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  1. All cell bodies/Soma for serotonergic neurons are in the:
    Hindbrain region: pons and medulla in a series of nuclei along the midline called the Raphe nuclei
  2. Serotonergic neurons Enter what brain parts:
    • Midbrain, limbic structures (hypothalamus and hippocampus), cerebral cortex (cortical and subcortical innervations)
    • down the spinal chord = regulate information processing and pain perception
  3. 5HT3 receptor is what type of receptor
    Ligand gated ion channel = excitatory receptor expressed in the brain
  4. All seratonin receptors except 5HT3 are what type?
  5. “off” switch for serotonin transmission:
  6. Pre-synaptic seratonin receptor, local negative feedback:
    5HT1a autoreceptor and b
  7. SSRIs target SERT of 5HT1A or B?
    5HT1A or B
  8. What can MAOIs treat?
    Treat depression, OCD, ADHD, and to control appetite
  9. Amphetamine stimulates serotonin release be what action?
    Depends on it binding to and being transported by the reuptake pump
  10. Seratonin reuptake pump is the target for what drugs?
    TCAsa nd SSRIs
  11. Differences between the TCAs and SSRI.:
    • SSRIs = relatively selective for the serotonin transporter, safer
    • TCAs = block both serotonin and NE transporters
  12. SImilrities between the TCAs and SSRI.:
    Same ceiling/efficacy
  13. iproniazid MOA:
    MOAI - Blocked the reuptake of biogenic amines
  14. Why respirine taken off the market?
    HTN treatment - caused profound depression/suicide b/c deleted biogenic amines
  15. Why is biogenic amine theory not correct?
    • 1. Some antidepressants don’t block reuptake of biogenic amines and they’re not MAOI
    • 2. biogenic amines elevated in the synaptic cleft 30 minutes after you take one
  16. Supersensitivity of receptors in the brain leads to depression?
  17. chronic antidepressant treatment affects what receptors?
    HHT, alpha 1 adrenergic and B-adrenergic
  18. Action of 5HT1A:
    hyperpolarizes the membrane
  19. Action of SSRIs after first dose on neural firing:
    • Inhibit SERT
    • 5-HT1A:
    • increases 5-HT1A and decreases rate of firing
  20. Action of SSRIs after chronic dose on neural firing:
    • 2-4 wks:
    • normalizes: raphe 5-HT neuron activity
    • downregulation of 5-HT1A receptors
    • elevate serotonergic transmission - unimpeded
  21. Cell bodies for NE neurons in the brain are in the:
    BRAIN STEM’S Locus Ceruleus - blue body
  22. NE neurons send their projections:
    • In the descending manner to the spinal cord
    • Ascending manner to the forebrain structures (limbic: hypothalamus and hippocampus) and cerebral cortex
  23. Post-synaptic noradrenergic receptors:
    Alpha adrenergic or beta adrenergic receptors
  24. Pre-synaptic noradrenergic receptors:
    Alpha-2 adrenergic receptor
  25. DA cell bodies are located:
    Midbrain: VTA or Substantia nigra
  26. Nigrostratal tract
    Substantia nigra to the striatum = Parkinson’s disease
  27. Mesolimbic dopamine pathway
    VTA to limbic structures = nucleus accumbens and the amygdala (reward circuitry pathway)
  28. Meso-Cortical dopamine pathway
    VTA to the cerebral cortex = Regulates/contributes to thoughts = target for antipsychotic drugs
  29. Dopamine cell bodies Project to:
    Limbic structures as well as the cerebral cortex
  30. 5 different post-synapatic dopamine receptor subtypes, what type of receptor are they:
    All G-protein coupled receptors
  31. VTA and Substantia nigra dopamine cell bodies = what are the somato-dendritic auto-receptors - inhibit the firing rate?
    D2 dopamine receptors - coupled to K+ channels
  32. Opioids bind mu opiod receptors on:
    • GABAergic interneurons in the VTA
    • Leads to Release dopamine in the nucleus accumbens = rewarding or pleasurable experience
  33. Psychostimulant like cocaine or an amphetamine affects what receptors?
    Inhibits the dopamine transporter, DAT
  34. Cholinergic pathway that goes to the hippocampus = very important for:
    Short-term memory
  35. Block muscarinic receptors at hippocampus = difficulty with:
    Short-term memory
  36. Where are Ach neuron cell bodies located and where do they proect to?
    BMSI nucleus sends cholinergic projections to the cerebral cortex- Alzheimer’s
  37. (True/False) Muscarinic and nicotinic cholinergic receptors are important for brain function.
    True – mediate reward of nicotine
  38. Desipramine has a little bit of selectivity for :
    NE over serotonin
  39. Metabolite of imipramine is:
    Desipramine = both are biologically active TCAs.
  40. Mechanism of action of TCAs:
    inhibit the reuptake of NE and serotonin
  41. TCAs can produce sedation, related to their:
    alpha-1 adrenergic receptor affinity
  42. TCA cardiac toxicity is related to what feature?
    Ion channel blockade
  43. TCA adverse effect: Atropine-like side effects: dry mouth, constipation, blurred vision, mydriasis, metallic taste, urine retention is related to what receptors?
    muscarinic blockade
  44. TCA adverse effect: Orthostatic hypotension is related to what receptors?
    a1-AR and possibly a2-AR blockade.
  45. TCA adverse effect: Drowsiness, sedation and weight gain is related to what receptors?
    Histamine-receptor blockade
  46. Alternate receptor interaction of TCAs, put in order of most to least:
    Amitrylptyline >Doxepin> Imipramine = Clomipramine
  47. SSRI most potent in blocking SERT:
    Paroxetine (does not equate to efficacy)
  48. SSRI most selective for the SERT vs NET
    Escitalopram (does not equate to efficacy)
  49. SSRI most potent against DAT:
    • Sertraline
    • (Not a high affinity blocker of DAT, but amongst the SSRIs, it has the highest affinity)
  50. SSRI most potent anticholinergic agent:
  51. Potential Clinical Consequences of 5-HT Reuptake Blockade:
    • Sexual dysfunction
    • Impaired cognition (No more likely to impair cognition than a TCA)
    • Antidepressant effect
    • GI issues
  52. SSRI with highest rates of sexual dysfunction:
    Paroxetine (Paxil)
  53. SSRI with worst side effects:
    Paroxetine (Paxil)
  54. When there is non-compliance due to adverse effect, is it reasonable to switch to one SSRI to another?
  55. SSRI with a flat-dose response curve:
    Escitalopram (Lexapro)
  56. Escitalopram (Lexapro) Potency of blocking 5-HT is comparable to:
  57. SSRI NOT metabolized by CYP 3A4:
    Escitalopram (Lexapro)
  58. SSRIs from activating to sedating:
    Proxac – Zoloft – Escitalopram – Fuvoxamine – Paxil
  59. MOA Mirtazapine :
    • Doesn’t block serotonin or NE transport = increases vesicular release =Potentiation of NE transmission in the CNS
  60. MOA Nefazodone:
    • = congener of trazodone
    • Same kind of profile as trazadone = some 5-HT2 blocking activity = ability to block serotonin transport = some ability to block norepinephrine transport
    • Low efficacy
  61. Why does Tyramine cause negative effects:
    • Vasorepressor
    • promotes the release of NE in the periphery
    • Causes MABP surge in periphery
  62. Do MOAs produce adaptive changes in CNS similar to TCAs and SSRIs?
  63. Irreversible inhibitors of MAO-A and MAO-B:
    (isocarboxazid and Phenelzine)
  64. reversible inhibitors of MAO-A and MAO-B:
  65. BP effect of MOAIs:
    May lower, not profound
  66. Describe Ketamine
    • glutamate receptor antagonist
    • N-methyl-D-Aspartate (NMDA) subtype of glutamate receptor
    • IV
    • Couple of hours = improvement in mood
  67. SJW effects what receptor types?
    DA, 5HT, NE, GABA, Glutamte – all with low potency
  68. Molecular mechanism of action of HYPERFORIN:
    • -not competitive inhibitor
  69. Hyperforin or hypericin cross the BB well?
  70. GI distrubance = very high with fluoxetine, BUT almost non-existant in:
    St. John’s Wort
  71. Adverse effects of SJW:
    • Photosensitivity
    • Serotonin Syndrome
  72. MOA of Lithium:
    • alter the coupling of receptors with G-proteins.
    • Inhibits breakdown of IP2 to IP1
    • depletion of DAG and IP3 and ¯ [Ca2+]
    • - not really selective
    • Activates phospholipase C
    • disrupts glycogen synthase/adenylyl cyclase activity
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