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Nerves and Muscles
How a nervous impulse becomes
A muscular contraction
Anatomy of a Motor Neuron
Nerve cell body
Nucleolus
Nissel Bodies
Axon
Schwann Cell
Synaptic Knob
Nucleus
Dendrite
Axon Hillock
Nodes of Ranvier
Myelin Sheath
Synaptic Vesicle
The Nervous ImpulseMembrane potential
• Potential difference
• -is the difference in charge between 2
points –inside and outside the
membrane.
• -cells are said to be polarized
Resting potential
• -the potential difference in a
neuron when there is no impulse.
• -negative ions build up in the
cytosol of the neuron next to the
membrane
• -positive ions build up in the
extracellular fluid next to the
membrane
Charge distribution inside and
outside a nerve cell
Out + + + + + + + + + + + + + + + + + + +
Na
• _____________________________________
• ------------------------------ K
• In + - + - + - + - + - + - + - +
• ------------------------------ • ------------------------------------------------------------Out + + + + + + + + + + + + + + + + + + +
+
The Facts
• Out side the nerve membrane is positive
due to Sodium ions
• Inside the membrane has positive
potassium ions but also
– Negatively charged ions (like phosphate)
– Negatively charged amino acids
– And the inside of a resting nerve cell is
NEGATIVE!
Potential Difference
• The potential difference of a typical
neuron is -70 millivolts.
• *The minus sign indicates the inside
is relatively negative to the outside.
• Most body cells are “polarized”
Why there is a resting potential:
Unequal distribution of ions across the
membrane
-Extracellular fluid rich in Na+ and Cl-K+ is the main intracellular cation and
phosphates and amino acids are the
main
anions
Relative membrane permeability to Na+
and K+
-permeability of plasma membrane is
50-100 times greater for K+ in a resting
neuron or
muscle fiber.
Potassium ions and resting
potentialRemember diffusion?
-if the membrane were freely
permeable to K+ but impermeable to
other cations,
then K+ would leave the cell until the
electrical gradient (holding K+ inside
the cell) was equal to the chemical
gradient (pushing K+ out of the cell).
The Whole Picture
• transmembrane potential of –90+mV
is the equilibrium potential for K
• The –70 mV membrane potential
+
reflects the effects of Na
• The equilibrium
potential for Na+ is
+
+66 mV (Na would flow inward)
Active Forces Maintaining Resting
Potential
• There is a slow Na+ leak inward
• There is also a slow K+ leak outward.
• These are countered by the action of Na/K
pumps and ATPase
• Sodium pumps are electrogenic
– contribute to electronegativity
– pump 3 Na+ out for each 2 K+ in
Graded Potentials
excitable tissue responds to environmental
stimuli
• response is a small change in membrane
potential
• -results from opening or closing of
membrane channels
• membrane can become more polarized
-hyperpolarization
• membrane can become less polarized
-hypopolarization
• -60
-60
•
********
•
******
• -70
****
-70
•
******
•
**
• -80 *******
-80
____________________________________________
_
time (msec)10
time (msec)
10
•
• Hyperpolarization
Hypopolarization
Important points:
• Graded membrane potentials
are localized
• Only spread a short distance
down the membrane
ACTION POTENTIALS
• A sequence of events that will result in a
•
•
•
•
reversal of membrane potential and then
restore resting potential.
Result from the opening of 2 types of voltage
gated channels
-1st lets Na+ rush into the cell = depolarization
-2nd lets K+ flow out of the cell = repolarization
-whole process takes 1 msec
GENERATION OF AN ACTION
POTENTIAL
Definitions:
• Leakage channels: always open
• Voltage gated channel: opens in
response to a change in membrane
potential -has 2 separate gates:
• Inactivation gate= open during
resting potential
• Activation gate= closed during
resting, opens when the threshold is
reached
1. Depolarization to Threshold
• Depolarizing graded potential
(local currents)
• Potential difference reaches
threshold (-55mV)
Activation of Sodium Channels,
Rapid Depolarization
• Voltage gated Na+ channels
rapidly start to open
• -Inactivation channels stay open
in resting potential
• -Activation channels open,
membrane becomes more
permeable to Na+
Next………
• Inrush of Na+ results in
depolarization
• Depolarization causes inflow of
Na+, which causes further
depolarization, which increases
Na+ inflow -a positive feedback
system.
• Membrane potential goes from –
55mV to +30 mV in one millisec.
Sodium Channel Inactivation and Potassium
Channel Activation. -Repolarizing Phase
• Positive potential results in a closing
of Na inactivation channels
• Threshold depolarization opens
voltage gated K+ channels
• K+ gated channels open slowly
• Na+ channels close- Na+ inflow slows
• Both electrical and chemical
gradients favor the movement of K+
out
• Loss of positive charges
restores the membrane
potential to the resting
levels
• Na+ Channels remain
inactivated until
membrane reaches the
threshold
• Remain closed but can
open at this time
And……
• When membrane reaches
normal resting potential, K+
channels begin to close
• Membrane reaches –90 mV
before K+ channels are
closed.
Refractory Period
• Absolute refractory period
• Period where the membrane cannot
respond to stimulation
• Period begins from the point that all
the Na voltage gated channels open
at the threshold –(cannot open
more!)
• Period ends when sodium channels
regain their normal resting condition.
More..
• Relative refractory period is the
period of hyperpolarization before
resting potential is restored that
requires a higher stimulation.
And…..
• Local anesthetics work by blocking
the opening of the voltage gated
sodium channels.
• Propagation of the impulse: spreads
to adjacent regions along the neuron.
SIGNAL TRANSMISSION AT SYNAPSES
• Important terms….
• Presynaptic neurons
• Postsynaptic neurons
• Synaptic cleft
Types:
• Electrical synapses:
• Gap junctions
-Tubular proteins called
connexons
-100 / gap junction
-Connect cytosol of 2 cells
-Provides a path for ions
(current)
• Visceral smooth muscle
• Cardiac muscle
Advantages
• -faster -direct
• -synchronization of the
activity of a group of neurons
or muscle fibers
• -produce coordinated
contractions
• -2 way transmission
Chemical Synapses
• Action potential arrives at synaptic bulb
•
•
•
•
(knob)
Depolarization opens voltage gated Ca2+
channels
Increase in Ca2+ concentration triggers
exocytosis of synaptic vesicles
Neurotransmitters are released into the
synaptic cleft
Diffuse across cleft and bind to
neurotransmitter receptor sites
Jump!
• Binding of neurotransmitter to
receptor is part of a ligand gated
channel, these will open
• Open channels allow the flow of ions
across the membrane.
• Change in the polarization of the
membrane will result.
• One way transfer.
• Acetylcholine is the neurotransmitter
of skeletal muscle
Questions you need to be able to
answer:
•
•
•
•
•
•
•
1. What is potential difference?
2. What is resting potential in a neuron?
3. What is a graded potential?
4. What is an action potential?
5. What is the sequence of events in an action
potential?
6. What is the role of neurotransmitters?
7. What is the sequence of events in the release
of neurotransmitters?
NEUROMUSCULAR JUNCTIONS:
Chapter 10, p315
• Definition: the synapse between a motor
neuron and a skeletal muscle fiber. NMJ
are usually at the middle of long skeletal
muscle fibers.
• Motor neuron divides into many synaptic
“bulbs”
• Motor end plate is the region of the
sarcolemma that is adjacent to the
synaptic bulb.
Important structures in “Jump”!
• Motor Unit: Muscle fibers controlled by a
motor neuron
• Motor Unit
• Motor Neuron
• Neuromuscular Junction
• Motor End Plate
• Sarcolemma
GENERATION OF A MUSCLE
ACTION POTENTIAL
• Motor Neuron releases acetylcholine
(Ach) from the synaptic bulbs
• ACh binds receptors on the
sarcolemma
• Gated
ion channels open letting in
Na+
• Na makes the inside of the muscle
fiber more +
• Triggers muscle action potential
And then…..
• -travels along the sarcolemma
• -into the T tubules
• One nerve impulse triggers one
muscle action potential
• ACh is broken down by
acetylcholinesterase (AChE) –
attached to collagen fibers in the
synaptic cleft
• Muscle action potentials cease
Clinical Correlations:
• Botulinum Toxin: blocks the exocytosis
of synaptic vesicles at NMJ. ACh is not
released and contractions do not occur.
Paralysis
• Curare: binds the ACh receptor so the
gated channel does not open. Paralysis
• Anticholinesterase agents: slow the
activity of cholinesterase. Prolongs the
time ACh is in the synaptic cleft.