Introduction Mechanism Discovry

1. GABA NEUROTRANSMITTER
PARUL INSTITUTE OF PHARMACY AND
RESEARCH
Simran

2. CONTENTS
INTRODUCTION
DISCOVERY
SYNTHESIS , STORAGE AND
DEGRADATION
GABA RECEPTOR
FUNCTION
DRUG ACTING ON GABA RECEPTOR
MECHANISM OF ACTION
AGONIST AND ANTAGONIST
DEFICIENCY AND DISEASES
RERATED
CONCLUSION

3. INTRODUCTION
GAMMAAMINO BUTYRIC ACID ( GABA )
GABA Is the major neurotransmitter of the mammalian brain.
It is the broadly distributed in the brain.
Implicated in broad range of neuropsychiatric disorders like seizures , anxiety
,schizopharenia, alcohol dependence etc.
Location - all locating of CNS
Mechanism – ligand gated ion channel and G. protein coupled receptor .
Nature inhibitory

4. DISCOVERY
In 19thcentury – was know as a metabolite of
plant andmicrorganisums.
In early 20thcentury – was isolated as an
amino acid in the brain of mouse through
paper chromatography.
In 1950 Robert and Frankel discovered
GABA in brain.
GABA patches : inhibitory effects

5. SYNTHESIS , STORAGE AND DEGRADATION
Glutamine
Glutamate
Gamma Amino butyric acid (GABA)
Succinate semialdehyde
Succinate

6. SYNTHESIS , STORAGE AND
DEGRADATION

7. STORAGE AND RELEASE
• Newly synthesized GABA store in synaptic vesicle by means of
vesicular transporter.
• Store GABA release into synaptic cleft stimulated by depolarisation of
presynaptic neurons.
• GABA diffuse across the cleft to target receptor on postsynaptic
surface .
• The action of GABA is terminated by reuptake into both presynaptic
nerve terminals & glial cells.

9. FUNCTION
• Relieving anxiety.
• Improving mood .
• Relieving premenstrual syndrome (PMS).
• Regulating the release of sex hormones .
• Treating attention deficit hyperactivity disorder
(ADHD).
• Promoting lean muscle growth.
• Burning fat.
• Stabilizing blood pressure.
• Relieving pain.
• Lower elevated blood sugar levels in diabetics.

12. Mechanism of GABAA Receptor

15. Binding of GABA to the extracellular domain of
B1
Allosteric change in the B2 subunit (coupled to G
protein)
Inhibit adenylyl cyclase
Activate K+ channels
Ca2+ conductance
Se Neurotransmitter release & Action potential

18. GABA
RECEPTOR
 Agonists:
 Muscimol(amanita muscaria)
 Alcohol
 Benzodiazepines
 Barbiturates
 Antagonist:
 Picrotixin

19. DEFICIENCY AND DISEASES
RERATED
 Epilepsy – GABA decreases
GABA increases – BENZODIAZEPINS
BARBITURATES
 Anxiety – GABA decreases
GABA increases - BZD
BARBITURAYES
 USE :-
 General anesthesia – BZD
 Alcohol – BZD prevent alcohol withdrawal syndrome.
BARBITURATES
 Sedative & hypnotics : BZD
skeletal muscle relaxant : DIAZEPAM

20. CONCLUSION
 GABA is a amino acid made in brain cells
from glutamate .it function as an
inhibitory neurotransmitter , meaning it
blocks nerve impulses. without GABA ,
nerve cells fire too often too easily.

21. THANK YOU