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10. Antidepressants.docx

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University of Otago
Kristin Hillman

Week 10. Antidepressants 8/23/2013 2:30:00 PM • At times, we’ve all felt sad/depressed • What are some causative factors (in terms of life) in depression?  Weather  Post-natal depression  Stress  Death  Loss of activity/ability  Injury/chronic illness  Nothing clear - genetic disposition  Relationship breakup  Trauma  Insomnia/too much sleep  Failure  Malnutrition • How do we deal with it?  Distraction  Exercise  Food  Talk to people  Remove yourself from negative/triggering environment  Drugs (e.g. antidepressants) • Periods of sadness/despair are a normal part of life • Can argue an important part of life?  Develop coping skills  Strengthen social bonds  Prompt self-reflection and learning (for the next time) Depression • When periods of sadness are intense and persistent  depression • Affective disorder • Defined by a loss of interest/pleasure in usual things/activities  intense and persistent sadness  low activity…  fatigue…  recurrent… • Serious depression, if left untreated, can be fatal (suicide) • Recent stats for depression rates = 1 in 6 NZs, 1 in 7 before the age of 24 • High levels of depression in NZ, and suicide rate too – not good!!!! • What constitutes depressive behaviour?  Talking about feelings  Recall the definition of behaviour in week 1 – depressive behaviour can be seen…but most of it comes from feelings being said. How to treat depression? • 1. Recognition of depression (within self, and/or within someone else) • 2. Agreement to some course of therapy  Psychotherapy  Pharmacotherapy  Or both combined • 3. Adherence to therapy Pharmacotherapy to treat • To treat depression pharmacologically, need to know what’s going on at the biochemical level • Biological (or biogenic) Amine Hypothesis  Developed in 1960s  Idea = if you increase NE and 5HT in the brain, can treat depression  therefore, if this is true, then a deficiency of NE and 5HT must account for depression???  Shortcomings? o Consistent deficits in biological amines not always seen in depression o Mismatched time course in therapy between amine increase and improved affect  If this hypothesis was true, then in every depressed brain you should see low levels of these neurotransmitters (not the case) and you should see improved mood if you increase these (not the case) • Receptor Sensitivity Hypothesis  Imbalance of receptors  Idea = Receptors have been sensitized and you’ve created an imbalanced system = causes depression • Today, we’re seeing a shift towards examining long-term, network level changes  (e.g. changes in BDNF, CREB-mediated transcription, neurogenesis)  Disequilibrium in the amine…  Nevertheless, antidepressant drugs still primarily target the amine neurotransmitters (NE and 5HT etc) Remember four targets:  Synthesis  Relases  Post0synaptic recepotrs  Clearance • This lecture, focus is on NE and 5HT Norepinephrine • Comes from DA • MAO-A = breaks down NE • NET – transporter • Receptors:  alpha 1 - Gq  alpha 2 (2a, 2b, 2c) (want to know this one) o can find it presynaptically = metabotropic, Gi o Dont worry about 3 subtypes of it  beta - Gs Serotonin: • Comes form tryptophan • Loaded into vesicles • 5 subtypes:  3 – ionotropic (excitatory)  1 - autoreceptor (presynaptically, Gi, inhibitory) • Clearance  SERT  MAO-A to breakdown History of antidepressants • Prior to the development of these antidepressant drugs, what were some other drugs used to treat depression  Alcohol  Cannabis  Opioids • 1950s  MAO inhibitors (MAOIs brought to market)  Tricyclic antidepressants (TCAs) brought to market o didn’t work for psychosis, but did for depression • 1960s  Biological amine hypothesis developed • 1970s  2nd generation antidepressants developed • 1980s • 1990s • 2000s • 2010s  antidepressant drug design today – lots and lots being made (make a lot of money) Rates of depression • Are more people depressed in 2011 than say 1980?  Prescription rates for antidepressant drugs are steadily increasing  E.g., NZ Rx = 700,000 in 2002, Rx = 1.2 million in 2008 • Why are we seeing higher rates of depression in 21 century?  Recent world events? o e.g. Chch earthquake  Public awareness and decline of stigma to seek help? o There are a number of ads today, may increase public awareness  Better recognition and diagnosis? o By self and/or GP  Application to other disorders?  Drug advertisements? o Huge pushes for adverts  An undermining of the Westernized life? o E.g. “The American nightmare” – expecting too much out of life? Four major classes of drugs we talk about today:  MAO inhibitors  Tricyclic antidepressants  SSRI  Dual action SSRI + 5HT2 Monoamine Oxidase Inhibitors (MAOIs) • Mechanism  Inhibits MAO  Binds non-selectively and irreversibly to MAO  What’s another MAOI we’ve talked about? o  What’s another irreversible enzyme inhibitor weve talke about? o Nerve gases • Mode  Improve affect and activity levels in depressed individuals • Downfall?  Use is limited by serious drug-drug and drug-food interacti
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