Antidepressants and schizophrenia treatments

Serotonin, Dopamine, Norepinephrine

Monoamine Oxidase Inhibitor

The proteins that break down monoamines

The brain (in the synapse) and the liver

Selective Serotonin reuptake inhibitor

Least amount of side effects 

• 1. sexual dysfunction 
• 2. sleep disturbances 
• 3. Stomach problems 
• 4. hallucinations (auditory and visual) 
• 5. confusion

Tricyclic antidepressants

Block the reuptake of serotonin in the axon terminal by blocking serotonin receptors on the axon

Serotonin is in the synapse for longer and is more active

Serotonin can leave the terminal but cannot come back

TCA's prevent the re-uptake of monoamines by blocking specific receptors in the axon terminal

chemical compound found in dairy, meat, bread, alcohol, chocolate, etc.

MAO's break down tyramine in the liver

When MAOI's are introduced, they decrease the amount of MAO's in the liver significantly. 

Less MAO's = more tyramine in the liver 

Too much tyramine is toxic

• High blood pressure 
• Headache
• Sweating 
• Nausea 
• Stroke

• Memory deficits 
• Drowsiness 
• Cardiotoxicity (mostly high blood pressure) 
• Motor impairment

Electroconvulsive therapy

Electrodes send electrical impulses through the frontal cortex (bilaterally or unilaterally) to improve electrical firing of the neurons

Decreases depression but can cause memory loss if performed more than three times a week

• 5 or more symptoms for at least two weeks
• must include depressed mood or feelings of worthliness

• Depressed mood 
• Low self esteem 
• Psychomotor agitation/retardation
• Cognitie deficits
• Anhedonia 
• Fatigue
• Change in sleeping patterns 
• Thoughts of suicide 
• Weight change

• Thoughts of grandour 
• Decreased need for sleep 
• Talkativeness
• Racing thoughts
• Distractability 
• Increased goal activity 
• Excessive involvement in pleasurable activities

Type of prevalence rate

proportion of subjects who match each other in symptomology

60%

25%

37%

18%

80%

17%

The higher the percentage of DNA shared, the more likely the chance that they will both get the disorder

• Decreased grey matter
• Decreased frontal lobe activity 
• Damage to hippocampus/hypothalamus/amygdala

The HPa axis is especially sensitive, and negative feedback loop does not stop when it is supposed to so it eats away at the hypothalamus

• Decreased HPA activity 
• Increase protein to increase health of hippocampus neurons 
• Increase MA activity

• Monamines naturally reside in the synapse 
• MAO's breakdown MA's so that they are not able to travel to the dendritic terminals 
• MAOI's breakdown MAO's to prevent them from harming MA's

• Emotional disregulation
• Anhedonia
• flat affect (lack of facial expression)

• Impaired motivation
• Alogia (reduced speech) 
• Social withdrawal

• Psychotic
• Hallucinations
• Delusions

• Disorganized 
• Inappropriate behavior 
• cognitive impairment 
• Disordered speaking/thinking

Drug that effects mood, psychology, cognition, behavior, perception in some way

Directly effect synapse transmission

Water and fat

• buzz/high 
• relaxation 
• sedative
• cognitive deficits
• disinhibition 
• decreased emotional control 
• decreased sleep quality 
• association with crime/accidents/violence
• blackout

• CNS depressant 
• Decreased respiration 
• Pain reliever 
• diuretic 
• Anticonvulsant 
• motor deficits
• dilates superficial blood vessels (lowers body temperature)

Alcohol blocks glutamate cells from leaving the axon and attaching to the dendrite

antagonist

increases synaptic transmission

Slows down synaptic transmission

• Continuously drinking means that glutamate cannot travel through the synapse
• Dendritic terminals make more glutamate receptors in order to receive all glutamate that escapes the alcohol and comes through the synapse 
• The person drinks more to get drunk 
• The neurons cannot fire because there is too much alcohol in the body that is blocking glutamate from entering the synapse 
• Dendrites continue to make more receptors in response

When there is no alcohol in the body the neurons are too active, which leads to the symptoms of withdrawal

• Anxiety 
• Foggy Thinking 
• Shaking 
• Irritability 
• Sweating 
• Headache 
• Nausea 
• Fever 
• Seizures

1. Fatty liver- due to triglyceride over accumulation (causes inflammation in the liver cells) 

• 2. Alcoholic hepatitis- acetaldehyde over accumulation 
• 3. Liver cirhosis- massive cell death in the liver due to over accumulation of acetaldehyde and triglycerides

• Liver damage
• Vitamin B deficiencies (can cause brain damage)

• Opioid antagonist 
• taken with alcohol 
• reacts with the alcohol to make the person sick and associate negatively with alcohol 
• must be taken consistently

• Acetaldehyde dehydrogenase antagonist 
• makes you sick by stopping the creation of acetic acid

They must be taken continuously so they require cooperation from the person taking them in order to be effective