Psychiatric Disorders

(presence of abnormal features)

(Absence of normal features)

-Old treatment for Schizophrenia

-Chlorpromazine (sedating). Reserpine (effective but dangerous drop in blood pressure)

Loss of DA= Parkinsons. Too much DA= schizophrenia

• -Supported by: Reserpine depletes DA (leak vesciles)
• -Chlorpromazine blocks DA receptors
• -Problems: takes weeks to work (cant be all D)

• -Depression/mania. More sufer from unipolar than bipolar
• -Amygdala/Prefrontal Cortex/Mesotelencephalic damaged (depression)

• -Treatment: MAOIs- Prevent breakdown of monoamines
• -Tricyclic antidepressants- block reuptake of serotonin/norepinephrine (safer then MAOIs)
• -SSRIs- Very successful
• -Lithium- lots of side effects
• -Sleep deprivation improves depression

Underactive serotonin/norepinephrine

-inherited genetic susception to depression

-HPA axis not as responsive to normal negative feedback

stress/anxiety in absence of causal stimulus

- anxiety triggered by stimulus

-onset rapid stress physiological response

-anxiety producing obsessive relieved by compulsive actions

continuing stress following extreme stress

• -Treatments: Benzodiazepines (hypnotics, muscle relaxants) GABA agonist. Increases probability of channel opening
• -Serotonin agonists- Reduce anxiety without sedation/best long term treatment

• Too little serotonin/GABA neurotransmission=anxiety.
• Amygdala (fear/defensive maybe responsible)

setative/increased duration of GABA channel opening

involuntary movement/vocalization

• -Major genetic component
• -Hard to study/ no animal models
• -Treated with neuroleptics
• -Suggest basal ganglia-thalamus-cortex problem

hyperactive impulsive, inattentive, combined hyperactive impulsive and inattentive

Smaller prefrontal cortex/cerebellum, lower levels of dopamine

• -Atomoxetine- Norephinephrine reuptakeinhibitor
• -Amphetamine salts (adderall/retalin) increase dopamine, serotonin and norepinephrine concentrations in synapse