1What are the the 8 excitatory neurotransmitters?
, , , , , ,
What are the the 8 excitatory neurotransmitters?
Acetylcholine, aspartate, dopamine, histamine, norepinephrine, epinephrine, glutamate, 5‐ hydroxytryptamine (serotonin)
2What are 3 inhibitory neurotransmitters?
1.
2.
3.
What are 3 inhibitory neurotransmitters?
1. Glycine
2. Taurine
3. GABA
3What are the 4 stages of neurotransmission?
1.
2. : Calcium activates the release of Ach on to Ach receptors. Binding of neurotransmitters causes depolarization (Na+/K+)
3. : Metabolic degredation of Ach in synaptic cleft
What are the 4 stages of neurotransmission?
1. Resting
2. Excitation: Calcium activates the release of Ach on to Ach receptors. Binding of neurotransmitters causes depolarization (Na+/K+)
3. Termination: Metabolic degredation of Ach in synaptic cleft
4In the case of neurotransmitter
, it is taken up into ,
before it is
In the case of neurotransmitter
serotonin, it is taken up into presynaptic neuron (Reuptake),
before it is degraded
5 are supporting, neuronal cells that maintains the normal
physiology of the nervous system
Glial Cells are supporting, neuronal cells that maintains the normal
physiology of the nervous system
6Oligodendrocytes provide the that insulate the axon.
Oligodendrocytes provide the fatty myelin
sheaths that insulate the axon.
7When the axonal connections die
off it results in
(movement and balance
disruptions as well as vision
imbalance). (influenced by lack of )
When the axonal connections die
off it results in Multiple Sclerosis
(movement and balance
disruptions as well as vision
imbalance). (influenced by lack of oligodendrocytes)
8-Microglia protects the neuron from infection through phagocytosis. The microglia are activated by inflammatory signals
-The signals from the damaged cells include
-Microglia protects the neuron from infection through phagocytosis. The microglia are activated by astrocyte inflammatory signals TNF-alpha, IL-6, and NO
-The signals from the damaged cells include ATP and CX3CL1
9What is an example of something that is trans acetylated? What is the effect?
Histones. Acetylation if histones activates them.
10 can be used in neurotransmitter synthesis.
Acetyl CoA can be used in neurotransmitter synthesis.
11Acetylcholine causes the opening of
channels in nerve after a nerve stimulus
Acetylcholine causes the opening of
Na+/K+ channels in post synaptic nerve after a nerve stimulus
12 is one of the fastest enzymes. Such a high turnover
is expected, since recovery from depolarization occurs within seconds.
Acetylcholinesterase is one of the fastest enzymes. Such a high turnover
is expected, since recovery from depolarization occurs within seconds.
13choline goes to acteyl coline using
choline goes to acteyl coline using
choline acteyltrasnferase + CoA 
14acteylcholine is degraded and becomes + by a reaction using
acteylcholine is degraded and becomes
choline +
acetate by a
hydrolysis reaction using
cholinesterase 
15 , ,
: competes with
acetylcholine receptor.
Tubocurarine, alpha‐bungarotoxin,
cobra toxin: competes with
acetylcholine receptor.
16Physostigmine and neostigmine
inhibit by
carbamoylating residue at
the active site.
Physostigmine and neostigmine
inhibit acetylcholinesterase by
carbamoylating serine residue at
the active site.
17DIPF (organophosphate) reacts
with active site and
modifies the enzyme.
DIPF (organophosphate) reacts
with active site serine and
covalently modifies the enzyme.
18DIPF reacts with the active site serine and covalently modifies enzyme
DIPF reacts with the active site serine and covalently modifies enzyme irreveseribly
19Receptor targeted inhibitors (alpha bungartoxin, cobra toxin, etc) function as
Receptor targeted inhibitors (alpha bungartoxin, cobra toxin, etc) function as comptetive inhibitors
20 and and have selenocystine
Glutathione peroxidase and deiodinase and have selenocystine
21What is the universal methyl group donor?
SAM
22Methionine is a amino acid
Methionine is a conditional amino acid
23Proline is synthesized from
Proline is synthesized from glutamate
24Glutamate becomes using and . It then forms a intermediate. Using a and , it forms .
Glutamate becomes
glutamate semialdehyde using
ATP and
NADH. It then forms a
gamma pyroline 5 carboxylate intermediate. Using a
reductase and
NADPH, it forms
proline.

25Hydroxylation of occurs as a
posttranslational modification (hydroxylases
require (ascorbate, lack of it
causes Scurvy).
Hydroxylation of proline occurs as a
posttranslational modification (hydroxylases
require Vitamin C (ascorbate, lack of it
causes Scurvy).
263‐hydroxyproline and 4‐hydroxyproline are
found in .
3‐hydroxyproline and 4‐hydroxyproline are
found in collagen.
27Glutathione peroxidase contains
Glutathione peroxidase contains selenocysteine.
28In the mRNA for selenoproteins, the codon , which generally serves as a termination codon, codes for selenocysteine
In the mRNA for selenoproteins, the codon UGA, which generally serves as a termination codon, codes for selenocysteine
29Selenocysteinyl-tRNA is added to ribosomes to make
Selenocysteinyl-tRNA is added to ribosomes to make selenoproteins.
30Selenocysteinyl tRNA is formed by adding using ATP to
Selenocysteinyl tRNA is formed by adding
selenide using ATP to
seryl-tRNA 
313 examples of seleno proteins are , , and
3 examples of seleno proteins are glutathione peroxidase, deiodinase, and thioredoxin reductase
32 is used to convert any hormone into more active form (i.e. T4 to T3).
Deiodinases is used to convert any hormone into more active form (i.e. T4 to T3).
33Phenylalanine becomes using and and
Phenylalanine becomes
tyrosine using
phenylalanine hydroxylase and
THB and
O2 
34THB is formed using and
THB is formed using GTP and beneficial bacteria
35The gene symbol for phenylalanine hydroxylase is
The gene symbol for phenylalanine hydroxylase is PAH
36PAH deficiency leads to classical
PAH deficiency leads to classical PKU
37PKU results in the accumulation of the products , , and
PKU results in the accumulation of the products phenylalanine, phenylpyruvate, and pheyllactate
38PKU results in a (core unique symptoms), light
pigmentation; peculiarities of
gait, stance, and sitting posture;
eczema; and epilepsy
PKU results in a mousy odor (core unique symptoms), light
pigmentation; peculiarities of
gait, stance, and sitting posture;
eczema; and epilepsy
39PKU is an
PKU is an autosomal recessive disorder
40In PKU (PHU deficinecy), you would want to have low and high in the diet.
In PKU (PHU deficinecy), you would want to have low Phe and high Tyr in the diet.
41In non-classical PKU, there are people who cannot make
In order to fix this, take
In non-classical PKU, there are people who cannot make biopterin supplement (THB)
In order to fix this, take Kuvan/sapropterin
42Consumption of a Large numbers of neutral amino acids LNAA can also be used to address the
Consumption of a Large numbers of neutral amino acids LNAA can also be used to address the non-classical pathway
43Tyrosine becomes which then can form
Tyrosine becomes
homogentistate which then can form
fumarate and acetoacetate 
44Lack of will cause which is the build up of homogenistate
Lack of
oxygenase will cause
alcaptonuria which is the build up of homogenistate

45Accumulation of
homogentisate, which upon
accumulation forms dark
brown polymer, gets
deposited into joints, causing
Accumulation of
homogentisate, which upon
accumulation forms dark
brown polymer, gets
deposited into joints, causing
arthritis
46SAM is formed from
SAM is formed from methionine
47Methionine + ATP come together to form using
Methionine + ATP come together to form SAM using methionine adenosyltransferase
48SAM is the main
SAM is the main methyl trasnferase
49Methyl Group Acceptor
Guanidoacetic acid
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
Guanidoacetic acid
Methylated Product
Creatine phosphate
Metabolic Pathway
Creatine synthesis
50Methyl Group Acceptor
Phosphatidyl ethanolamine synthesis
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
Phosphatidyl ethanolamine synthesis
Methylated Product
Phosphatidyl choline
Metabolic Pathway
Phospholipid
51Methyl Group Acceptor
Norepinephrine
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
Norepinephrine
Methylated Product
Epinephrine
Metabolic Pathway
Catecholamine
52Methyl Group Acceptor
rRNA & tRNA
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
rRNA & tRNA
Methylated Product
Methylated RNA
Metabolic Pathway
RNA synthesis
53Methyl Group Acceptor
Protein bound lysine
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
Protein bound lysine
Methylated Product
Trimethyl lysine
Metabolic Pathway
Carnitine synthesis
54Methyl Group Acceptor
Histones (Chromatin)
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
Histones (Chromatin)
Methylated Product
Methyl Lys or Arg of histones
Metabolic Pathway
Chromatin Modelling
55Methyl Group Acceptor
DNA
Methylated Product
Metabolic Pathway
Methyl Group Acceptor
DNA
Methylated Product
CpG islands
Metabolic Pathway
Gene Expression
56 : (Many Proteins at the
Amino Terminal end residues such as
Met, Ser, etc…
N‐Acetylation: (Many Proteins at the
Amino Terminal end residues such as
Met, Ser, etc…
57 : (Histones on Lys and
Arg Residues)
N‐Methylation: (Histones on Lys and
Arg Residues)
58 : (Histones on Lys
Residue)
N‐Ubiquitination: (Histones on Lys
Residue)
59 : (Histones on
Serine Residues) -> adds potential energy to a protein
O‐Phosphorylation: (Histones on
Serine Residues) -> adds potential energy to a protein
60Histones are methylated on and
Histones are methylated on lysine and arginine
61Methionine + ATP is converted to SAM using . SAM transfers a methyl and becomes . From that step, forms. From there, + forms cystathionine. Gamma cystathionase + B6 then forms + (can then become )
Methionine + ATP is converted to SAM using
MAT (methionine adenosyltransferase) . SAM transfers a methyl and becomes
S-adenohomocysteine. From that step,
homocysetine forms. From there,
cystathionine B-synthase +
vitamin B6 forms cystathionine. Gamma cystathionase + B6 then forms
cysteine +
alphaketobutyrate (can then become
propinoyl CoA)

62Defect in cystathionine synthase, results in
the accumulation of and
in the blood and
in the urine. Symptoms include skeletal abnormalities,
thrombosis and mental retardation.
Defect in cystathionine synthase, results in
the accumulation of homocysteine and
methionine in the blood and homocystine
in the urine. Symptoms include skeletal abnormalities,
thrombosis and mental retardation.
63Problems with the enzyme , , or addition of causes homocystinuria.
Problems with the enzyme cystathionine B-synthase, vitamin B6, vitamin B12 or addition of serine causes homocystinuria.
64Problems with the enzyme or causes cystathionuria
Problems with the enzyme gamma cystathionase or vitamin B6 causes cystathionuria
65To make succinyl CoA from propinoyl COA is done using and
To make succinyl CoA from propinoyl COA is done using methyl malonyl mutase and B12
66To regenerate methionine from homocystesine, you need , , and
To regenerate methionine from homocystesine, you need methione synthase, B12, and N5-CH3-THF
67In the regeneration of methionine from homocystine can have a methyl group donated from either a or
In the regeneration of methionine from homocystine can have a methyl group donated from either a serine or glycine
68Only 2 enzymes require B12 as cofactor: and
Only 2 enzymes require B12 as cofactor: methionine synthase and methyl malonate mutase
69Sulfur amino acids can oxidize two cysteines to make a disulfide bond
(between 2 cysteines makes , 2 homocysteines become )
Sulfur amino acids can oxidize two cysteines to make a disulfide bond
(between 2 cysteines makes cystine, 2 homocysteines become homocystine)
70-Cystinuria: Defect in membrane transport of
through epithelial cell
-Cysteine gets oxidized to which has poor
solubility and it precipitates in the urinary tract
and forms .
-Cystinuria: Defect in membrane transport of
dietary cysteine through epithelial cell
-Cysteine gets oxidized to cystine which has poor
solubility and it precipitates in the urinary tract
and forms kidney stones.
71Homocysteine can form homocysteinethiolactone. This is a reactive intermediate that
which aggregates and eventually forms .
Homocysteine can form homocysteinethiolactone. This is a reactive intermediate that thiolates LDL
which aggregates and eventually forms atheromas.
72Tryptophan degradation gives you as a byproduct and and as products
Tryptophan degradation gives you
formate as a byproduct and
glutarate and
niacin (B3) as products

73Valine and Isoleucine are broken down into (which then becomes that can enter ). Leucine becomes because it is .
Valine and Isoleucine are broken down into
propinoyl coa (which then becomes
succinyl CoA that can enter
TCA). Leucine becomes
acteyl CoA because it is
ketogenic.

74The enzyme used to break down valine, isoleucine, and leucine is
The enzyme used to break down valine, isoleucine, and leucine is
BCAA dehydrogenase 
75BCAA dehydrogenase reqires
BCAA dehydrogenase reqires
thiamin (B1), lipoic acid, CoA (B5), riboflavin B2, and Niacin B3 
76Maple Syrup Disease
Symptoms: Urine has maple syrup odor, vomiting, brain damage
Treatment: Reduced in diet
Type of disorder:
Maple Syrup Disease
Symptoms: Urine has maple syrup odor, vomiting, brain damage
Treatment: Reduced
branched chain amino acids in diet
Type of disorder:
Autosomal recessive 
77Propinoyl CoA makes , , , and on being degraded.
Propinoyl CoA makes methionine, threonine, isoleucine, and valine on being degraded.
78Methylmalonic acidemia is a deficiency in or . Causes metabolic acidosis and mental retardation.
Methylmalonic acidemia is a deficiency in
methyl malonyl CoA mutase or
vitamin B12. Causes metabolic acidosis and mental retardation.

79Histidine breaks down into and from using
Histidine breaks down into
glutamate and
N-Foramino THF from
N-foramino gultamate using
THF 
80The enzyme histidase is highly expressed in and . In skin,
is one of the components of .
The enzyme histidase is highly expressed in skin and liver. In skin,
urocanate is one of the components of sweat.
81Lysine is to form (required for of fatty acids)
Lysine is trimethylated (3 SAM) to form carnitine (required for B oxidation of fatty acids)
82Phosphocreatine is an
Phosphocreatine is an energy storage molecule
83Glycine + Arginine yields and with becomes which then forms using
Glycine + Arginine yields
Guanidinoacetate and with
SAM becomes
Creatine which then forms
Phosphocreatine using
ATP 
84What are the 3 componenents of folic acid (vitamin B9)?
1. Pterydine ring
2. PABA
3. Polyglutamate
85Microorganisms converts and
into folic acid. Humans
synthesize folic acids. Folic acid is an
.
Microorganisms converts pteridine
precursors and para‐aminobenzoic acid
into folic acid. Humans cannot
synthesize folic acids. Folic acid is an
essential vitamin.
86Folic acid synthesis is inhibited by
(anti microbial agent).
Folic acid synthesis is inhibited by
sulfonamides (anti microbial agent).
87Methotrexate blocks dihydrofolate reducatse from to
Methotrexate blocks dihydrofolate reducatse from
DHF to
THF 
88THF is a carbon carrier
THF is a one carbon carrier
89What is the folate trap?
Responsible for trapping in the
What is the folate trap?
Responsible for trapping
folic acid in the
N5 methyl THF form 
90The folate trap leads to insufficent formation of due to
The folate trap leads to insufficent formation of
methionine due to
B12 deficiency 
91The folate trap leads to inhibition of which does conversion of to . Inhibition causes .
The folate trap leads to inhibition of
thymidylate synthase which does conversion of
dUMP to
dTMP. Inhibition causes
slowed cell division .

92Serine + THF produces
Serine + THF produces
glycine + N5-N10-Methylene THF 
93Glycine produces
1.
2.
3.
4.
5.
Glycine produces
1. Heme
2. Serine
3. Purine
4. Collagen
5. One carbon donors
94Taurine is produced from
Taurine is produced from
cysteine 