Escolar Documentos
Profissional Documentos
Cultura Documentos
Physiology
By Dr Adeela Shahid
Professor of Physiology
SMDC
Objectives
Nervous Tissue is
composed of two type
of cells
Neurons
Neuroglial
cells
Ability
Nerve
Cable
In
Structure of a
Neuron
Cell Body / Soma
Dendrites
Axon (Nerve Fiber)
Neuron
Neurons
(continued)
Cell Body
Cell body
Has a nucleus with one or two nucleoli but
no centrosome. Lost the power of division.
Cytoplasm
Organelles
Mitochondria, ER, Ribosomes,
Lysosomes, Golgi Apparatus
Nissl bodies / Nissl granules
Composed of endoplasmic reticulum
with abundance of ribosomes. It is the
site of protein synthesis
Neurofibrils
Neurotubules
& neurofilaments
Melanin, cu, Iron
Lipofuscin
Yellow brown granular pigment
composed of lipid containing
residues of lysosomal digestion
which accumulate as the neuron
ages.
Nissl Bodies
Two
kinds of processes
Dendrites
Axon
Dendrites
Axon
Axon is a long thin cylindrical projection that originates from thickened cone
shaped elevation called Axon hillock.
The part of the axon closest to the axon hillock is called Initial segment. It is
highly excitable.
AXON
Axon
Axonal Transport
Axonal
transport
Movement of materials from or to the
cell body by axoplasmic flow is called
axonal transport.
Types of flow
Orthograde Flow
Retrograde Flow
Axonal transport uses two molecular
motors DYNEIN and KINESIN and
transport occurs along microtubules.
Orthograde Transport
Movement toward the synapse is called
anterograde /orthograde transport.
Proteins and polypeptides are
transported to the axonal endings by
Axoplasm flow.
Fast axonal transport 400mm/day
Slow axonal transport 0.5-10mm/day
Retrograde Transport
Movement
Coverings of Axon
Axolemma
Myelin
sheath
Neurilemma
Outermost transparent
cell membrane of
shawann cell.
Endoneurium
CT which surround the Neurilemma
Perneurium
Bundles of nerve fiber surrounded
by CT
Epineurium
Many Bundles bounded together by
CT
Objectives
Nodes of Ranvier:
Physiologic Importance of
Nodes
Nodes of Ranvier:
Periodic constrictions that are about 1mm
apart are called nodes of Ranvier
Unmyelinated areas between adjacent
Schwann cells
Produce nerve impulses
Important for exchange of ions between the
interior of axon & the external environment.
nerve fibers
Unmyelinated nerve fibers
Enveloped by Shawann
cells
Schwann cells:
Successive wrapping
of the cell membrane
forms myelin sheath
Provide insulation.
Provide structural &
nutritive support
Repair nerve fiber after
damage
Myelination
Nerve fiber invaginate the Shawann cell
Point of fusion of Shawann cell
membrane with nerve fiber is called
Mexacon.
Mexacon wraps around the axon in a
spiral manner.
Axon surrounded by several layers of
shawann cell membrane form myelin
sheath. No cytoplasm (white in color)
This process is called myelination
Myelination
Myelination
Myelination
nerve fibers
Unmyelinated
fibers
Oligodendrocytes
Each has
extensions that
form myelin
sheaths around
several axons.
Insulation.
Un-myelinated Nerve
Fibers
Supported
by mass of
surrounding tissues.
Functions of Myelin
Sheath
Provides
insulation
Support
Nutrition
Increases
Composition of Myelin
sheath
The
CLASSIFICATION
OF NEURONS
Classification of Neurons
Structural/Histological classification
Functional/Physiological
classification
Classification according to the size
Classification according to the
location
Structural/Histological
classification.
Uni-polar
Psuedo-unipolar
Structural/Histological
Classification
Bi-polar
Functional/Physiological
classification
Functional Classification of
Neurons
Classification according to
the size
Golgi type-1-neurons
Have a very long axon found in
brain.
Golgi type-2-neurons.
Have small thick, plump axons
found in spinal cord
Classification According to
the Location
Upper motor Neurons
Brain
Lower motor neurons
Cranial nerve nuclei in brain.
Spinal cord
Alpha & Gamma Motor Neurons
in the anterior horn of spinal cord
NEUROGLIA
/SUPPORTING CELLS
Neuroglia /Supporting
Cells
Astrocytes
1.
2.
3.
4.
5.
6.
Supporting cells
Nutritive Function
End feet of astrocyte surround capillaries
take up glucose from the blood
Take up some neurotransmitters released
from the axonal terminals of neurons.
Blood Brain Barrier (BBB)
Phagocytosis
Healing
Neuroglial Cell
(continued)
Oligodendrocytes
Form myelin sheath around nerve fibers in
CNS.
Microglia Cells
Phagocytic cells, remove debri resulting from
injury, infection, and disease (eg, multiple
sclerosis and Alzheimer disease).
Satellite Cells
Surround cell bodies in ganglia, provide
support & nutrition to cell bodies
Schwann Cells
Membrane
Potential
Dr Adeela Shahid
Professor of Physiology
SMDC
Objectives
Membrane Potential
It is the separation of opposite
charges across the membrane.
OR
Difference in the charges across
the membrane.
Membrane Potential
caused by Diffusion
Potassium Diffusion /
Equilibrium potential
No further movement of K+
occurs when the inward electrical
force /electrical gradient pulling
the K ions inside exactly counterbalances the outward force of
diffusion/ concentration gradient.
The MP at this point is called
equilibrium potential for K+
The potential difference is 94 mv
with negativity inside the fiber
membrane.
Diffusion Potential is -94 mv
Equilibrium Potentials
Nernst Potential
The
Nernst Potential
Magnitude is determined by the
ratio of concentration of the ion on
the two side of the membrane.
The greater this ratio, the greater
the tendency for the ion to diffuse
in one direction, and therefore the
greater the Nernst potential
required to block net diffusion.
Nernst equation
Nernst Potential
Nernst potential is the potential inside the
membrane. Potential in the ECF outside
the membrane remains at zero potential.
If a positive ion is diffusing from outside
to inside the sign will be +ve.
If positive ion is diffusing from inside to
outside the sign will be ve.
SIGN Indicates the polarity of the excess
charge inside of the membrane.
Outside
Inside
Na
4 mEq/L
140 mEq/L
Calculation
Nernst potential for K
Concentration of K+ inside the cell is
greater than outside (140 mEq/L inside
compared to 4 mEq/L outside)
K+ inside/ K+ outside = 140/4= 35
Log of 35 is 1.54
61 x 1.54 = 94
Nernst Potential will be -94 mv
Objectives
outside
Permeability of the ion
Charge of each ion
Goldman equation
Goldman equation
1.
2.
3.
Resting
Membrane
Potential
Resting Membrane
Potential of Nerves
Potential difference across the
membrane at rest is called resting
membrane potential.
OR
The membrane potential of a cell that is
not producing impulses is called RMP.
The Potential at rest is called RMP.
RMP
Large nerve fiber
Neuron cell body
SA node
mv
Skeletal muscle
-90 mv
-70 mv
-55 to -60
-90 mv
RMP
RMP exist because of a build up of
ve charges on inner side of the
membrane & an equal buildup of
+ve charges on the outer side.
Such separation of +ve & -ve
charges have potential energy
measured in mv.
Greater the difference in the charges
greater would be the potential.
1.
2.
3.
Origin of Normal
RMP
Contribution of the K Diffusion Potential
Contribution of the Na Diffusion Potential
Contribution of the Na-K Pump
OR
K+ leak channels
Na+ leak channels
Na+/ K+ pump
Origin of Normal
RMP
Contribution of K
diffusion
K+ outside: 4 mEq/L
K+ inside: 140 mEq/L
K+inside/K+outside = 35.0
Nernst potential of K=-94mv
Contribution of Na
diffusion
RMP = -90 mv
-86
is due to Na & K
diffusion.
-4 is due to Na/K pump
RMP
Measurement of Membrane
Potential
Evidences
Change the concentration of K + in ECF
causes disturbance of RMP
In Hyperkalemia Membrane potential
becomes less negative (decrease in RMP) &
membrane becomes hyper excitable. i.e. early
depolarization.
lethal injections of KCl (raising the extra
cellular K+ concentrations and depolarizing
cardiac cells.).
In Hypokalemia there will be increase in RMP.
Objectives
ACTION
POTENTIAL
Stimulus
Any change in the external environment that
is strong enough to initiate an action potential.
Types
Electrical
Chemical
Hormonal
Thermal
Mechanical
Electromagnetic Radiation
Levels of Stimulus
Subthreshold
Threshold
Suprathreshold
Action Potential
A
Action Potential
It
is a large change in
membrane potential from a
value of -90/-70mv to a peak
of about +35mv & back to
-90/-70mv.
Action
potential is generated at
the axon hillock where density of
voltage gated Na channels is
greatest.
Duration
Action Potential
It begins when signals from the dendrites &
cell body reach Axon Hillock & causes
membrane to depolarize.
As the Axon Hillock depolarizes the voltage
gated channels for Na open rapidly
increasing membrane permeability to Na.
In action potential there is reversal potential .
Inside becomes +ve
Outside becomes ve
Phases
Resting
Membrane
Potential
Depolarization
Repolarization
Hyperpolarization
PHASES OF ACTION
POTENTIAL
Resting Membrane
Potential
Stimulus Artifact
Latent Period
1. Initial Depolarization/Slow Phase
2. Threshold level / Firing level
3. Rapid Depolarization
4. Over shoot potential
5. Rapid Repolarization
6. Slow after Depolarization/negative after potential
7. Hyperpolarization / Positive after potential
-65
6
-90
7
Resting stage
Before
action potential
begins, the membrane is in
resting stage & is said to be
polarized because of -90mv
RMP.
Stimulus artifact
When
Latent Period
The
-65
6
-90
7
Initial Depolarization/Slow
Phase
The
stimulus
causes opening of
some Na channels
resulting in initial
20mv 25mv
depolarization.
FIRING LEVEL
Rapid Depolarization
Inactivation gates
never open once
closed unless
membrane
potential becomes
near the RMP
(Threshold).
Inactivation of Na
gates at +35mv
open K gates
Slow to open &
slow to close
-65
6
-90
7
Overshoot
Potential
The Action
Potential curve
reaches the zero
potential rapidly
& then
overshoots the
zero line up to
+35 mv.
Rapid Repolarization
Stage
K gates open slowly &
K gates open slowly &
K moves out
K efflux continues
Inside becomes -Ve
Return of negativity
inside the membrane.
This re-establish the
normal RMP. This is
called Repolarization
Spike Potential
The
-65
6
-90
7
Hyperpolarization/
Positive
After
Potential
When potential has
Phases
Objectives
Changes in Na and K
conductance during Action
Potential
Depolarization Phase
At threshold stimulus there is
sudden opening of large number of
Na channels. Na moves in resulting
in depolarization up to +35mv.
Na channels are inactivated & Na
gates close at +35mv.
Hyperpolarization /
Positive After
Potential
Slow
Evidences
Changing the concentration of K+ in ECF
there is disturbance of RMP
In Hyperkalemia Membrane potential
becomes less negative & membrane becomes
hyper excitable. i.e. early depolarization.
lethal injections of KCl (raising the extra
cellular K+ concentrations and depolarizing
cardiac cells.).
In Hypokalemia membrane will become
more Ve
Initiation of Action
Potential
Properties of Action
Potential
APPLIED
PHYSIOLOGY OF
ACTION POTENTIAL
Objectives
Local
Anesthetics
Procaine
Tetracaine
Lidocaine
Local Anesthetics
Block
Voltage Clamp
It
Measure voltage
of
membrane
potential
conduct electric
current
Periods of Action
Potential
Latent
Period
Refractory Period
Absolute Refractory
Period
Relative Refractory
Period
Refractory Period
It
Types of Refractory
Period
Absolute
Refractory Period
(ARP)
Relative Refractory Period
Absolute Refractory
Period (ARP)
The
Relative Refractory
Period
The relative refractory
period is that period
during which a
greater than normal
strength of stimulus
is required to produce
second action
potential.
It is due to continuous
K efflux.
Objectives
PROPAGATION OF THE
ACTION POTENTIAL
Local circuits of
current develops
between
depolarized
point & adjacent
resting areas.
Myelin Sheath is
interrupted by nodes of
Ranviers.
All Channels are present
along the node of
Ranvier.
Action potentials only
occur at nodes.
Action potential/nerve
impulse jumps down the
fiber from node to node.
Significance
Fast conduction of action potential. (5-50
times more conduction velocity).
Less energy expenditure due to less ionic
changes. Ionic fluxes are occurring only at
nodes & no change is occurring at internodes.
Due to insulation by myelin sheath at the
internodal area there is decrease in
membrane capacitance which allows
repolarization to occur with very little transfer
of ions at the nodes of Ranvier.
Objectives
Physiological Properties of
Nerve Fibers
Excitability
Conductivity
All or None Law
Refractory Period
Absolute Refractory Period
Relative Refractory Period
Strength Duration Curve
Excitability
When
a nerve is stimulated it
produces a wave of
depolarization i.e. nerve
impulse. This shows that it
has the property of
excitability.
Conductivity
It
Refractory period
Refractory
Period
Absolute Refractory Period
Relative Refractory Period
The relationship
between intensity
of stimulus
(voltage) & the
duration of
stimulus (time) is
called strengthduration curve.
RHEOBASE
It the minimum voltage or current which when
applied for an adequately prolonged time will
be able to reach threshold and will give rise to
action potential.
UTILIZATION TIME
The minimum time required for current equal
to the rheobase to induce action potential.
CHRONAXIE
It
Physiological Importance
Tissues which are more excitable
will have shorter CHRONAXIE.
Nerve fibers have shorter chronaxie
than muscles. Nerve fibers are more
excitable.
When injury to a motor nerve
chronaxie is increased
Objectives
Classification of Nerve
Fibers
Type A fibers (myelinated)
Alpha
Beta
Gamma
Delta
Type B fibers (myelinated)
Type C fibers (unmyelinated)
Compound Action
Potential
Multi-peaked action
potential recorded
from a mixed nerve
is a compound
action potential
It is due to different
type of fibers which
are present in a
mixed nerve.
Compound Action
Potential
Compound Action
Potential
Nerve fiber with the largest
dia shows following
features.
Greater conduction
velocity.
Greater magnitude of
action potential.
Shorter duration of spike
potential.
Shorter refractory period.
Advantage of Compound
action Potential
On
CLASSIFICATION
OF NERVE
FIBERS
Classification of Nerve
Fibers
Type A fibers (myelinated)
Alpha
Beta
Gamma
Delta
Type B fibers (myelinated)
Type C fibers (unmyelinated)
Fiber
Diameter
(m)
Conduction
Velocity
(m/s)
Proprioception;
somatic motor
12-20
70-120
Touch, pressure
5-12
30-70
Motor to muscle
spindles
3-6
15-30
2-5
12-30
Preganglionic
autonomic nerves
<3
3-15
Spike
Duration
(milli-sec)
Absolute
Refractory
Period
(milli-sec)
0.4-0.5
0.4-1
1.2
1.2
Dorsal root
Pain,
temperature
Sympathetic Postganglioni
c sympathetic
Fiber
Diameter
(m)
Conducti Spike
Absolute
on
Duration Refractory
Velocity
(milliPeriod
(m/s)
sec)
(milli-sec)
0.4-1.2
0.5-2
0.3-1.3
0.7-2.3
Hypokalemia
- Hyperpolarization
Hyperkalemia
Depolarization
Hypocalcemia
Increase excitability
Hypercalcemia Decrease
excitability
(Membrane Stabilizer)
Recording of Action
Potential
Cathode Ray
Oscilloscope
Mono-Phasic AP
Microelectrode is inserted
inside of the fiber & the
other electrode is placed
outside.
GRADED
POTENTIAL /
LOCAL POTENTIAL
Objectives
At the end of lecture 1st yr
MBBS student should be able to
Differentiate between graded
potential and action potential
Classify Nerve fibers
Graded Potential
Action Potential
Threshold
Amplitude
Fixed
Refractory
Period
No R.P
Has R.P
All or none
Law
Duration
Prolonged in duration
Short duration
Self
Propagation
No self Propagation.
Decremental in character.
Decrease with distance.
Self Propagated
Nature
Excitatory or
inhibitory/hyperpolarization
Depolarization with
overshoot potential
Sites
Nerve, muscle
A fibers (myelinated)
Sensitive to pressure
Type B fibers (myelinated)
Sensitive to hypoxia
Type C fibers (unmyelinated)
Sensitive to local anesthetics
Objectives
Conduction Velocity
of Nerve Fibers
The
Conduction velocity
Distance is 4.5 cm
Latent period is 1.5ms
Conduction velocity ?
S=V/T
V=S/T
Clinical importance
Diagnosis
Physical examination
Testing of reflexes
Walking and other directed movements
Muscle weakness, proprioception , and the sense of
touch.
Tests
Nerve conduction study and Electromyography
Disorder of
Myelin Sheath
Multiple
Sclerosis
Multiple Sclerosis
Age 20-50yrs
Sex : more common in Females
Inflammatory and neuro- degenerative
disease
CAUSES
Causes
Genetics
Environmental
factors
such as viruses
Genetics
Environmental Factors
Viruses
Patho-physiology
Antibodies and WBC attack myelin sheath
and cause inflammation and injury to the
myelin sheath & the nerves.
Gradual destruction of Myelin sheath around
axons of the brain & spinal cord.
Leakage of K+ through voltage-gated
channels results in hyper-polarization and
failure of transmission of nerve impulse.
impulse
Types
Transient
episodes appear
suddenly
Progressive form of the
disease
weakness
Fatigue
Diminished
coordination
Slurred speech
Blurred or hazy vision
Bladder & bowl dysfunction
Sensory disturbances
DIAGNOSIS
Diagnosis
Diagnosis
History & Physical Examination
TESTS
1. Nerve conduction tests
detect slow conduction in motor and
sensory
pathways
2. CSF analysis
oligoclonal bands indicative of an abnormal
immune reaction against myelin
3. Magnetic resonance imaging (MRI)
multiple scarred (sclerotic) areas in the brain.
Treatment
No
cure for MS
Immunosuppressant drugs like interferon
suppress the immune response
& reduce the severity and slow
the progression of the disease.
Treatment
GUILLAIN-BARRE
SYNDROME
Objectives
Guillain-Barre Syndrome
Auto immune disease
It is polyneuropathy
When the body's defense (immune)
system mistakenly attacks part of the
PNS.
This leads to nerve inflammation &
demyelination of the peripheral
nerves.
GB Syndrome
Diagnosis
History
Physical Examination
Nerve conduction test
Cerebrospinal fluid
Electromyography (EMG) tests the electrical
activity in muscles
Pulmonary function tests
T/M
Objectives
DEGENERATION &
REGENERATION OF
NERVE FIBER
Degeneration of Nerve
Fiber
CAUSES
Trauma
Crushing
Section
Toxic
substance
Interference with blood
supply
Degenerative changes
depend upon the extent of
injury
In
Impulses
conducted for 3
days after injury, later on it
decreases. After 5 days no
conduction of nerve impulse.
Degenerative changes
take place at three
levels
Cell
body
Proximal stump
Distal stump
Changes in Proximal
stump
Degeneration process also
extends one or two nodes
upwards. Soon followed by
regeneration
changes
in the distal segment
were observed by A H
Waller hence given the
name Wallerian
Degeneration.
Schmidt-Lanterman
clefts/Incisures
In
Regeneration
Cell
Body
Distal stump
Regeneration
Within 96 hours of the injury,
the proximal end of the nerve
fiber sends out sprouts / fibrils
upto 50 to 100 in number
towards the endoneurial tubes.
The fibrils move towards the
distal cut end of the nerve fiber
and some of the fibrils enter the
endoneurial tube of distal end
and form axis cylinder
Rapid
In
Regeneration
If distance between cut ends is more than
3mm then tumor like swelling is formed
called Neuroma
No regeneration in optic nerve and CNS
No endoneurial tubes so the regenerating
axon cannot be guided
No schawan cells instead
oligodendrocytes are present
SYNAPSE
Objectives
At the end of lecture 1st yr MBBS
student should be able to:
Define synapse
Classify synapse
Discuss chemical and electrical
synapse
Synapse
It
is a functional
connection between a
neuron and another
neuron or effecter cell.
Impulses
Synapse
Neurons are linked to one another to form
conducting pathways. These links or
interneuronal junctions are called
SYNAPSE.
It is a junction where axon or some other
part of the neuron terminates on the
soma, dendrite or axon of other neuron .
First incoming neuron is presynaptic
neuron & second neuron to which activity
is transmitted is postsynaptic neuron.
Anatomical Classification of
Synapse
Axo-somatic
Axo-dendritic
Axo-axonic
Somato-dendritic
Somato-somatic
Dendro-dendritic
Classification of Synapse on
Geometric Basis
Simple synapse
Single pre-synaptic
component in contact
with one post-synaptic
structures.
Complex synapse
One pre-synaptic
component comes in
contact with two postsynaptic structures.
Serial synapse
3 structures are
arranged serially, activity
from one conducted to
second and then to third.
Reciprocal synapse
Activity passes from one
cell to second cell and
from the second cell
back to the first one.
Neuron will have
presynaptic & postsynaptic functions.
Functional
classification of
synapse
Electrical Synapse
Chemical Synapse
Mixed synapse
Electrical
Synapse
Electrical Synapse
The membranes of the pre- and
postsynaptic cells are joined by GAP
junctions at electric synapses.
The two membranes are very close to
each other (synaptic cleft 2nm). They
are connected to each other through
GAP junctions.
There is rapid transmission of electrical
signals between cells due to gap
junctions.
Gap
Electrical Synapse
Gap junctions:
Adjacent cells
electrically joined
through a channel
formed by Connexin
proteins, arranged in
a hexagonal pattern
forming gap
junctions.
These channels link
the cytoplasm of 2
cells.
Chemical
Synapses
Chemical Synapses
Chemical
synapses are
specialized junctions through
which neurons send chemical
signals to each other and to nonneuronal cells such as those in
muscles or glands.
Chemical Synapse
Functional Anatomy of
Synapses
It is a classical synapse,
formed between axon
Chemical Synaptic
Transmission
When an
action potential
travels along the
axon of a neuron and
reaches at synapse it
causes release of
neurotransmitter
which bind to
receptors in the
membrane of post
synaptic neuron
Events in Synaptic
Transmission
Calmodulin
activates an enzyme
called protein kinase.
Protein kinase causes
phosphorylation of protein synapsin
in the membrane of synaptic vesicle.
Fusion of synaptic vesicles with the
plasma membrane.
Release of neuro-transmitter by
exocytosis.
Chemical Synapse
Amount of NTs
released
depends upon
frequency of AP
Post-synaptic
membrane
contains
receptors for
binding the NTs
Synaptic Transmission
Synaptic Transmission
(continued)
EPSP: depolarization.
IPSP: hyperpolarization.
Questions
Mechanism
of transmission
of nerve impulse across
chemical synapse?
Synaptic transmission?
Objectives
Post-synaptic potential
Depending
upon the
neurotransmitter involved,
chemical transmission results in
either an EPSP or IPSP .
Post-synaptic potential is of two
types.
EPSP
IPSP
Advantage of EPSP
EPSP
Action
Potential
Magnitude
low
high
Refractory
Period
No R.P
Has R.P
All or none
Law
Response is graded,
Obeys All & None
doesnt obey all & none law Law
Duration
Prolonged in duration
Self
No self Propagation.
Propagation Decremental in character.
Decrease with distance.
Short duration
Self Propagated
Pre-synaptic inhibition
Presynaptic inhibition
Pre-synaptic knob (B) has
additional synapse with
nerve terminal (A) & from
this additional synapse
there is release of NT
which will inhibit the presynaptic knob (B).
The amount of an
excitatory NT released at
the end of an axon (B) is
decreased by the effects of
a inhibitory NT from
neuron (A).
Post-synaptic inhibition
When the inhibitory neurotransmitter
is released there is inhibition of post
synaptic membrane and the Post
synaptic membrane is hyperpolarized
Post-synaptic inhibition when
potential in the post synaptic neuron
changes from
-70 to -80mv or -90mv.
Summation
Summation
When
Summation
There are 1000 synapse on a single motor
neuron.
Neuron receives multiple inputs from
excitatory & inhibitory neurons.
A single impulse cannot excite motor
neuron. In order to excite motor neuron
there must be summation of the effects of
stimuli.
Generation of action potential depends
upon summation of these multiple inputs.
Types of Summation
Types
Temporal
Summation
Spatial
Summation
Temporal Summation
When 2 subthreshold stimuli are
applied one after the
other, the effects are
added & excitation
occurs.
2nd stimulus falls
when the effect of
first stimulus is still
there.
Spatial Summation
Properties of
Synaptic
Transmission
Properties of Synaptic
Transmission
Uni-Directional Conduction
Synaptic Delay
Summation
Fatigue of Synaptic Transmission
Dales law
Effected by Hypoxia, Drugs,
Anesthetics, Acidosis, Alkalosis &
Ischemia.
Uni-Directional
Conduction
Impulses are conducted through the
Synaptic Delay
It
Summation
Temporal
summation
Spatial summation
Fatigue of Synaptic
Transmission
Dales law
Tetanus toxin
Botulinum toxin
These are bacterial products that cause
paralysis by preventing
neurotransmission.
Clinical Aspects
in Lower Esophageal
Sphincter is given to relieve
ACHALASIA
Injection
BIPHASIC ACTION
POTENTIAL
Therefore,
Alzheimers disease
Accomodation
Neurotransmitters
Acetyl-choline
Epinephrine
Norepinephrine
Dopamine
Serotonin
Glycine
GABA
Substance P
Acetylcholine (ACh) as NT
Acetyl-Choline Receptors
Skeletal muscle
Autonomic ganglia
Smooth muscle
Cardiac muscle
In cells of particular glands
Ligand-Operated ACh
Channels/
Nicotinic Ach receptors
Schmidt-Lanterman
clefts/Incisures
Ligand-Operated ACh
Channels/
Nicotinic
Ach
receptors
Ion channel run through
receptor.
Receptor has 5
polypeptide subunits
that enclose ion channel.
2 subunits contain ACh
binding sites.
Permits diffusion of Na+
into and K+ out of
postsynaptic cell.
Produces EPSPs.
G Protein-Operated ACh
Channel/ Muscrinic ACh
Receptors
G Protein-Operated ACh
Channel/ Muscrinic ACh
receptors
Only 1 subunit.
Ion channels are
separate proteins
located away from
the receptors.
Binding of ACh
activates alpha Gprotein subunit.
Alpha subunit
dissociates.
Alpha subunit or the
beta-gamma
complex diffuses
through membrane
until it binds to ion
channel, opening it.
Alzheimers disease
Myasthenia Gravis
ACh in CNS
Cholinergic neurons:
ACh in PNS
Norepinephrine (NE) as NT
CNS:
General behavior.
Monoamines as NT
Monoamine NTs:
Epinephrine.
Norepinephrine.
Serotonin.
Dopamine.
Inhibition of Monoamines
as NT
Reuptake of
monoamines into
presynaptic
membrane.
Enzymatic
degradation of
monoamines in
presynaptic
membrane by MAO.
Enzymatic
degradation of
catecholamines in
postsynaptic
membrane by COMT.
Mechanism of Action
Monoamine NT do not
directly open ion channels.
Act through second
messenger, such as cAMP.
Binding of norepinephrine
stimulates dissociation of
G-protein alpha subunit.
Alpha subunit binds to
adenylate cyclase,
converting ATP to cAMP.
cAMP activates protein
kinase, phosphorylating
other proteins.
Open ion channels.
Serotonin as NT
Dopamine an NT
Norepinephrine (NE) as NT
CNS:
General behavior.
Amino Acids as NT
Hyperpolarization.
Polypeptides as NT
CCK:
Substance P:
Synaptic plasticity
(neuromodulating effects):
Polypeptides as NT
Endogenous opiods:
Endogenous Cannabinoids,
Carbon Monoxide
Endocannabinoids:
Carbon monoxide:
EPSP
No threshold.
Decreases resting
membrane
potential.
Closer to threshold.
Graded in
magnitude.
Have no refractory
period.
Can summate.
Synaptic Integration
Spatial summation:
Numerous boutons
converge on a single
postsynaptic neuron
(distance).
Temporal summation:
Successive waves of
neurotransmitter
release (time).
Long-Term Potentiation
Synaptic Inhibition
Presynaptic inhibition:
Amount of excitatory NT
released is decreased by
effects of second neuron,
whose axon makes
synapses with first
neurons axon.
Postsynaptic inhibition
(IPSPs):
No threshold.
Hyperpolarize
postsynaptic membrane.
Increase membrane
potential.
Can summate.
No refractory period.
1. The supporting cells that form myelin sheaths in the peripheral nervous
system are
a. oligodendrocytes.
b. satellite cells.
c. Schwann cells.
d. astrocytes.
e. microglia.
2. A collection of neuron cell bodies located outside the CNS is called
a. a tract.
b. a nerve.
c. a nucleus.
d. a ganglion.
3. Which of these neurons are pseudounipolar?
a. sensory neurons
b. somatic motor neurons
c. neurons in the retina
d. autonomic motor neurons
Key Nerve
1. c
2. d
3. a
10. c
11. b
12. d
4. a
5. c
6. d
13. d
14. b
15. a
7. d
8. a
9. c
16. c
17. a