Lecture 65: Biogenic Amine Neurotransmitters

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Lecture 65: Biogenic Amine Neurotransmitters
2010-04-25 15:17:22

Neuroscience Week 6
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  1. Do biogenic amines produce fast or slow transmission in neurotransmitters?
  2. What kind of structure does Serotonin have?
    indoleamine structure
  3. What converts tryptophan to 5-hydroxytryptophan?
    tryptophan hydroxylase
  4. What is the molecular precursor to serotonin and what is the difference between the two molecules?
    • 5-hydroxytryptophan
    • serotonin is the decarboxylated form of 5-hydroxytryptophan
  5. What happens when there is serotonergic dysfunction in the CNS?
    • depression
    • anxiety
    • OCD
    • panic attacks
  6. How much of the brain is composed of serotonin pathways?
  7. Where do serotonin pathways come from and go to?
    from ralphe nuclei and go to cortex (& down spinal cord)
  8. What is the pre-synaptic release modulating receptor in serotonin pathways?
  9. What is "SERT"?
    Plasma Membrane Serotonin Transporter: it removes serotonin from the synaptic cleft
  10. What are four common TCAs?
    • amitryptiline
    • imipramine
    • clomipramine
    • doxepin
  11. What does TCA stand for?
    Tri-cyclic Antidepressants
  12. What are 6 common SSRI's?
    • fluoxetine
    • paroxetine
    • fluvoxamine
    • sertraline
    • citalopram
    • escitalopram
  13. What does SSRI stand for?
    Selective Serotonin Reuptake Inhibitor
  14. What is depression the result of?
    Reduced levels of biogenic amines in the CNS
  15. What are two discrepancies in the biogenic amine theory?
    • Drugs take 2-3 weeks to work, even though the molecular aspect is working in several days
    • Not all anti-depressant drugs inhibit transport of 5-HT or NE or MAO
  16. What does the updated biogenic amine theory say?
    • That first there is receptor signalling dysfunction
    • Then there is receptor supersensitivity and that drugs chronically work to reverse this
  17. Describe SSRIs and their effects on 5-HT1A.
    Acutely: elevates Serotonin in Dorsal Raphe Nuclei and causes activation of 5-HT1A Receptors. This causes a decrease in firing of the serotonergic receptors. Meanwhile SSRIs increase serotonin release in the forebrain. The combination of decreased firing and increase release is canceled out acutely.

    Chronically: eventually cell bodies in the Dorsal Raphe Nuclei are normalized and normal firing resumes. Now, the SSRI can act in the forebrain unimpeded and increases the release of biogenic amines.
  18. How do the short and the long alleles of the 5-HTT gene differ with one another?
    • They differ with respect to expression of the transporter and therefore serotonin uptake
    • People with the s- or ss copies of the 5-HTT gene mean decrease in 5-HTT, increase in synaptic 5-HT, increase in excitatory 5-HT receptors
    • In other words, people with the ss alleles are more likely to develop depression under similar stress factors
  19. What is the effect of high expression of the 5-HT1A Receptor?
    increase in inhibition at somotodentritic sites, decreasing frequency of action potentials, decreasing release of serotonin (biogenic amines), increasing behavioral despair (depression)
  20. Will a neuron that has high expression of 5-HT1A receptors respond well to fluoxetine?
  21. What is the difference between the serotonergic dysfunction of depression and OCD?
    • anatomy really
    • orbitofrontal cortex is where the problem for OCD lies
    • Pre-frontal cortex is where the problem for depression lies
  22. What is attributed to the enhanced release of serotonin in the orbitofrontal cortex?
    densensitization of terminal 5-HT1B Receptors
  23. Why do SSRIs have fewer side effects than TCAs?
    because SSRIs, such as fluoxetine, have little to no affinity for alpha1, histamine, and muscarinic receptors
  24. What is the locus ceruleus associated with in the brain?
    noradrenergic pathways
  25. How many subtypes of noradrenergic receptors have been demenstrated in the brain?
    • 8:
    • alpha1A, 1B, 1C, 2A, 2B, 2C
    • beta1, 2
  26. What role do adrenergic receptors play in the CNS?
    regulation of mood, vigilance, and cardiovascular function
  27. Which pathway of catecholaminergic neurons degenerates in PD?
    Nigrostriatal pathway
  28. Which dopamine pathways constitute the reward pathways of the brain?
    • mesolimbic
    • mesocortical
  29. What controls pro-lactin release?
    dopamine projection from the arcuate nucleus of the hypothalamus to the intermediate lobe of the pituitary
  30. Where do the reward pathways of the brain originate?
    ventral tegmentum
  31. Describe the dopaminergic synapse
    • Well, dopamine is synthesized from tyrosine->L-Dopa->Dopamine.
    • Dopamine is transported into vessicles whose formation is regulated by synthesis modulating autoreceptor
    • There is also a release modulating autoreceptor
    • finally there are Ca++ channels that determine when the vessicles should be released
  32. How is the affinity for D2 Dopamine receptors related to the anti-psycotic dose?
    They are directly related. The greater the affinity, the less the dose
  33. Describe the mesolimbic dopamine rewards loop.
    • Well, it starts in the ventral tegmentum whose axon projects to the Nucleus Accumbens. These are the rewards when NT is released and there is also a -feed back loop from the nucleus accumbens and interneurons that project back to the ventral tegmentum
  34. Where do opiods and alcohol affect the rewards systems?
    On the somatodendritic parts of the interneuron, nucleus accumbens and the synapses to the cortex
  35. Where can you find cholinergic nuclei in the brain?
    No where in particular, they are very wide spread
  36. Does Nicotine affect the rewards circuitry?