Neuroscience Biochemistry Page 1 of 14

Neuro Biochem
By
Nabeerah Israr
D’24

Nabeerah Israr
Dowite’ 24
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Nabeerah Israr
Dowite’ 24
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“Neurotransmitters”

chemicals responsible for signal transmission between the nerve cells.

CNS have more than 50 Neurotransmitters. While PNS has just 2

neurotransmitters:

Acetylcholine Norepinephrine

“Criteria to classify substances as Neurotransmitters”

must be present in presynaptic terminal, pakaged in synaptic vesicles

must be released via exocytosis from nerve terminal on arrival of action

potential

specific receptors mist be present on post synaptic membrane.

“Synthesis of Neurotransmitters”

Histidine Histamine

Choline Acetylcholine

Tyrosine Dopamine Norepinephrine Epinephrine

Tryptophan 5-hydroxytraptamine Melatonin

Arginine Nitric Oxide

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“Chemical Classification of Neurotransmitter”

1. ACETYLCHOLINE

2. BIOGENIC AMINES
Catecholeamines (Dopamine, Norepinephrine, Epinephrine)

Serotonin

Histamine

3. AMINO ACIDS

GABA
(major inhibitory neurotransmitter in brain; derived from Glitamic Acid)

Glycine

Aspartate

Glutamate (excitatory transmitter in CNS~ 75%)

4. NEUROPEPTIDES
Substance P (pain transmission)

Endorphins and Enkephilins

Somatostatin, Gastrin, Oxytocin, Vassopressin, LH Releasing Hormone

5. PURINES
Adenosine

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ATP

6. GASES & LIPIDS

NO

CO

Cannabiniods

⭐⭐⭐⭐⭐⭐

ACETYLCHOLINE

Most abundant in BRAIN

Excitatory EXCEPT at parasympathetic endings of vagus nerve at cardiac

plexus.

released at:-
1. Neuromuscular Junction
2. preganglionic neurons of ANS (both symp + para symp)
3. Post ganglionic neurons of Parasympathetic neurons
Degraded by enzyme Ach Esterase (AchE)

“CHOLINERGIC RECEPTORS”
NICOTINIC RECEPTORS:
Location:
1. Autonomic Ganglia (Sympathetic + Parasympathetic)
2. Skeletal Muscles

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Agonist:
1. Ach 2. Nicotine

Antagonist:

Curare; competitive inhibitor at neuromuscular junction (nicotinic receptors)

Botulinum; binds presynaptic terminal and decreasing the release of Ach

containing vesicles. (It is also used in Botox Injection, uncintrolled blinking of eye
to treat muscle spasm.)
Thus Both are causing Flaccid Muscle Paralysis.

MUSCARINIC RECEPTORS:
Location:
1. Lacrimal, Salivary and Gastric Glands
2. Smooth M. (Bronchial, GI, Blood Vessels)
3. Heart (SA Node, AV Node)

Agonist:
1. Ach 2. Muscarine
Antagonsit:

Atropine blocks muscarinic receptor; used in opthalmic solutions and

ointments; from belladoma plant

SYNTHESIS:
In presynaptic neuron

Choline + Acetyl CoA Acetylcholine

Choline Acetyl Transferase (ChAT) — enzyme

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Sources of Choline:
a. Exogenous (Folic Acid, Vit B12)
b. Endogenous (from synaptic cleft, synthesized by Glycine, hydrolysis
of phosphatidyl choline, sphingomyelin)

Degradation:
By Acetylcholinesterase (AchE) found at post synaptic neuromuscular junction;
convert it into:
Choline: which is taken back by presynaptic nerve.

Accetate: which is is also taken back and converted into Acetyl CoA by Accetae
CoA Ligase.

Myasthenia Gravis

Aquired Autoimmune disease

Auto Ab against the Ach receptor (nicotinic) at Neuromuscular Junction

Symptoms: Diplopia, Ptosis, dysarthria, Dysphagia, limited faciao expressions

Neostigmine/Pyridostigmine is given to patient resulting in decresed

hydrolysis of Ach by AchE.

Alzheimer’s Disease

Neurodegenerative diorder

learning and memory impairment

Associated with Lack of Ach.

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⭐⭐⭐⭐⭐⭐

CATECHOLEAMINES

Dopamine, Nirepinephrine, Epinephrine

Synthesized by Tyrosine

Phenylalanine Tyrosine Dihydroxy Phenylalanine (DOPA) Dopamine

Norepinephrine Epinephrine

Phenyl ethanol amine-N-Methyl Transferase catalyze the conversion of NE

into Epinephrine; this enzyme is only present in Adrenal Medulla

DOPAMINE

Monoamine Neurotransmitter

High Conc. In:

a. Corpus striatum
b. Frontal cortex
c. Limbic system
d. Hypothalamus

Dopaminergic Pathways:
a. Mesolimbic
(associated with pleasure & reward)
b. Mesocortical
(Motivational & emotional responses)
c. Nigrostriatal
(ccordination of movement)
d. Tubuloinfundibular
(prolactin release + maternal behaviour)

Functions:

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a. Role in Movement
b. Pleasure and Motivation
c. Learning
d. Controls flow of information

Inactivation:
Reuptake
Degradation:
a. MonoAmineOxidase (MAO)
b. Catechol-O-Methyl Transferase (COMT)
c. Aldehyde Dehydrogenase (ALDH)
End product is Homovanillic Acid (HVA).

D1 Like Receptors:

a. Gs coupled (stimulatory) Adenylate cyclase Activate cAMP inc.

b. D-1 c. D-5

D2 Like Receptors:
a. Gi coupled (inhibitory)
b. D-2 c. D-3 d. D-4

Parkinson’s Disease

Progressive neurodegenerative disease

Pyramidal and Extra Pyramidal Tracts are involved

Parkinsonism is a clinical syndrome consisting of 3 cardinal symptoms:
1. Resting tremor
2. Bardykinesia
3. Muscke rigidity
Anteroflexed head and flexed knees and elbows
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Treatment

L-Dopa along with Carbidopa

Carbidopa doesnot cross BBB thus inhibits peripheral cinversion of DOPA into
dopamine.

Schizophrenia

Excessive Dopamine in the frontal lobes.

Hallucinations, Delusions, disorganized thinking, losing interest.

⭐⭐⭐⭐⭐⭐

SEROTONIN
(5-Hydroxy Tryptamine)
Monoamine Neurotransnitter derived from Tryptophan.

Found in:
a. GI Tract (90% of the body’s serotonin in enterochrimaffin cells)
b. Platelets
c. CNS
Functions:

a. Contribute in Feeling of well being and hapiness

b. Regulation of mood, appetite and sleep
c. Memory and learning🧠
d. Vasocinstrictor (when platelets bind to clot then release serotonin)
e. Promotes confidence, relaxation amd feelinhs of personal security.

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Sources:
a. Eggs b. Cheese c. Pineapple d. Nuts aand seeds
Vitamin B6

Synthesis:
Tryptophan hydroxylation decarboxylation Serotonin N-
Acetylation Melatonin

Degradation:
Serotonin MAO (monoamine oxidase) 5-hydroxyindoleacetic acid

Serotonin and PAIN:

a. Serotonin reduces the intensity of pain signals sent to brain.
b. It helps pain gates close!
c. It is released in the area of spinal cord where substance P is released thus
counteracting it.
d. lower in women than men.
e. In Maigraine & Headache; its level are lower.

Low Serotonin Levels:

Seen in Depression, Premenstrual Dysmorphic Disorder & Irritable bowel
syndrome

Moderately Low Serotonin Levels:

Feel so sleepy
Hungry all the time
Sad and insecure
Unexplained body sensations like headaches, stomach pains etc

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Dowite’ 24
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Severly Low levels:

Super speed thoughts about you cannot control. May be about horrible
scenes from past or imagined.
Overeact to small problems
Feel terrible
Head feels like about to explode

Serotonin Syndrome
a. MILD: Increased heart rate, shivering, sweating, dialated pupils, Overactive
reflexes (clonus), mental status changes

⭐⭐⭐⭐⭐⭐

“Formation & Fate of AMMONIA”

1. Amination of Ketoglutarate
📌 Results in formation of non essential amino acids.

📌 Alpha Keto glutarate + NH4+ ⏩ GLUTAMATE DEHYDROGENASE ⏩

Glutamate + H2O

2. Amination of Glutamate to Glutamine

📌 major buffering molecule for Ammonia

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📌Glutamate + NH4+ Mg-ATP ⏩ Glutamine Synthetase ⏩ Glutamine

+ Mg- ADP + Pi

3. Deamination of Alpha Amino acids In kidney

Glutamine⏩ Glutaminase ⏩ Glutamate + (free NH3) ⏩ Glutamate
Dehydrogenase ⏩ Alpha Keto acid +(free NH3)

4. Deamination of Glutamate In kidney And Liver

Glutamate ⏩ Glutamate Dehydrogenase ⏩ Imino acid ⏩ Alpha

Keto acid +(free NH3)

5. TOXICITY OF AMMONIA & BIOCHEMICAL CHANGES IN BRAIN

1. Enhances amination of alpha ketoglutarate to glutamate to
Glutamine
2. Slow down TCA Cycle
3. Low glutamic acid ➡️ Decreased formation of GABA
4. Increased glutamine outflow from brain cells Increases the inflow of
Tryptophan (same protein allows the influx) thus increased synthesis of
serotonin (Excitatory)

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6. Effects of ammonia toxicity

Slurring of speech
Blurring of vision
Lethargy
Vomiting
Mental retardation
Coma
Death

🙂 BEST OF LUCK 🙂

Nabeerah Israr
Dowite’ 24