Psyc 4130 1nd Edition Lecture 33 Outline of Last Lecture I. Evidence for DA HypothesisII. Classic AntipsychoticsIII. D2 Antags Are Not Well-ToleratedIV. The DA Hypothesis SequelV. The PFC modulates Activity in the VTAVI. Atypical AntipsychoticsVII. NMDA AgonistsOutline of Current Lecture I. Disorders of AffectII. Bipolar DisorderIII. DepressionIV. Diagnostic Criteria Highlights V. Signs and SymptomsVI. Common ComorbiditiesVII. Monoamine Hypothesis VIII. Evidence for MA Hypothesis IX. Resolving Lagtime IssuesX. BDNFXI. MAR BDNF Signaling CascadeXII. MA AutoR OverexpressionCurrent Lecture Disorders Of Affect- What qualifies as a disorder? Bipolar Disorder - Manic-Depression- Mania (or hypo) alternating with depressiono More delusions of grandiosity - Typical Cycleso Alternating periods- period of mania (few weeks- few months), after mania then nose dive into depression (3 times as long as manic stage)o Mania begets depression - Manic EpisodesThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.o Greatly reduced need for sleep (not insomnia!)o Boundless energy and behavioral hyperactivityo Rapid, relentless, “pressured” talko Grandiosity Megalomania o “Master plans”o Sexual acting outo Illegal behaviors (e.g. illicit drug use) Depression- Bipolar vs. Unipolar- Pervasive helplessness and hopelessness- Beck’s “cognitive triad” Diagnostic Criteria Highlights- Persistent Sadness/Irritability - Diminished Interest (Anhedonia)- Weight Change (70/30)- Dramatic Changes in Sleep- (Psycho)Motor Agitation (Obsvd by Others)- Fatigue- Inability to Concentrate- Helpless, Hopeless, Worthlessness, Guilt- Suicidal Ideation or Attempts Signs and Symptoms- Behavioral domain often includes:- Changes in sleep habits- Changes in appetite and eating - Weight changes- Behavioral domain often includes:- Slow, torpid, speech and movements, sometimes alternating with psychomotor agitation- Decreased sexual behavior- Decreased social involvements- Extreme self-deprecation- Strong, unfounded sense (delusions?) of guilt- Suicidal ideation (15-30% attempt suicide!) Common Comorbidities- Generalized Anxiety Disorder (GAD)- Panic Disorder- Agoraphobia- PTSD Monoamine Hypothesis- Reserpine- Blocks vesicular transport- Powerful decrease of monoamine activity Evidence for MA Hypothesis- Reserpine causes depression.- Brains of individuals who died by _______ show upregulation expression of monoamine receptors.- Tryptophan depletion causes relapse in patients with remitted depression.- Biosynthetic precursor for tryptophan (serotonin)- Rx: Drugs that increase MA levels:o Cocaine: Uber Coca (Freud)o Amphetamineso MA Oxidase Inhibitors (MAOIs)o Tricyclics (TCAs): NE & 5-HT RIso SSRIso SNRIso DRIs- Shortcomings of MA Hypothesiso Lagtime issueo Tryptophan depletion in people who are not vulnerable to MDD Resolving Lag Time Issues- Revised MA Hypothesis views depression as a consequence of neurodegeneration in the hippocampus and medial prefrontal cortex.- Vulnerabilities and stress team up to inhibit the expression of neurotrophic factors in these areas. BDNF- Brain-derived neurotrophic Factor- Essential for growth of new neurons and for the survival and receptor “budding” of intact neurons- BDNF functions within the nucleus to maintain vital cell processes and to enable the cell to express new receptor sites. MAR BDNF Signaling Cascade- MAR activity allows Ca++ influx. - Ca++ activates the second messenger cAMP- cAMP activates PKA- PKA travels to nucleus and activates CREB- CREBactivity increases expression of BDNF- BDNF promotes cell maintenance, survival and the expression of new monoamine receptors. MA AutoR Overexpression- Recall how autoreceptors work.- People who ___________ monoamine ______________ will therefore show lower-than-normal activity in postsynaptic monoamine
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