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Queen's University
Pharmacology and Toxicology
PHAR 100
Hisham Elbatarny

Drugs used in the treatment of mental illness – II (antidepressants) Outline • History • Depression • Causes • Symptoms • Theories of Depression • First Generation (Typicals) • TCAs • Monoamine Oxidase Inhibitors • Second Generation (Atypicals) • SSRIs • Dual-Action Antidepressants • Reference: Chapter 5 History • MAOI (monoamine oxidase inhibitor) were discovered accidentally • Drugs were developed to treat tuberculosis and found patients had elevated mood – felt better • MAOI still very effective with proper diet and dose • TCA (tricyclic antidepressant) also discovered by accident while doing research on antipsychotics • did not alleviate psychiatric symptoms, but did elevate mood • first SSRI (Selective serotonin reuptake inhibitor)– fluoxetine – was introduced in the US in 1987 Depression • sometimes we feel sad or “depressed” in response to certain events that happen to us ◦ e.g., loved ones leaving, end of holidays etc. (no physical symptoms and not long-lasting) • sometimes the “depressed” state persists or returns without reason • loss of appetite, loss of interest in activities etc. • depression can occur in persons that do not feel depressed • often the elderly show signs of depression (weight loss, insomnia) without feeling sad Major Depressive Disorder (MDD) • chronic, recurring and potentially life threatening • fourth most disabling disease worldwide • worsens the health of those with chronic illness • approx. 10% men and 25% women experience depression in their lifetime Symptoms • MDD is an ‘Affective’disorder – profound changes in emotion or mood • MDD (five symptoms daily for at least 2 weeks) ◦ depressed/irritable mood ◦ decreased interest in pleasurable activities/inability to experience pleasure ◦ weight gain/loss ◦ insomnia/hypersomnia ◦ psychomotor agitation/retardation ◦ fatigue/loss of energy ◦ feelings of worthlessness/excessive guilt ◦ diminished ability to think/concentrate ◦ recurrent thoughts of death/suicide Causes • chronic illness • situational ◦ unpleasant life circumstances ◦ negative thinking patterns ◦ substance abuse ◦ medication intended for therapeutic use (side effect) • biological ◦ genetic ◦ hormonal (women are particularly susceptible) ◦ neurobiological dysfunction ◦ symptoms from a second disorder (Parkinson’s Disease) Monoamine Theory of Depression • related to a deficiency in neurotransmitters, specifically the monoamines • restoring levels of these neurotransmitters would result in normal mood state • problem: changes should occur soon after drug administration, BUT the antidepressant effects develop more slowly ◦ why? ▪ changes in receptor sensitivity over time? ▪ changes on intracellular processes? (e.g., second messengers) Neurogenic Theory of Depression • based on two relatively recent discoveries ◦ existing neurons can repair themselves ◦ brain can make new neurons • stressful situations reduce the production of new neurons (and damage existing ones) in both the hippocampus (implicated in learning and memory, remember route to school) and frontal cortex (governs cognitive flexibility: risk taking, etc) ◦ hypoglycemia, toxins and hypoxia • antidepressants can repair neurons and increase their production (Neurogenesis) • therapeutic delay in clinical effects of antidepressants may be due to the time course for new neurons to develop, mature and become functional (~two weeks) Antidepressant Drugs • First-generation antidepressants ◦ Tricyclic antidepressants (TCA) ◦ Monoamine oxidase inhibitors (MAOI) • Second-generation antidepressants ◦ Selective serotonin reuptake inhibitors (SSRI) ▪ fluoxetine (Prozac) ▪ sertraline (Zoloft) • Dual-action antidepressants ◦ Serotonin and Norepinephrine reuptake inhibitors Tricyclic Antidepressants (TCA) • class of d
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