EXCITABLE TISSUES
(Neuron and Muscle)
By: Hotesa G. MSc Medical Physiology
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Outlines
General consideration
Nerve tissue and components:
Nerve cells
Glial cell
Synaptic Transmission:
Chemical Synapse
Electrical Synapse
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General consideration
Excitable Tissues
1. What Makes a Tissue "Excitable"?
 Definition: Excitable tissues (neurons and muscle fibers) possess the unique ability to
respond to a stimulus by rapidly generating and propagating electrical signals.
 The Majority of cells in the human body possess a membrane potential, only a specialized
few can actually alter or change that potential in response to stimulation.
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2. The Mechanism of the "Stimulus"
 Alterations in membrane potential are achieved by strictly varying the membrane
permeability to specific ions.
 Stimulus-Response: When a stimulus is detected, the cell opens or closes specific ion
channels, allowing ions like Na+ or K+ to rush across the membrane, flipping the
electrical charge.
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Introduction to Membrane Potential
 Electrical potentials are the voltages that exist across the plasma membranes of
almost all cells in the body.
Most cells exhibit a Negative Membrane Potential at rest, meaning there is an
excess of negative charges at the inner surface of the cell membrane compared to
the outside.
 This occurs because of two major reasons of ion permeability:
1. The membrane selective permeability to K+ ion at rest time, and
2. The Na+/K+ Pump
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Selective Ion Permeability (K+)
The primary reason for the internal negative charge is the behavior of Potassium (K+).
The Gradient: K+ concentration inside the cell is significantly higher than the outside
concentration.
The Movement: Because the membrane is "leaky" to K+ at rest, K+ ions move out of the
cell following their concentration gradient.
The Result: As positive K+ ions leave, they leave behind an excess of negative charges
(mostly from proteins and phosphates) on the inside of the cell membrane.
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The Na+/K+ Pump
The Na+/K+ pump is an active transport mechanism that acts as a second factor in maintaining
negativity.
Electrogenic Nature: It pumps three Na+ ions OUT and only two K+ ions IN.
Net Loss of Positivity: Since three positive charges leave for every two that enter, there is a net
loss of positive ions from the intracellular fluid.
Contribution: This unequal exchange directly contributes to the negative electrical environment
on the inner membrane surface
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Changes in Membrane Potential
 The membrane potential is not static; it changes when the cell needs to "work" or
communicate.
 Changes in the opening or closing of specific ion channels allow ions to flow across the
plasma membrane.
 Depolarization: If Na+ channels open, Na+ rushes in, making the inside less negative
(more positive). Inside of the neuron from -70mV (resting potential) it becomes to +30mV
 Hyperpolarization: If more K+ channels open or Cl− enters, the inside becomes more
negative (-80mV)
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Nerve Tissue
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Components of Nerve tissue
1. Neurons:
Basic unit of the nervous system
Produce and conduct electrical impulses
2. Neuroglia(Glia) : Numerous support cells.
Assist the functions of neurons
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Neurons = Nerve cells
 Basic structural and functional units of the nervous system
 Specialized to respond to physical and chemical stimuli, conduct
electrochemical impulses, and release chemical regulators.
 Sense and react to the chemical and physical changes occurring in their
surrounding environment.
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Neuron are responsible for most of the unique functions of the brain.
 Neurons sense changes in the environment,
 communicate these changes to other neurons, and
 command the body’s responses to these sensations.
 Primary neural functions include reception, conduction and transmission.
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 Neurons have three principal parts: Cell body, Dendrites, Axons
1) Cell body/Soma/:
- Contains the nucleus and Nissl bodies (densely staining areas of rough
endoplasmic reticulum)
- It’s Nutritional center of the neuron
Nuclei: collection of neuron cell body in CNS
Ganglia: collection of neuron cell body in Peripheral Nerve System
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2) Dendrites:
- Concerned with reception of stimuli from environment
- Transmits electrical impulses to the cell body
- dendrites function as the antennae of the neuron
3) Axons
Conducts impulses away from the cell body.
- Gives out collateral branches when the target consists of many cells
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Axoplasmic flow:
Axonal transport:
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Classes of Neurons
On functional basis: Sensory neurons, association neurons, motor neurons
Sensory neurons (= Afferent Neurons ):
• Transmit information / impulses from sensory receptors into the CNS
• e.g. pain receptors in skin to the CNS
Association neurons (=Interneurons):
• Located entirely within CNS
• accounts for 99% of all neurons
• performs the associative, or integrative functions of the nervous system
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Motor neurons (= Efferent Neurons ):
• Transmit information out of the CNS to effector organs (muscles or glands)
• Two types of motor neurons:
↘Somatic motor neurons:- responsible for reflex and voluntary
control of skeletal muscles.
↘Autonomic motor neurons:-innervate (send axons to) the
involuntary effectors: smooth muscle, cardiac muscle, and glands.
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Types of neurons
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Motor neuron
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Neuroglia =Glial cell
 Supports the functions of neurons
 About 5x more abundant than neurons
 Glial cells are able to divide by mitosis.
 This why brain tumors in adults are usually composed of glial cells rather
than of neurons.
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Continue glial cells………
- Neurons gain efficiency through special glial cells.
- Surround the neuron, adhering to their surface &
- Helping to remove problem of resistance to the conduction of excitation.
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Types of Glial cells:
 Four in CNS:
 Astrocytes: Provide physical support, transport nutrients to neurons & help
to regulate the external environment of neurons in the CNS.
 Microglia: Involved in phagocytosis and brain immune function
 Oligodendrocytes: Provide physical support and form the myelin sheath of
CNS axons
 Ependymal cells: line the ventricles (cavities) of the brain and the central
canal of the spinal cord.
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 Functions of astrocytes:
 Astrocytes take up K+ from the extracellular fluid:
K+ diffuses out of neurons during the production of nerve impulses, this is
important in maintaining the proper ionic environment for neurons.
 Astrocytes take up some NT released from the axon terminals of
neurons:
• For example: NT glutamate is taken into astrocytes and transformed into
glutamine.
• Glutamine is then released back to the neurons, which can use it to reform
the NT glutamate.
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 Astrocyte end-feet surrounding blood capillaries take up
glucose from the blood:
Glucose is metabolized into lactic acid, or lactate. Lactate is then
released and use as an energy source by neurons
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 Astrocytes appear to be needed for the formation of synapses in the
CNS:
Normal synapses in the CNS are ensheathed by astrocytes
 Astrocytes induce the formation of the blood-brain barrier/BBB:
Provides selective permeability of substances between the brain CSF
and blood plasma
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 Neuroglia cells are two in PNS:
 Schwann cells:
- Form myelin sheaths (around peripheral axons)
 Satellite cells or ganglionic gliocytes:
- Support neuron cells bodies within the ganglia
of the PNS.
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Formation of a myelin sheath around axon
PNS axon
CNS axon
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Functions of glial cells
 Mechanical supportive elements of neurons
 Phagocytic defense mechanism
 Modifiers of electrical activity in neuron
 Regulation of metabolism in neuron
 Producers of myelin sheath
 Development assistance in neuronal circuitry
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Synaptic Transmission
 Synapses: specialized cell-to-cell contacts
 There is a Gap between two neurons or neuron & muscle cell
- Allow the information encoded by action potentials to pass to another cell.
- Occur at the junction between the processes of two neurons or
between a neuron and an effector cell (muscle or gland)
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 Synapse has two sides: presynaptic and postsynaptic
• Presynaptic side consists of an axon terminal and release
chemical transmitter called neurotransmitter(NTs) to the gap
• Postsynaptic side may be a dendrite or the soma of another neuron and
contain specific receptor for binding of the released chemical transmitter
 Synaptic cleft: space between the presynaptic and postsynaptic membranes
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 Synaptic connection:
 On average single neuron forms about 103 synaptic connections.
 Human brain contains 1012 neurons
 1012 x 103 = 1015 synaptic connections
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 Synaptic transmission:
 Transfer of information at the synapse from one neuron to another
 Two types: Chemical synaptic transmission
Electrical synaptic transmission
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I. Chemical synaptic transmission:
- Involve the release of a chemical transmitter by one cell that acts upon
another cell.
- Action potentials in a presynaptic cell cause the release of the chemical
transmitter, which crosses a narrow cleft to interact with specific
receptors on a postsynaptic cell.
- Unidirectional (forward transmission only)
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Components of a chemical synapse
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 Neurotransmitters (NT’s) are chemical signaling
molecules released by neurons to communicate with other
neurons, muscles, or glands.
 They can function as excitatory or inhibitory substances
Mechanism of NT release:
 Action Potential arrives at axon terminal
• Opening of voltage gate for Ca2+ on presynaptic
membrane
• Ca2+ influx and Phosporylation of Synapsin-P
• Vesicle detachment from cytoskeleton
• Attachment of vesicle to release (docking) site
• NT release by exocytosis.
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Neurotransmitter Classes and Actions
Class
Small
Molecule
Examples
Duration
of Action
Glutamate, GABA,
Dopamine
Fast signaling: Acts on ion channels (ionotropic)
Rapid/Shor or G-proteins (metabotropic) for quick
t
excitation or inhibition.
Primary Action/Mechanism
Endorphins,
Neuropeptide Substance P
Neuromodulation: Often modulates the
Slower/Pro intensity of other signals; involved in pain,
longed
mood, and long-term changes.
Gaseous
Direct Diffusion: Crosses membranes without a
Very Short receptor; induces vasodilation and retrogradely
(instability) signals back to the sender cell.
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Nitric Oxide (NO)
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 Neurotransmitter receptors: on postsynaptic neuron memb
1. Ion channel coupled receptors usually by amino acid and amine
NT (fast acting) Ionotropic Receptors (Ligand-Gated Ion
Channels).
2. G-protein coupled receptors by proteins NT (slowly acting),
affecting metabolism thus metabotropic receptors :
 Activates cellular enzymes
 Activation of gene transcription
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Neurotransmitter
Ionotropic Receptors (Ligand-Gated Ion
Channels)
Metabotropic Receptors (G-Protein-Coupled
Receptors)
Acetylcholine (ACh)
Nicotinic cholinergic receptors
Muscarinic cholinergic receptors (M1–M5)
Glutamate
NMDA(N-Methyl-D-Aspartate), AMPA(AlphaAmino-3-Hydroxy-5-Methyl-4Isoxazolepropionate), Kainate receptors
Metabotropic Glutamate Receptor/ mGlu₁–mGlu₈
GABA
Gamma-Aminobutyric Acid /GABA_A
GABA_B
Glycine
Strychnine-sensitive glycine receptor
None identified
Dopamine
None
D₁–D₅
Norepinephrine
None
α₁, α₂, β₁, β₂, β₃ adrenergic receptors
Epinephrine
None
α₁, α₂, β₁, β₂, β₃ adrenergic receptors
Serotonin (5-HT)
5-HT₃/ 5-Hydroxytryptamine (Serotonin)
5-HT₁, 5-HT₂, 5-HT₄–5-HT₇
Histamine
None
H₁, H₂, H₃, H₄
Adenosine
None
A₁, A₂A, A₂B, A₃
Opioid Peptides
None
μ (Mu), δ (Delta), κ (Kappa), ORL₁ (NOP)
/Nociceptin/Orphanin FQ Peptide Receptor
Nitric Oxide
No classical receptor; activates soluble guanylyl
cyclase
Intracellular second messenger signaling46
 Excitatory neurotransmitters: depolarize the postsynaptic membrane,
producing an excitatory postsynaptic potential/EPSP/
 Effect on post synaptic membrane:
 Change in internal metabolism to alter number of channel proteins
 Opening of sodium channel
 Closing of K+ and Cl- channel
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 Inhibitory neurotransmitters: hyperpolarize the postsynaptic
membrane, producing an inhibitory postsynaptic potential/IPSP/
 Effect on post synaptic membrane:
 Opening of K+ channel
 Opening of chloride channel
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Summary
Excitatory Neurotransmitters
Glutamate
Aspartate
Acetylcholine (at neuromuscular
junction)
Inhibitory Neurotransmitters
GABA
Glycine
Major Monoamines
Dopamine
Norepinephrine
Epinephrine
Serotonin
Histamine
Special Neurotransmitters
Purines (ATP, Adenosine)
Neuropeptides (Substance P, Opioids)
Gas (Nitric Oxide)
Only Important Ionotropic Monoamine
Receptor
5-HT₃ (Serotonin receptor)
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 Summation of postsynaptic potentials: Summation is the additive
effect of multiple postsynaptic potentials that influences the generation of
an action potential.
1. Temporal summation
Addition of postsynaptic potentials produced by rapid successive impulses
from a single presynaptic neuron.
2. Spatial summation
Addition of postsynaptic potentials produced simultaneously by multiple
presynaptic neurons.
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 Properties of chemical synaptic transmission:
 Unidirectional: Forward direction
Focused, discrete, goal directed signal transmissions
 Synaptic delay : 0.05 -1.0ms
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Continue………
 Convergence: From multiple source or from a single source (pool)
This gives rise to temporal or spatial summation that facilitate neurons for discharge.
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Continue………
 Divergence:
Amplifying divergence in the same pathway
A single Betz cell excite 10,000 spinal motor neuron.
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Continue………
 Synaptic fatigue:
• Decline in the response of output neuron due to long period of high
frequency stimulation.
• Decline in response following prolonged activity results from:
• Exhaustion of NT,
• Inactivation of some postsynaptic receptors by metabolites,
• Accumulation of high concentration of Ca2+ in post synaptic neuron,
opens K+ channel and results in hyperpolarization of cells.
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 Synaptic after discharge (signal prolongation):
Persistence of output signal after stoppage of signal
Due to: Delay in inactivation of NT, repeating
stimulation
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 Synaptic plasticity:
 Ability of neurons (synapse) to alter/change during development, disease,
damage and repair processes, and during the processes of learning and
memory.
• Property of synapses to change their characteristics/structural + chemical/
• Changes may be presynaptic or postsynaptic, or both, and may be short or
long lasting.
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6.
# of Dendritic spine
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 Synaptic potentiation:
Synaptic potentiation is an increase in postsynaptic response caused by
prior repetitive stimulation.
1. Short term potentiation
2.
•
Lasts for several minutes
•
Often follows brief low-frequency stimulation
•
Caused by increased presynaptic Ca²⁺ concentration or
•
Release of modulatory neurotransmitters such as serotonin (5-HT)
Long term potentiation: Follows brief high-frequency stimulation (tetanic
stimulation)
 Can persist for hours, days, or longer
 Considered a major cellular mechanism underlying learning and memory
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 Synaptic depression (Inhibition, Habituation):
• Gradual decrease in post synaptic potential when stimulation of presynaptic
neuron is frequently repeated
• Due to progressive closure or inactivation of Ca2+ channels in
presynaptic neuron
• Responsible for negative memory by enabling the brain to ignore
insignificant stimulus
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Property
Definition
Unidirectional transmission
Signal passes only from presynaptic to postsynaptic neuron
Synaptic delay
Brief delay (≈0.5–1.0 ms) before postsynaptic response
Convergence
Many inputs to one neuron
Divergence
One neuron influences many neurons
Synaptic fatigue
Decreased response after prolonged high-frequency
stimulation
After-discharge
Continued response after stimulus ends
Synaptic plasticity
Ability of synapses to change structurally and functionally
Potentiation
Enhanced synaptic response after repeated stimulation
Synaptic depression
Reduced response with repetitive stimulation
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II. Electrical synaptic transmission:
- Occur where two cells are joined by gap junctions,
- Conduct current from cell-to-cell via non selective pores.
- Cardiac muscle is an example of cells that are electrically coupled via gap
junctions. SA node to AV to ….depolarization from atria to Vent
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Muscle Tissue
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Outlines
 Muscle tissue: overview
 Smooth muscle
• Types
 Types of muscle tissues
 Skeletal muscle:
• Functional structure
• Mechanism of contraction
• Excitation contraction coupling
• Mechanism of contraction

Cardiac muscle

Clinical correlates
• Rigor mortis &Tetanus
• Myasthenia gravis
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Muscle tissue: overview
 Can be excited chemically, electrically + mechanically
 Muscle is specialized to contraction to produce force & movement
 45-50% of the total body mass ( 600 muscles)
 25% total bodily O2 consumption at rest is consumed by the muscles.
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Types of muscle tissues
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Skeletal muscle:
• Attached to bones & moves skeleton
• Have well developed cross striations (interdigitating thick
and thin filaments).
• Voluntary muscle tissue: Contracts when exclusively
stimulated by a somatic motor neuron.
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 Cardiac muscle:
• Have cross striation (banding pattern of thick and thin
filaments).
• Involuntary muscle tissue.
• Have intercalated disc with gap junctions.
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Smooth Muscle:
 Non-striations: Alternating dark and light bands are absent.
 Involuntary muscle
 Lines the walls of most hollow organs: vascular,
gastrointestinal, respiratory, urinary, and reproductive
systems
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Skeletal muscle
 Functional structure:
 Skeletal muscles are usually attached to bone
by tendons composed of connective tissue.
 Connective tissue ensheaths the entire muscle &
is called epimysium.
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 Skeletal muscles consist of bundles
called fascicles.
 Fascicles are also surrounded by
connective tissue (perimysium)
• Each fascicle is composed of numerous
muscle fibers (muscle cells).
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 Muscle cells are ensheathed by endomysium, and
consists many myofibrils;
 Myofibrils are made up of long protein molecules called
myofilaments.
 There are two types of myofilaments: thick
myofilaments and thin myofilaments.
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• Has striated appearance: produced due to the alternating arrangement of
dark(thick) and light(thin) filaments in the myofibrils
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 Sarcomere:
• Functional unit
• Contractile segment of muscle
• It is the distance between two z-lines.
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Molecular geometry
A-Band (A= Anisotropisch):
 Darker area in the center of the
sarcomere.
 It occurs due to the orderly
arrangement of thick filaments.
 Thin filaments may extend into
the A-band.
H-Band (H = Hensen’s disc):
 It contains only myosin tails (no
myosin heads/no cross-bridges)
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M-line (M= Mittelmembran):
 Join tail of two thick filaments
together
 It contains 2 important proteins:
• Myomesin: a structural protein that links
neighboring thick filaments
• Creatinine Phosphokinase: an enzyme
that maintains adequate ATP conc. in
working muscle fibers.
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I-Band (I= Isotropisch):
 The lighter area on either side of the z-
lines.
 Each sarcomere contain half of the two I-
bands.
 Thin filaments
Z-Line/Disc (Z = Zwischenscheibe)
 Dense line in the center of each light
band.
 Separates one sarcomere from the next.
 It is the attachment site for the thin filaments.
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Classification based on speed of shortening
Muscles have different proportions of fibers, slow and fast twitch fibers
Two types of muscle fibers:
 Slow twitch/ type I/ fiber: resist fatigue for higher
endurance activity
 Fast twitch/ type II/ fiber: for better sprinter
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Skeletal muscle contraction
 Sliding Filament Theory of Contraction:
 When a muscle contracts it decreases in length as a result of the shortening
of muscle fibers.
 Shortening of the muscle fibers is produced by shortening of their myofibrils
 Shortening of myofibrils occurs as a result of the shortening of the distance
from Z line to Z line.
 Shortening of sarcomere length occurs due to sliding of thin filament over the
thick.
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Motor unit: Each somatic motor neuron, together with all of the muscle fibers that it
innervates
- Each muscle fiber receives a single axon terminal from a somatic
motor neuron.
1:100 to
1:2,000
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 Motor neuron stimulates the muscle fiber to contract by liberating acetylcholine
at the neuromuscular junction(NMJ).
 Motor end plate: specialized region of the sarcolemma of the muscle fiber at NMJ.
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Mechanism of skeletal muscle contraction:
1. Events at NMJ:
 Presynaptic somatic motor neuron end:
 AP in presynaptic somatic motor neuron propagates to the axon terminals
 This depolarize plasma membrane of the presynaptic somatic motor
neuron axon terminals, causes
 Opening of voltage gated Ca2+ channels at the active zones →↑Ca2+
permeability and entry of Ca2+ into neuron axon terminals
 Release of Ach from the synaptic vesicles into the synaptic cleft
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2. Motor end plate:
Diffusion of Ach to post junctional membrane → combination of Ach with
nicotinic Ach receptor on the motor endplate
 Opening of the Ach gated Na+ channel→↑ permeability of the motor end plate
to Na+
 Transient change in the Motor end→ depolarization → Endplate potential/EPP/
 EPP depolarizes areas of muscle membrane adjacent to endplate and causes
initiation of AP on sarcolemma
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3. Sarcolemma & Sarcoplasm Reticulum
 Propagation of AP across sarcolemma into the T-tubule
 T-tubule: rapid transmission of AP into interior of muscle fiber.
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o AP opens voltage - gated Ca2+ channel (DHPR) on T-tubule and
Ca2+- Release Channel (RyR) in sarcoplasm reticulum membrane.
Depolarization of the T-tubule
↓
Opening of DHPR(Dihydropyridine Receptor) – RyR (Ryanodine
Receptor) Ca2+ channels
(Connected by a foot process whose length is 20nm)
↓
Calcium flows out of the terminal cisternae into the sarcoplasm
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DHPR and RyR Calcium channels
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4. Activation of muscle protein & Contraction:
Influx of Ca2+
↓
Binds to Troponin C (4Ca2+)
↓
Conformational change in troponin
↓
Tropomyosin moves aside
↓
Exposes the myosin-binding sites on actin
↓
Myosin cross-bridge on the thick filament bind to actin filamentscontraction
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5. Relaxation of Muscle:
 Removal of Ca2+ from the sarcoplasm into the SR.
 For Ca2+ removal from the sarcoplasm the third ATP is consumed by Ca2+-
ATPase/SERCA
 After removal of Ca2+ :
• Troponin returns to its original conformational state.
• Tropomyosin inhibition of Myosin-Actin interaction is restored.
• Cross-bridge cycling stops and the muscle is returned to its resting state.
 Breakdown of Ach by AChE.
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 Regulatory function of ATP:
 Actin + Myosin +ATP + Ca2+
Contraction
 Actin+ Myosin + ATP – Ca2+
Relaxation
 3 ATP molecules are needed:
• For energizing the myosin cross-bridges
• For dissociation of actin-myosin complex and initiation of relaxation
• To pump out Ca2+ from the sacroplasm to sequester it into the SR(Ca2+pump/SERCA)
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Changes in banding pattern
Relaxed
muscle
Partially contracted
muscle
Fully contracted
muscle
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Excitation-Contraction Coupling
 Process by which an action potential initiates the contractile process.
 1st – Action potential is propagated thru T-tubule to
the interior and there is release of Ca2+ from terminal cisternae of sarcoplasmic
reticulum
2nd –Muscle protein is activated by Ca2+
3rd –Tension is generated by the muscle proteins
4th – Ca2+ removed
5th –Relaxation of the muscle
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Summary
Discharge of motor neuron
↓
Release of Ach at motor endplate
↓
Binding of Ach to nAchR
↓
↑gNa+ in endplate membrane
↓
Generation of EPP
↓
Generation of AP in muscle fibers
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2
Generation of AP in muscle fibers
↓
Inward spread of depolarization along T-tubules
↓
Release of Ca2+ from terminal cisterns of SR into sarcoplasm
↓
Binding of Ca2+ to troponin C, uncovering myosin-binding sites on actin
↓
Formation of cross-linkages between actin and myosin and sliding of thin
on thick filaments, producing contraction/movement/
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3
Steps in relaxation:
Ca2+ pumped back into SR
↓
Release of Ca2+ from troponin
↓
Cessation of interaction between actin and myosin
↓
Muscle return to resting state
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 Modes of skeletal muscle contraction:
Isotonic contraction??
Vs
Isometric contraction??
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 Clinical correlates:
?Rigor mortis????
?Tetanic contraction???
?Mysthenia graves???
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Clinical Correlates
Rigor Mortis- Several hours after death, all the muscles of the
body go into a state of contracture.
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Smooth muscle
 Lines the walls of most hollow organs
 Important therapeutic target to regulate : diameter of blood vessels,
Air ways, GIT,…
 Not striated in appearance=no sarcomere
 No T-tubule or muscle triad structure
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 Two types: single-unit & multi-unit smooth muscle
1) Single-unit(unitary) Smooth muscle:
 Mass of smooth muscle fibers contract together as a single unit.
 The fibers usually are arranged in sheets or bundles, and
 Their cell membranes are adherent to one another at multiple points and are
joined by many gap junctions;
 So that action potentials or ions can travel/flow from one fiber to the next
and cause the muscle fibers to contract together.
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 It is also known as syncytial smooth muscle because of its syncytial
interconnections among fibers.
 It is also called visceral smooth muscle because it is found in the walls of most
viscera of the body, including the gastrointestinal tract, bile ducts, ureters,
uterus, and many blood vessels.
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2) Multi-unit Smooth muscle :
 Composed of discrete, separate smooth muscle fibers
 Cells are not connected by gap junctions; function individually
 Each fiber contract independently of the others.
 Some examples of multi-unit smooth muscle are the ciliary & iris muscles of
the eye, and the piloerector muscles that cause erection of the hairs when
stimulated by the sympathetic nervous system.
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 Structure of smooth muscle:
• Smooth muscle does not have the same striated arrangement of actin
and myosin filaments.
• Large numbers of actin filaments attached to so-called dense bodies.
• Myosin filaments are interspersed among the actin filaments in the
muscle fiber.
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• Some of the membrane-dense bodies of adjacent cells are
bonded together by intercellular protein bridges.
• It is mainly through these bonds that the force of contraction is
transmitted from one cell to the next.
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Structure of smooth muscle:
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Structure of smooth muscle
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Mechanism of smooth muscle contraction

Nerve stimulation, hormonal stimulation, stretch, or change in the chemical
environment of the smooth muscle fiber depolarizes cell membrane of
smooth muscle cell

Increases intracellular calcium ions.

Smooth muscle contain calmodulin instead of troponin.
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Steps:
1) The calcium ions bind with calmodulin.
2) The calmodulin-calcium complex then joins with and activates myosin light
chain kinase.
3) Activated MLCK in turn phosphorylate regulatory chain of myosin
head(MLC).
4) Phosphorylated MLC initiates myosin head binding with actin filament
5) This pulls actin onto myosincontraction.
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 Cessation of Contraction:
- When the calcium ion is removed &
- Myosin LC phosphatase, deactivates MLCK
• Then the cycling stops and contraction ceases.
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Excitation-contraction coupling in smooth muscle.
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 Although most skeletal muscles contract and relax rapidly, most smooth
muscle contraction is prolonged tonic contraction, sometimes lasting for
long periods.
 This is called the latch bridge state, and results from slow rates of
cross-bridge detachment in smooth muscle.
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