Antidepressant Drugs

Types of Antidepressants
1. Tricyclics
  1. operate by blocking transporter proteins that reabsorb serotonin, dopamine & norepinephrine into presynaptic neurone after release
    1. results in prolong the presence of NT in synaptic cleft, continue stimulating postsynaptic cell
  2. Also block histamine receptors, acetycholine receptors & certain sodium channels
    1. blocking histamine causes drowsiness
    2. blocking acetycholine leads to dry mouth and hard to urinate
    3. block sodium channels causes heart irregularities
2. Selective Serotonin Reuptake Inhibitors (SSRIs)
  1. specific to NT serotonin
  2. prozac blocks reuptake of serotonine
  3. produce milder side effects than try but effectiveness is about the same
  4. Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)
    1. block the reuptake of serotonin and norepinephrine
3. Monoamine Oxidase Inhibitors (MAOIs)
  1. block enzyme monoaime oxidase (MASO
    1. presynaptic terminal enzyme that metabolises catecholamines and serotonin into active forms.
      1. when block this enzyme the presynaptic terminal has more of its transmitter available for release
  2. last resort after try and SSRI
  3. must avoid foods containing syramine (cheese etcs
    1. combo of tyramine and MAOIs increases blood pressure
4. atypical antidepressant
  1. buropion inhibits reuptake of dopamine and to some extent norepinephrine but not serotonin
5. St Johns Wort
  1. advantage of being less expensive than anti depressants
  2. advantage/disadvantage available without a prescription
    1. can end up taking inappropriate amounts which is dangerous
  3. all mammals have liver enzyme breaks down plant toxin
    1. increases effectiveness of that enzyme
      1. this also breaks down medicines and makes them ineffective
How do Antidepressants work
1. increase presence of serotonin or other NT at sun apse so problem is too little of the NT
  1. blood metabolites, people with sep have approx normal levels of release of NT
    1. some studies show people with dep have increase in serotonin release
      1. BARTON ET AL 2008
      2. possible to decrease serotonin levels suddenly by consuming all amino acids except tryptophan, procurer to serotonin
        decrease in serotonin doesn't provoke any feelings of dep
        NEUMEISTER ET AL 2004
2. would expect drugs to have diff effects but most have equal effects on NT
  1. two studies, patients failed respond to antidep drug
    1. one added second drug and other switched
      1. patients who didn't respond to first, responded to second
        RUSH ET AL 2006
    2. neither did control group so no conclusions found
3. time course is threat in term of NT
  1. antidep produce effects on NT in synapses within min-hrs depending on drug
    1. takes 2 weeks for it to start working
      1. delay of benefits suggests increase level of NT at synapses doesn't explain the benefits of drugs
4. focus on neurotophins
  1. neurotophins aid in survival, growth and connections of neurons
  2. most with deo have lower levels of neurotrophin called brain-derived neutotrophic factor BDNF
    1. important for synaptic, plasticity,learning and proliferation of new neurones in hippo
    2. low BDNF people with dep have smaller hippo, impaired learning, reduced production of new hippo neurons
  3. prolonged use of antidep increases BDNF prod and improves learning and formation of new neurons
    1. takes weeks
      1. time course for BDNF and changes in hippo matches time course for behavioural recovery
        procedures block neuron production also block behavioural benefits of antidep drugs
  4. BDNF alone doesn't auto elevate mood but helps by facilitating new learning that builds new synapses and removes old ones
    1. mode of action explains why antidep help people in dep but fail to elevate mood for normal people

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	Creado por n.c.wetmore hace más de 11 años