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ANS
1. AUTONOMIC NERVOUS SYSTEM
JAMIA HAMDARD
CENTRE FOR CLINICAL AND TRANSLATIONAL RESEARCH,
SCHOOL OF CHEMICAL AND LIFE SCIENCES
PRESENTED BY:
SABIYA MIRZA
SHAISTA AHMED
SNIGDHA BANERJEE
UZMA NAYEEM
3. Autonomic nervous system is an involuntary system that primarily
controls and modulates the functions of the visceral organs.
Autonomic nervous system innervates:
• Smooth muscles of the vessels
• Smooth muscles of the digestive system
• Smooth muscles of the urinary bladder and urethra
• Smooth muscles of the lower airways
• Cardiac muscle
• Sweat, digestive and lacrimal glands
• Adrenal medulla
INTRODUCTION
4. FUNCTION OF THE ANS
• Fight or flight
• Rest and Digest
• Largely co-ordinates visceral and reflexive actions
• Mostly not under conscious control (there are exceptions)
• Senses the internal environment of the body and acts
accordingly – Consists of both visceral sensory and motor
neurons
• Also called “involuntary nervous system”
8. NEUROTRANSMITTERS
• Neurotransmitters are chemical messengers that transmit
signals from a neuron to a target cell across a synapse
• Target cell may be a neuron or some other kind of cell like a
muscle or gland cell
• Necessary for rapid communication in synapse
• Neurotransmitters are packaged into synaptic vesicles -
presynaptic side of a synapse
9. CRITERIA FOR BEING A
NEUROHUMORAL TRANSMITTER
• It should be present in the presynaptic neuron.
• It should be released in the medium following nerve stimulation.
• Its application should produce responses identical to those produced
by nerve stimulation.
• Its effects should be antagonized or potentiated by other substances
which similarly alter effects of nerve stimulation.
11. ACETYLCHOLINE (ACh)
• Acetylcholine was the first neurotransmitter to be discovered
• Isolated in 1921 by a German biologist named Otto Loewi
• Uses choline as a precursor - cholinergic neurotransmitter
• Used by the Autonomic Nervous System, such as smooth
muscles of the heart, as an inhibitory neurotransmitter
• Responsible for stimulation of muscles, including the muscles of
the gastro-intestinal system
• Related to Alzheimer's Disease
12. DOPAMINE
• Is synthesized in three steps from the amino acid tyrosine
• Associated with reward mechanisms in brain
• Generally involved in regulatory motor activity, in mood,
motivation and attention
• Schizophrenics have too much dopamine
• Patients with Parkinson's Disease have too little dopamine
13. NOREPINEPHRINE (Nor Adrenaline)
• Synthesized directly from dopamine
• Direct precursor to epinepherine
• It is synthesized in four steps from tyrosine
• Norepinephrine is strongly associated with bringing our nervous
systems into "high alert”
• It increases our heart rate and our blood pressure
• It is also important for forming memories
14. GLUTAMATE
• It is an amino acid
• It the most commonly found excitatory
neurotransmitter in the brain
• It is involved in most aspects of normal brain function including
cognition, memory and learning
• Glutamate is formed from α – ketoglutarate, an intermediate of
Kreb’s cycle
15. γ-AMINO BUTYRIC ACID (GABA)
• Synthesized directly from glutamate
• GABA is the most important inhibitory neurotransmitter
• Present in high concentrations in the CNS, preventing the brain
from becoming overexcited
• If GABA is lacking in certain parts of the brain, epilepsy results
16. SEROTONIN (5-HT)
• Synthesized in two steps from the amino acid tryptophan
• Regulates attention and other complex cognitive functions,
such as sleep (dreaming), eating, mood, pain regulation
• Too little serotonin has been shown to lead to depression,
anger control etc
18. STEPS IN NEUROHUMORAL TRANSMISSION
I. IMPULSE CONDUCTION
• Resting transmembrane potential (70 mV negative inside) due to:
-high K+ permeability and concentration of axonal membrane
- low Na+ permeability and its active extrusion from the neuron
• Stimulation or arrival of an electrical impulse causes:
-sudden increase in Na+ conductance
-depolarization and overshoot (reverse polarization: inside becoming 20
mV positive)
-K+ ions then move out and repolarization is achieved
-ionic distribution is normalized during the refractory period by the
activation of Na+ K+ pump
• This Action Potential generates local circuit currents, which activate ionic
channels at the next excitable part of the membrane, and it is propagated
further without decrement
19.
20. Tetrodotoxin (from puffer fish) and
saxitoxin (from certain shell-fish)
selectively abolish increase in Na+
conductance in nerve fibres and
thus block impulse conduction
Pharmacological
viewpoint
21. II. TRANSMITTER RELEASE
2)Nerve impulse
promotes fusion of
vesicular and
axonal membranes
through Ca2+ entry
which fluidizes
membranes
1)The transmitter
(excitatory or
inhibitory) is stored in
prejunctional
nerve endings within
synaptic vesicles
3)All contents of
the vesicle (transmitter,
enzymes,other
proteins) are extruded
(exocytosis) in the
junctional cleft.
4) Modulation of the
release process:
-Transmitter itself
Activation of specific
receptors
eg. α2 and muscarinic
agonists inhibit
(ACh)release at
autonomic
neuroeffector sites
22. Pharmacological
Viewpoint
Drug targets to modify junctional
transmission
1)Proteins located on the vesicular
and axonal membranes that participate
in the docking and fusion of the
synaptic vesicles resulting in
exocytosis.
Eg.synaptotagmin, synaptobrevin,
neurexin, syntaxin and synaptophysin
2) Some mediators like NO,
prostaglandins, endocannabinoids are
synthesized on demand and reach
their target by diffusion or by active
transport.
23. III. TRANSMITTER ACTION ON POSTJUNCTIONAL
MEMBRANE
The released transmitter combines with specific receptors on the postjunctional
membrane and depending on its nature induces an excitatory postsynaptic
potential (EPSP) or an inhibitory postsynaptic potential (IPSP)
EPSP
•Increase in permeability
to cations
•Na+ or Ca2+ influx
•Causes depolarization
followed by K+ efflux
•Passive ionic
movements as the flow is
down the concentration
gradients
IPSP
•Increase in permeability
to anions
•Cl- influx
•Increase in selective
permeability to K+ ions,
which move out
•Causes hyperpolarization
of the membrane
24. IV. POSTJUNCTIONAL ACTIVITY
• Neurotransmitter release into the nerve or nerve effector cell
• This combines with the receptor present on the post junctional
membrane, this causes increase in ionic permeability
• When EPSP is generated, it initiates a propagated nerve action
potential in the post junctional nerve
• When an IPSP is initiated, it opposes the simultaneous excitatory
potentional at the post junctonal site
25. V. DESTRUCTION OF THE TRANSMITTERS
After the transmitter serves the function it is either destroyed
enzymatically or removed
26.
27. COTRANSMISSION
Release of more than one neurotransmitter from the same
nerve terminal
On being released by nerve impulse the
cotransmitter may:
• modify responsiveness of the effector to the
primary transmitter or substitutes for it
• act on prejunctional receptors and modulate release of
the transmitters
28. REFERENCES
• Essentials of Medical Pharmacology, sixth edition, KD Tripathi.
• The Sympathetic and Parasympathetic Nervous Systems cartoon
https://youtu.be/S62DBpjS1EI
• https://www.britannica.com/science/autonomic-nervous-system
• R Bankenahally, MBBS DA FRCA FCAI, H Krovvidi, MBBS MD
FRCA, Autonomic nervous system: anatomy, physiology, and
relevance in anaesthesia and critical care medicine, BJA Education,
Volume 16, Issue 11, November 2016