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Mood & Thought Disorders (Biological Basis of Affective Disorders…

- - - - reserpine – depletes monoamines (used to treat high blood pressure) caused depression in 20% of cases
      - monoamine oxidase inhibitors (MAO inhibitors) – used to treat tuberculosis –> marked elevation in mood
      - antidepressant drugs elevate level of serotonin, norepinephrine, and/or dopamine in synapse
        
        depression thought to arise from deficit in one of these monoamine neurotrans. so antidepressants restore them
        
        SSRIs – enhance serotonin action by blocking reuptake of serotonin
        
        MAO inhibitors – enhance NE & 5-HT action by preventing enzymatic destruction
        
        tricyclics – enhance NE & 5-HT (serotonin) by blocking reuptake
    - - some drugs target 5-HT & other NE?
      - do not work in up to 40% of patients
      - drugs require long time to achieve clinical efficacy
  - - - CRH released by hypothalamus –> ACTH released by pituitary –> cortisol released by adrenal glands
    - - abnormality = corrected w/ successful treatment of depression
    - - porsolt forced swim test
        
        mice forced to swim in container they can't escape
        
        eventually stop trying to climb out & just float (learned helplessness)
        
        treatable w/ antidepressants
      - inescapable shock
        
        dog put into box w/ no way to escape
        
        learned helpless behavior
        
        early morning wakefulness
        
        decreased feeding
        
        reduced sexual motivation
        
        reversed by antidepressants
  - - - onset = after extremely stressful events
      - HPA anomalies – elevated cortisol, ACTH & enlarged adrenals
      - excess brain CRH – elevated CRH in CSF
    - - copious cort receptors in hippocampus
      - hippocampal lesions lead to prolonged stress response due to loss of negative feedback w/ hypothalamus
      - antidepressants increase cort receptors in hippocampus
  - - - elevated cort
      - elevated CRH
      - enlargement of amygdala
      - reduced volume of hippocampus –> exerting less negative feedback
    - - human health benefits from touch
      - maternal care modulates stress response
        
        rat mothers vary in maternal behaviors – licking & grooming (LG) & arched back nursing (ABN)
        
        pups w/ least amount of maternal care experience most stress as grown ups (& vice versa)
        
        cross fostering
        
        shows that stress response ≠ inherited
        
        pups w/ low care biological mother but high care foster mother have decreased stress response
        
        tactile stimulation affects gene expression which dictates amount of cortisol receptors animal will have for life
        
        more receptors = better stress response
        
        serotonin neurotransmission in hippocampus (result of tactile stimulation) –> gene expression of cortisol receptors on hippocampus
- - - - Mania
        
        persistent, abnormal elevated mood
        
        grandiosity, decreased need for sleep
        
        racing thoughts, increased talkativeness
        
        impulsive behaviors, rapid onset
        
        hypomania: increase in efficiency, creativity
      - Type I
        
        severe mania w/ severe depression
      - Type II
        
        hypomania w/ extreme depression
      - Treatment
        
        urgency
        
        onset in childhood/teenage years
        
        often multiple suicide attempts
        
        lifelong condition
        
        psychosocial therapy
        
        medications
        
        lithium – stabilize mood but negative side effects
        
        antipsychotics – (DA receptors agonist) help control mania
        
        antidepressants – DO NOT help treat bipolar depression
  - - - Treatment
        
        cognitive behavioral therapy – effort to overcome negative though processes
        
        antidepressant medications
        
        tricyclics
        
        monoamine oxidase inhibitors
        
        SSRIs & SNRI (prozac, zoloft, etc)
        
        ketamine (hallucinogenic glutamate agonist) – rapid improvement but long-term value unclear
        
        ECT (electroconvulsive therapy) of temporal lobes – used when suicide risk = high; immediate result
        
        deep brain stimulation
        
        stimulate anterior cingulate, recruits inhibitory neurons to reduce activity
        
        awake patients describe sudden calmness
        
        electrodes left in place w/ battery-operated stimulator
        
        does not work for everyone
      - symptoms
        
        cognitive difficulties
        
        overeating, appetite loss
        
        fatigue & decreased energy
        
        suicide ideation & attempts
        
        feelings of hopelessness & pessimism
        
        feelings of guilt, worthlessness, or helplessness
        
        insomnia, early-morning wakefulness or excessive sleeping
- - - - new mutations
      - epigenetics
      - environmental factos
        
        drug use
        
        maternal infection during pregnancy
        
        hypoxia during fetal development
    - - metabotropic glutamate receptors
      - NMDA recptors
      - postsynaptic density proteins
      - activity-regulated cytoskeletal-associated protein
      - calcium channels
  - - - loss of gray mstter in prefrontal cortex – region critical for working memory
      - loss of gray matter in temporal lobe, amygdala, hippocampus – regions integrate cognition & emotion
- - - - delusions & hallucinations
    - - reduced expression of emotions
      - withdrawal from social interactions
      - impoverished content of thought & speech
      - difficulty in initiating goal-directed behaviors
    - - impaired working memory & executive function
      - seen in healthy relatives of patients w/ schizophrenia – reflect genetic predisposition
  - - - most effective @ diminishing positive symptoms
      - no medications reliably benefits cognitive symptoms
      - neuroleptics
        
        antagonist @ dopamine receptors subtypes
        
        combat (+) symptoms
        
        side effects
        
        persistent motor impairments
        
        parkinson-like symptoms
        
        eventual tardive dyskinesia
      - atypical neuroleptics
        
        bind to serotoni & dopamine receptors (possibly also GABA)
        
        effective against (+) & (–) symptoms
        
        less severe side effects
      - 3rd generation durgs
      - new focus = drugs that increase NMDA receptor responsiveness