I was greatly appreciated :)

2. Presented by:
Kritika Sarkar
B.D.S. Final year

3.  Neuro- anatomy
 The neuron.
 Definition.
 Classification.
 Structure of sensory neuron.
 The configuration of neurons.
 Electrophysiology of nerve conduction.
 Electrochemistry of nerve conduction.
 Resting potential.
 Membrane excitation:
 Depolarization.
 Repolarization.
 Impulse propagation.
 Impulse spread.
 Unmyelinated nerves.
 Myelinated nerves.
 Physiology of peripheral nerves.

4.  Pain.
 Definition.
 Theories.
 Physiology (Pathway).
 Mediators.
 Receptors.

5. It is the structural &
functional unit of the
nervous system.
It transmits messages b/w
the CNS and all parts of the
body.

7.  Depending upon the function:
 Sensory (afferent)
 Motor (efferent).
 Relay (Interneuron).
 Depending upon number of poles:
 Unipolar neurons.
 Bipolar neurons.
 Multipolar neurons.
 Depending upon the length of axon:
 Golgi type I.
 Golgi type II.

10.  They are capable of transmitting
pain & consist of 3 main parts.
1. Dendritic zone-most distal
segment, respond to
stimulation, provoking an
impulse centrally in the axon.
2. Axon-thin cable like structure
which has similar arborizations
like that of the dendrites. They
may be quite long (giant squid
axon measures 100-200 cm)
3. Cell body-it is located away from
the axon/the main pathway of
impulse transmission in the
nerve. Its main function is to
provide vital metabolic support.

11.  Axon is the long cylinder of neural cytoplasm
(axoplasm) encased in a thin sheath, the nerve
membrane (axolemma).
 The axoplasm, a gelatinous substance, is separated from
extracellular fluids by continuous nerve membrane.
 In some nerves this membrane is itself covered by an
insulating lipid rich layer of myelin.
 The membrane consists of bi-lipid layer of
phospholipids, associated proteins, lipids &
carbohydrates.
 The lipids are oriented with their hydrophilic/polar ends
facing the outer surface & the hydrophobic/non-polar
ends projecting in the middle of the membrane.

12. •Proteins are visualized as the primary organizational
elements of membranes.
•They are classified as:
•Transport proteins (channels, carriers or pumps)
•Receptor sites.
•Channel proteins are thought to be continuous pores
through the membrane, allowing some ions (Na+, K+, Ca++)
to flow passively, whereas other channels are
“gated”, permitting ion flow only when the gate is “open”.
•Some nerves are covered with lipid layer of myelin.
•The Myelinated nerve fibers are enclosed in spirally
wrapped layers of lipoprotein myelin sheaths, which are
actually a specialized form of Schwann cell.
•There are constrictions at regular intervals (approx. 0.5-0.3
mm) along the myelinated nerve fibers- NODES OF
RANVIER.

13.  The function of the nerve is to carry messages in the form
of electrical action potentials, which are called impulses.
 Action potentials are transient depolarization of the
membrane that result from a brief increase in the
permeability of the membrane to sodium, & usually also
from a delayed increase in the permeability to potassium.

14. Resting potential
Rapid Repolarization
(0.7 msec)
Slow Depolarization
(0.3 msec)
Stimulus
Resting
potential

15.  Resting state- in its resting state the nerve
membrane is:
 Slightly permeable to Na+ [Na+ migrates inwardly
because both the concentration(greater outside) & the
electrostatic gradient favor such migration. Resting
membrane is relatively impermeable to Na+ prevents
massive influx of the ion.]
 Freely permeable to K+ [It remains in the axoplasm,
despite its concentration gradient, because the
negative charge of the nerve membrane restrains the
positively charged ions by electrostatic attraction.]

16.  Excitation of a nerve segment leads to an increase in permeability of
the cell membrane to sodium ions.
 The rapid influx of sodium ions to the interior of the nerve cell causes
depolarization of the nerve membrane from its resting level to its firing
threshold of approximately -50 to -60 mV.
 A minimum 15 mV voltage potential is required to generate an action
potential.
Firing threshold – the magnitude of
the decrease in negative
transmembrane potential that is
necessary to initiate an action
potential (impulse).

17.  The action potential is terminated when the membrane
repolarized.
 This is caused by the extinction of increased permeability
to Na+.
 In many cells permeability to K+ increases, resulting in
influx of K+, & leading to a more rapid membrane
repolarization & return to its resting potential.

18. Na+ diffuses into the cell and K+ diffuses out of the cell
BUT, membrane is 75x’s more permeable to K+ than Na+
Thus, more K+ diffuses out than Na+ diffuses in
This increases the number of positive charges on the outside of the membrane
relative to the inside.
BUT, the Na+-K+ pump carries 3 Na+ out for every 2 K+ in.
•Number of charged molecules and ions inside and outside cell nearly equal
concentration of K+ higher inside than outside cell, Na+ higher outside than inside.
•Potential difference: unequal distribution of charge exists between the immediate inside and immediate outside of the plasma
membrane: -70 to -90 mV.

19.  A stimulus excites the nerve, leading to the following sequence of events:
A. An initial phase of slow depolarization. The electrical potential within the
nerve becomes slightly less negative.
B. When the falling electrical potential reaches a critical level, an extremely
rapid phase of repolarization results. This is termed as threshold potential,
or firing threshold.
C. This phase of rapid depolarization results in a reversal of the electrical
potential across the nerve membrane. The interior of the nerve is now
electrically positive in relation to the exterior. An electrical potential of +40
mV exists on the interior of the nerve cell.

20.  After these steps of depolarization, repolarization occurs.
 The electrical potential gradually becomes more negative
inside the nerve cell relative to outside until the original
resting potential of -70mV is again achieved.
 The entire process requires 1 millisecond :
 Depolarization=0.3 msec.
 Repolarization=0.7 msec.

22. Current flows from
Transmembrane
Stimuli depolarized to
potential
resting segment
Production of local Action potential in
Disruption of RMP
current the next segment
Cell’s interior: -ve Cell’s exterior: +ve
Carried on……
to +ve to –ve

23. In myelinated & un-myelinated nerve fibers.

24. Fiber class Subclass Myelin Function
A + Motor, propioception
+ Motor, propioception
+ Muscle tone
+ Pain, temperature, touch
B + Various autonomic functions
C sC - Various autonomic functions
d C - Various autonomic functions; pain,
temperature, touch

26. An unpleasant emotional experience
usually initiated by a noxious
stimulus & transmitted over a
specialized neural network to the
CNS where it is interpreted as such.

27. Theories

28.  Classical description was provided by Descartes in 1644, when he
conceived pain system as a straight through channel from skin to the
brain.
 The concept changed little until 19th century when Muller postulated
the theory of information transmission only by the way of sensory
nerves.
 Von Frey developed the concept of specific cutaneous receptors for the
mediation of touch, heat, cold & pain.
 Free nerve endings were implicated as pain receptors.
 A pain centre was thought to exist within the brain, which was
responsible for the development of all overt manifestations of the
unpleasant experience.

29.  In 1894 Goldscheider was the 1st to propose that stimulus intensity &
central summation are the critical determinants of pain.
 The theory suggested that particular patterns of nerve impulses that
evoke pain are produced by summation of sensory input within the
dorsal horn of the spinal column.
 Pain results when the total output of cells exceeds a critical level.
 For example, touch plus pressure plus heat might add up in such a
manner that pain was the modality experienced.

30.  The gate control theory, proposed by Melzack & Wall in 1965 & recently
reevaluated, is presently receiving considerable attention.
 Although the theory may be simply stated, its ramifications are extremely
complex.
 The gate control theory postulates:
1. Information about the presence of injury is transmitted to the CNS by small
peripheral nerves.
2. Cells in the spinal cord or nucleus of 5th cranial nerve, which are excited by
these injury signals, are also facilitated or inhibited by other large peripheral
nerves that also carry information about innocuous events.
3. Descending control systems originating in the brain modulate the excitability
of cells that transmit information about injury.
 Therefore the brain receives messages about injury by the way of the gate
control system, which is influenced by:
1. Injury signals.
2. Other types of afferent impulses &
3. Descending control.

33. Cyclooxygenase
pathway
• vascular
permeability.
•sensitizes nociceptor

34.  Cell injury  tissue acidity  Kallikrein  Bradykinin  vascular permeability
 activates nociceptor
 synthesis & release of prostaglandins
 Substance P (released by free nerve endings)  sensitize nociceptor
 vascular perm., plasma extravasation
(neurogenic inflammation)
 releases histamine (from mast cells)
 Calcitonin gene related peptide (free nerve endings)  dilation of peripheral capillaries
 Serotonin (released from platelets & damaged endothelial cells)  activates nociceptor
 Cell injury  potassium  activates nociceptor.

35.  Sensory nerve endings that mediate pain (nociceptor) are
actually chemo receptors. It is currently believed that there are
both mechano-receptive & chemo-receptive nociceptors.
 Criteria for a substance to be classified as a chemical pain
mediator are:
 General accessibility & activation as a consequence of
injury, infection or mechanical tissue damage.
 Suppression of mediator formation resulting in prevention of pain
fiber activation.
 Easy formation from labile precursors, release from sensitive storage
sites, and short half-life.
 Pain caused by exogenous application onto nociceptors.
 All criteria are met within the dental pulp by the
peptide, substance P. In other parts, other chemical agents are
significant, with bradykinin being one of the most active.

36.  Monheim’s Local anesthesia & pain control in dental practice (7th
edition).
 Malamed’s Handbook of local anesthesia.
 Ganong’s review of Medical physiology.
 Textbook of medical physiology by Guyton & Hall.
 www.iasp-pain.org
 www.google.com
 www.bioalive.com
 www.ncbi.org
 www.wikipedia.org
 www.slideshare.net
Thank you!