Psyc 4130 1nd Edition Lecture 33 Outline of Last Lecture I Evidence for DA Hypothesis II Classic Antipsychotics III D2 Antags Are Not Well Tolerated IV The DA Hypothesis Sequel V The PFC modulates Activity in the VTA VI Atypical Antipsychotics VII NMDA Agonists Outline of Current Lecture I Disorders of Affect II Bipolar Disorder III Depression IV Diagnostic Criteria Highlights V Signs and Symptoms VI Common Comorbidities VII Monoamine Hypothesis VIII Evidence for MA Hypothesis IX Resolving Lagtime Issues X BDNF XI MAR BDNF Signaling Cascade XII MA AutoR Overexpression Current Lecture Disorders Of Affect What qualifies as a disorder Bipolar Disorder Manic Depression Mania or hypo alternating with depression o More delusions of grandiosity Typical Cycles o 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 Episodes These 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 hyperactivity o Rapid relentless pressured talk o Grandiosity Megalomania o Master plans o Sexual acting out o 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 Amphetamines o MA Oxidase Inhibitors MAOIs o Tricyclics TCAs NE 5 HT RIs o SSRIs o SNRIs o DRIs Shortcomings of MA Hypothesis o Lagtime issue o 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 thannormal activity in postsynaptic monoamine receptors
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