This document presents information about the neurotransmitter GABA (gamma-aminobutyric acid). It discusses that GABA was first identified as an amino acid in plants and microorganisms in the 19th century, and was isolated from mouse brain in the 20th century. It also notes that in 1950, Robert and Frankel discovered that GABA acts as an inhibitory neurotransmitter in the human brain. The document provides brief descriptions of how GABA is synthesized from glutamic acid by the enzyme GAD, stored in synaptic vesicles, and released into the synaptic cleft upon neuronal stimulation.

1. G A B A -
N E U R O T R A N S M I T T E R
( g a m m a - a m i n o
b u t y r i c a c i d )
P R E S E N T E D B Y :
N O O R A F S H A N M E M O N ( B M - 8 6 - 2 0 1 8 )
R I M S H A A Z M AT ( B M - 8 7 - 2 0 1 8 )
A I S H A JA M A L I ( B M - 8 5 - 2 0 1 8 )

2. G A B A ( g a m m a - a m i n o - b u t y r i c
a c i d )
• is an inhibitory neurotransmitter that is very widely distributed
in the neurons of the cortex.
• GABA contributes to motor control, vision, and many other
cortical functions. It also regulates anxiety or fear.
• it calms the activity of brain.

3. D I S C O V E R Y O F G A B A :
• in 19th century, it was
known as the metabolite of
plants & micro organisms.
• in 20th century , through
the process of
chromatography it was
isolated as amino acid from
the brain of the mouse.
• In 1950, Robert & Frankel
discovered that GABA acts
as a inhibitory
neurotransmitter in human
brain.

4. •Synthesized from amino acid (L- glutamic acid) In the
presence of GAD.
•Glutamic acid decarboxylase ( GAD ) present in
neurons, pancreatic cells & in body fluid.
• GAD acts as a catalyst that removes carboxyl group
from glutamate and produces GABA.
S Y N T H E S I S O F G A B A :

5. S TO R A G E O F G A B A :
• Newly synthesized GABA is stored in synaptic vesicle by
means of vesicular transporter.
•These are stored at post synaptic terminal until action
potential is released.
R E L E A S I N G O F G A B A :
•The stored GABA releases into synaptic cleft stimulated by
depolarization of pre synaptic neurons.
•GABA diffuses across the cleft to target receptors on post
synaptic surface.
•The action of GABA is terminated by presynaptic nerve
terminal & glial cells

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