Biochemistry

Question 1

What’s serotonin made from, and what’s serotonin also known as?

Answer 1

Made from Tryptophan 5-hydroxytriptamine 5-HT

Question 2

Where is most of the serotonin in your body located? What are some other places it resides and what are its functions there?

Answer 2

Intestines-help regulate digestion CNS neurotransmitter It’s also named after its role as blood pressure regulator in endothelial cells- sero (serum) tonin (tones the blood vessels)

Question 3

Describe the highlights of serotonins biosynthesis?

Answer 3

Synthesized from Tryptophan-the enzyme tryptophan hydroxalase adds a hydroxy group- gets complicated and involves co-factor tetra-hydro-biop-terin which is similar in nature to tetrahydrofolate? Eventually we get 5-hydroxytriptamine (5-HT)

Question 4

Describe serotonins progression from biosynthesis to excretion in general terms

Answer 4

Tryptophan to 5-HT in the presynaptic neuron, release into the synaptic cleft, breakdown by MAO into 5-HIAA, excretion in urine etc.

Question 5

GLUT transporters are what type of transporter?

Answer 5

Facilitated diffusion which is a form of passive transport. There is simply a pore that allows it to flow in either direction. It stays in the cell after phosphorylation by hexokinase.

Question 6

Your grandma was recently prescribed neostigmine to help with her dementia. She likes to garden, but the other day took a sip of pesticide by accident and was taken to the hospital. Why might she be at greater risk for neurological issues complications than her grandson?

Answer 6

The neostigmine is a AchE inhibitor which already increases Ach in the synapse helping her with memory function, but taking too much AchE (pesticide) can lead to dangerous levels of Ach accumulation in the synapse and hyperexcitability of the post synaptic neuron. Her grandson doesn’t have the added complication of the neostigmine.

Question 7

You have a patient with a unique genetic disease that mutates his astrocytes in such as way that they are unable to undergo lactose fermentation, but are still able to use both anaerobic and aerobic respiration. What would you council him to be aware of? A) high intake of phenylalanine B) Ketogenic diet C) fatty desserts D) Fasting

Answer 7

D- Fasting. Why? b/c this would create a situation where neurons would be starved for glucose and have to rely on astrocytes for the production of lactate, which the neurons would typically uptake and convert to pyruvate for use in the kreb cycle during times of fasting. Your patient genetic condition would prevent this and lead to the starvation of neurons. B) ketogenic diet might be tempting, but ketones would be broken down into acetyl CoA and used by the brain with no problems.

Question 8

How might the interaction of astrocytes with neurons change should a gain of function mutation lead to the development of Glu-6-phosphatase in astrocytes? A) Astrocytes would transport glucose rather than lactate B) Astrocytes would convert glucose more readily to pyruvate C) Neurons would be able to store glycogen D) Neurons would uptake lactate more readily

Answer 8

A is correct- This enzyme would dephosphorylate glucose allow for it’s direct transport to neurons from astrocytes. This would be a more direct method that to use anaerobic metabolism and lactose fermentation. B- This plays on the false notion that this enzyme will help with glycolysis when in fact it does not. C-This makes no sense D- Unrelated to this enzymatic function