Lecture 65: Biogenic Amine Neurotransmitters
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Do biogenic amines produce fast or slow transmission in neurotransmitters?
What kind of structure does Serotonin have?
What converts tryptophan to 5-hydroxytryptophan?
What is the molecular precursor to serotonin and what is the difference between the two molecules?
- serotonin is the decarboxylated form of 5-hydroxytryptophan
What happens when there is serotonergic dysfunction in the CNS?
- panic attacks
How much of the brain is composed of serotonin pathways?
Where do serotonin pathways come from and go to?
from ralphe nuclei and go to cortex (& down spinal cord)
What is the pre-synaptic release modulating receptor in serotonin pathways?
What is "SERT"?
Plasma Membrane Serotonin Transporter: it removes serotonin from the synaptic cleft
What are four common TCAs?
What does TCA stand for?
What are 6 common SSRI's?
What does SSRI stand for?
Selective Serotonin Reuptake Inhibitor
What is depression the result of?
Reduced levels of biogenic amines in the CNS
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
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
Describe SSRIs and their effects on 5-HT1A.
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.
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.
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 receptorsIn other words, people with the ss alleles are more likely to develop depression under similar stress factors
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)
Will a neuron that has high expression of 5-HT1A receptors respond well to fluoxetine?
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
What is attributed to the enhanced release of serotonin in the orbitofrontal cortex?
densensitization of terminal 5-HT1B Receptors
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
What is the locus ceruleus associated with in the brain?
How many subtypes of noradrenergic receptors have been demenstrated in the brain?
- alpha1A, 1B, 1C, 2A, 2B, 2Cbeta1, 2
What role do adrenergic receptors play in the CNS?
regulation of mood, vigilance, and cardiovascular function
Which pathway of catecholaminergic neurons degenerates in PD?
Which dopamine pathways constitute the reward pathways of the brain?
What controls pro-lactin release?
dopamine projection from the arcuate nucleus of the hypothalamus to the intermediate lobe of the pituitary
Where do the reward pathways of the brain originate?
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 autoreceptorThere is also a release modulating autoreceptorfinally there are Ca++ channels that determine when the vessicles should be released
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
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
Where do opiods and alcohol affect the rewards systems?
On the somatodendritic parts of the interneuron, nucleus accumbens and the synapses to the cortex
Where can you find cholinergic nuclei in the brain?
No where in particular, they are very wide spread
Does Nicotine affect the rewards circuitry?
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