Introduction to Neurotrans

Excitatory Neurtransmitters:  ,  ,  ,  ,  ,  ,  

Inhibitory neurotransmitter:  ,  ,  

1.   Presynaptic vessicles
2.  Binding of Neurotransmitter (Depolarization Na+/K+)
3.   Metabolic degradation of neurotrasnmitters in the pre-synaoptic neuron or in the nueral cleft.

In the case of neurotransmitter serotonin, it is taken up into the   (reuptake) before it is degraded.

 cells are the supporting nueronal cells that maintain normal physiology of system

  are cells that provide fatty myelin sheaths that insulate axons. When the axonal connections die, you can end up with  

-Microglia protects the neuron from infection through phagocytosis. The microgla are activated by   inflammatory signals  
-The signals from the damaged cells include  

Acetylcholine causes the opening of
 channels in   nerve after a nerve stimulus

  is one of the fastest enzymes. Such a high turnover
is expected, since recovery from depolarization occurs within seconds.

Acetl CoA has a role in , ,  ,  ,  , and  

What is an example of something that is trans acetylated? What is the effect?

Choline becomes acteylcholine using   and  

Acetylcholine becomes acetate and choline using   and  

Physotigmine and neostigmine inhibit acteylcholinesterase by carbamoylating   at active site.

What does DIPF (organophosphate) target?

DIPF reactuves with the active site serine and   enzyme irreveseribly

Tubocuraine, alpha bungarotoxin, and cobra toxin compete with  

Receptor targeted inhibitors (alpha bungartoxin, cobra toxin, etc) function as  

  and  have selenocystine

What is the universal methyl group donor?

Methionine is a  amino acid

Proline is synthesized from  

Glutamate become   (needs   and  ) which becomes  which then becomes proline ( )

Hydroxylation of   occurs as a
posttranslational modification (hydroxylases
require   (ascorbate, lack of it
causes Scurvy).

3‐hydroxyproline and 4‐hydroxyproline are
found in  

Glutathione peroxidase contains  

In the mRNA for selenoproteins, the codon  , which generally serves as a termination codon, codes for selenocysteine

Selenocysteinyl tRNA is formed by adding   using ATP to  

Selenocysteinyl tRNA makes  ,  ,  , and 

Pheylalanine is the precursor for  

Phenylalanine is converted into tyrosine using   and cofactor  

Phenylalanine to tyrosine occurs using enzyme   with a gene symbol  

THB is formed using   and  

Classical Phenylketonuria
(PKU)=   deficiency

PKU is an autosomal recessive disorder that causes  , light pigmentation, gait issues low IQ, epilepsy, etc...

3 proudtcs accumulates in PKU  ,  ,  

In PKU (PHU deficinecy), you would want to have low  and high   in the diet.

In non-classical, there is people who cannot make   (THB)
In order to fix this, take 

Consumption of a Large numbers of neutral amino acids LNAA can also be used to address the  

Accumulation of
 , which upon
accumulation forms dark
brown polymer, gets
deposited into joints, causing
arthritis.

Methionine + adenosinetripphosphate forms s-adenosylmethionine (SAM) using enzyme  

SAM combines with an  , transfers a  , and becomes results in a   and  

Creatinine recieves phosphate from ATP when there is   to store it in cardiac muscles, brain, etc.

Guanidoacetic acid
Methylated Product:   Metabolic Pathway:  

Phosphatidyl ethanolamine
Methylated Product:   Metabolic Pathway:  

Norepinephrine
Methylated Product:   Metabolic Pathway:  

rRNA & tRNA

Methylated Product:   Pathway:  

Protein bound lysine
Methylated Porduct:  Pathway:  

The precursors of carnitine are   and  

Histones (Chromatin)
Products:  
Pathway:  

DNA CpG islands Gene Expression
Products:  
Pathway:  

N‐Acetylation: (Many Proteins at the
Amino Terminal end residues such as
Met, Ser, etc…) Comes from  

• N‐Methylation: (Histones on   and
  Residues)

N‐Ubiquitination: (  on  
Residue)

O‐Phosphorylation: (Histones on
  Residues)

Keep   on sickle cell hemoglobin type is a new theraputic method for sickle cell anemia

Lysein is methylated to   to  to 

Arginine is methylated until the   is formed

Defect in  , results in
the accumulation of homocysteine and
methionine in the blood and homocystine
in the urine.
Symptoms include skeletal abnormalities,
thrombosis and mental retardation.

Methionine + ATP is converted to SAM using  . SAM transfers a methyl and becomes  . From that step, an adenosine is lost and   forms. From there,   +   +   forms cystathionine. Gamma cystathionase + B6 then forms   +