• Indoleamines – serotonin/5-HT
• Catecholamines – dopamine, adrenaline, noradrenaline
• Amino acids – glutamate, GABA
• Neuropeptides – enkephalin, endorphins, substance P
• Monoamines
• Indoleamines – serotonin/5-HT
• Catecholamines – dopamine, adrenaline, noradrenaline
• Amino acids – glutamate, GABA
• Neuropeptides – enkephalin, endorphins, substance P
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define neuromodulators
a substance that modulates the effectiveness of a neurotransmitter by influencing its release or receptor response to it.
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what happens at an inotropic ion channel?
1. NT binds
2. channel opens
3. ions flow across membrane
2. channel opens
3. ions flow across membrane
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what happens at a metabotropic or 2nd messenger gated ion channel?
1. NT binds
2. G-protein is activated
3. G-protien subunits or intracellular messenger modulate ion channels
4. ion channel opens
5. ions flow across membrane
2. G-protein is activated
3. G-protien subunits or intracellular messenger modulate ion channels
4. ion channel opens
5. ions flow across membrane
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define hebbian plasticity
a neuropsychology theory claiming that an increase in synaptic efficacy arises from a presynaptic cell's repeated and persistent stimulation of a postsynaptic cell.
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what is epigenetic modification?
environment factors can determine whether a gene becomes switched on or not.
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what is a gene knockout?
you deactivated a gene to see how that impacts their functions which helps you to find out what that gene is used for.
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What are the symptoms of depression and how many must they have to be diagnosed?
Depressed mood (5)
Marked diminished interest in almost all activities.
weight loss, weight gain, change in appetite.
Insomnia (lack of sleep) or hypersomnia
Psychomotor agitation/retardation
Fatigue or loss of energy
Feelings of worthlessness or i
Marked diminished interest in almost all activities.
weight loss, weight gain, change in appetite.
Insomnia (lack of sleep) or hypersomnia
Psychomotor agitation/retardation
Fatigue or loss of energy
Feelings of worthlessness or i
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define unipolar depression
depression that alternates with normal emotional states (twice as many women suffer from depression as men). MZ = 40%, DZ = 20%
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define bipolar depression
fluctuation between depressive periods and episodes of euphoric, positive mood/mania (equal numbers of men and women – less common than unipolar). MZ = 33-70% DZ = 0-13%
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what was the development of antidepressants?
Monoamine Oxidase Inhibitors – 1950s Iproniazid
Tricyclic Antidepressants – 1950s Tofranil
Catecholamines – NA, Adrenaline and Dopamine. Reduced levels in the brain/bodies of depressed patients? No
Selective Serotonin Reuptake Inhibitors – SSRIs are the m
Tricyclic Antidepressants – 1950s Tofranil
Catecholamines – NA, Adrenaline and Dopamine. Reduced levels in the brain/bodies of depressed patients? No
Selective Serotonin Reuptake Inhibitors – SSRIs are the m
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What is affected in depression neurally?
• 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.
• Decreased activity in neural systems supporting regulation of emotion e.g., dorsolateral prefrontal cortex.
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What is the treatment for bipolar disorder?
• 1940s: discovery of Lithium’s effect in Bipolar
• Without lithium – cycle every 14 months on average, with Lithium – every nine years.
• Detailed mechanism unknown – neurotropic and neurotransmitter systems affected.
• Without lithium – cycle every 14 months on average, with Lithium – every nine years.
• Detailed mechanism unknown – neurotropic and neurotransmitter systems affected.
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What are the symptoms for schizophrenia?
• Delusions
• Hallucinations
• Disorganised speech
• Grossly disorganised or catatonic behaviour
• Negative symptoms, such as diminished emotional expression
• Hallucinations
• Disorganised speech
• Grossly disorganised or catatonic behaviour
• Negative symptoms, such as diminished emotional expression
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What are the positive symptoms of schizophrenia?
- hallucinations
- delusions of grandeur persecution
-disordered thought processes
-bizarre behaviours
- delusions of grandeur persecution
-disordered thought processes
-bizarre behaviours
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What are the negative symptoms of schizophrenia?
- social withdrawal
- flat affect (blunted emotional response)
- anhedonia
- reduced motivation
-poor focus on tasks
- catatonia
- flat affect (blunted emotional response)
- anhedonia
- reduced motivation
-poor focus on tasks
- catatonia
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What genes are impacted in schizophrenia?
Neuregulin 1: participates in glutamate GABA and Ach receptor regulation.
COMT: catecholamines
G72: glutamatergic activity
COMT: catecholamines
G72: glutamatergic activity
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What is the concordance rates?
MZ = 30-50%
DZ = 3-18%
DZ = 3-18%
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What are brain abnormalities?
• Ventricular abnormalities - Enlargement not related to length of illness or duration of hospitalisation
• Grey matter loss
• Cellular disarray of the hippocampus in chronic schizophrenia
• Grey matter loss
• Cellular disarray of the hippocampus in chronic schizophrenia
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What is the hypofrontality hypothesis?
Decreased activity in right middle frontal gyrus (BA9) during a context processing task in patients with schizophrenia.
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What is the dopamine hypothesis?
schizophrenia is caused by an excess of dopamine in the brain, due either to an overproduction of dopamine or a deficiency of the enzyme needed to convert dopamine to norepinephrine
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What is the glutamate hypothesis?
ecreased activity of the excitatory neurotransmitter glutamate is responsible for the clinical expression of schizophrenia.
glutamate is being blocked by the drugs which causes schizophrenic like symptoms.
glutamate is being blocked by the drugs which causes schizophrenic like symptoms.
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What are the seven major groups of anxiety disorders?
• Panic Disorder
• Social Phobia/Anxiety
• Agoraphobia
• Specific phobias
• Generalised Anxiety Disorder
• Separation anxiety disorder
• Selective mutism
• Social Phobia/Anxiety
• Agoraphobia
• Specific phobias
• Generalised Anxiety Disorder
• Separation anxiety disorder
• Selective mutism
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Why could anxiety be a good trait?
• Promotes caution, and apprehension, while curbing excessive or careless behaviour.
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What are the cause of panic disorder?
• Psychological factors e.g., general stress or life transitions
• Stimulants e.g., caffeine, SSRIs
• Metabolic hypothesis of panic – triggers are lactate, carbon dioxide.
• Amygdala abnormalities
• Stimulants e.g., caffeine, SSRIs
• Metabolic hypothesis of panic – triggers are lactate, carbon dioxide.
• Amygdala abnormalities
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What are is the treatment for anxiety?
• Benzodiazepines – potent class of anxiolytics.
• 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 c
• 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 c
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Other cards in this set
Card 2
Front
what happens at synaptic transmission?
Back
An AP reaches a pre-synaptic terminal.
NT is released from vesicles inside the pre-synaptic terminal into the synaptic cleft. NT diffuses across the gap and binds to receptors on the post-synaptic terminal. The NT binding depolarises the post-synaptic te
NT is released from vesicles inside the pre-synaptic terminal into the synaptic cleft. NT diffuses across the gap and binds to receptors on the post-synaptic terminal. The NT binding depolarises the post-synaptic te
Card 3
Front
Why are receptors special?
Back
Card 4
Front
Give some examples of neurotransmitters
Back
Card 5
Front
define neuromodulators
Back
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