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CHAPTER I

INTRODUCTION

1.1. Background
With a mass of only 2 kg (4.5 lb), about 3% of total body weight, the
nervous system is one of the smallest and yet the most complex of the 11 body
systems. The nervous system is an intricate, highly organized network of
billions of neurons and even more neuroglia. The structures that make up the
nervous system include the brain, cranial nerves and their branches, the spinal
cord, spinal nerves and their branches, ganglia, enteric plexuses, and sensory
receptors1.
Nerve cells, or neurons, carry electrical signals rapidly and, in some cases,
over long distances. They are uniquely shaped cells, and most have long, thin
extensions, or processes, that can extend up to a meter in length. In most
pathways, neurons release chemical signals, called neurotransmitters, into the
extracellular fluid to communicate with neighboring cells. In a few pathways,
neurons are linked by gap junctions, allowing electrical signals to pass directly
from cell to cell2.
Using electrical signals to release chemicals from a cell is not unique to
neurons. For example, pancreatic beta cells generate an electrical signal to
initiate exocytosis of insulin- containing storage vesicles. Single-celled
protozoa and plants also employ electrical signaling mechanisms, in many cases
using the same types of ion channels as vertebrates do. Scientists sequencing
ion channel proteins have found that many of these channel proteins have been
highly conserved during evolution, indicating their fundamental importance2.
Although electrical signaling is universal, sophisticated neural networks
are unique to animal nervous systems. Reflex pathways in the nervous system
do not necessarily follow a straight line from one neuron to the next. One
neuron may influence multiple neurons, or many neurons may affect the
function of a single neuron. Thee intricacy of neural networks and their

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neuronal components underlies the emergent properties of the nervous system.
Emergent properties are complex processes, such as consciousness,
intelligence, and emotion, that cannot be predicted from what we know about
the properties of individual nerve cells and their specific connections. The
search to explain emergent properties makes neuroscience one of the most
active research areas in physiology today2.

1.2. Objectives
1.2.1.Activity 1: The Resting Membrane Potential
1. To define the term resting membrane potential.
2. To measure the resting membrane potential in different parts of a
neuron.
3. To determine how the resting membrane potential depends on the
concentrations of potassium and sodium.
4. To understand the ion conductances/ion channels involved in the
resting membrane potential
1.2.2. Activity 2: Receptor Potential
1. To define the terms sensory receptor, receptor potential, sensory
transduction, stimulus modality, and depolarization.
2. To determine the adequate stimulus for different sensory receptors.
3. To demonstrate that the receptor potential amplitude increases with
stimulus intensity.
1.2.3. Activity 3: The Action Potential: Threshold
1. To define the terms action potential, nerve, axon hillock, trigger zone,
and threshold.
2. To predict how an increase in extracellular K + could trigger an action
potential.

1.2.4. Activity 4: The Action Potential: Importance of Voltage-Gated Na+


Channels
1. To define the term voltage-gated channel.
2. To describe the effect of tetrodotoxin on the voltage-gated Na +
channel.

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3. To describe the effect of lidocaine on the voltage-gates Na+ channel.
4. To examine the effects of tetrodotoxin and lidocaine on the action
potential.
5. To predict the effect of lidocraine on pain perception and to predict
the site of action in the sensory neurons (nociceptors) that sense pain.

1.2.5. Activity 5: The Action Potential: Measuring Its Absolute and


Relative
Refractory Periods
1. To define inactivation as it applies to a voltage-gated sodium channel.
2. To define the absolute refractory period and relative refractory period
of an action potential.
3. To define the relationship between stimulus frequency and the
generation of action potentials.
1.2.6. Activity 6: The Action Potential: Coding for Stimulus Intensity
1. To observe the response of axons to longer periods of stimulation.
2. To examine the relationship between stimulus intensity and the
frequency of action potentials.
1.2.7. Activity 7: The Action Potential: Conduction Velocity
1. To define and measure conduction velocity for an action potential.
2. To examine the effect of myelination on conduction velocity.
3. To examine the effect of axon diameter on conduction velocity.

1.2.8. Activity 8: Chemical Synaptic Transmission and Neurotransmitter


Release
1. To define neurotransmitter, chemical synapse, synaptic vehicle, and
postsynaptic potential.
2. To determine the role of calcium ions in neurotransmitter release.
1.2.9.Activity 9: The Action Potential: Putting It All Together
1. To identify the functional areas (for example, the sensory ending,
axon, and postsynaptic membrane) of a two-neuron circuit.
2. To predict and test the responses in each functional area to a very
weak, subthershold stimulus.
3. To predict and test the responses in each functional area to a
moderate stimulus.
4. To predict and test the responses in each functional area to an intense

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stimulus.

1.3. Literature Review


1.3.1. The Resting Membrane Potential
2. The resting membrane potential exists because of a small buildup of
negative ions in the cytosol along the inside of the membrane, and an
equal buildup of positive ions in extracellular fluid along the outside
surface of the membrane. Such a separation of positive and negative
electrical charges is a form of potential energy, which is measured in
volts or millivolts (1mV = 0.001 V). the greater the difference in charge
across the membrane potential (voltage). The cytosol or extracellular
fluid elsewhere in the cell contains equal numbers of positive and
negative charges and is electrically neutral2.
3. In neurons, the resting membrane potential ranges from -40 to -90 mV.
A typical value is -70 mV. The minus sign indicates that the inside of the
cell is negative relatives to the outside2.
4.
1.1.2. Receptor Potential
2. All sensory receptors have one feature in common. Whatever the type of
stimulus that excites the receptor, its immediate effect is to change the
membrane electrical potential of the receptor. This change in potential is
called a receptor potential. Different receptors can be excited in one of
several ways to cause receptor potentials: by mechanical deformation of
the receptor, by application of a chemical to the membrane, by change
of the temperature of the membrane, or by the effect of electromagnetic
radiation3.
3. These four means of exciting receptors correspond in general with the
different types of known sensory receptors. In all instances, the basic
cause of the change in membrane potential is a change in membrane
permeability of the receptor, which allows ion to diffuse more or less
readily through the membrane and thereby to change the transmembrane
potential3.
1.1.3.3. The Action Potential

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.3.4.
Action potentials are brief, rapid, large changes in membrane potential
during which the potential reserves. During an action potential,
depolarization of the membrane from resting potential (-70 mV) to
threshold potential (-50 mV) triggers sequential changes in permeability
caused by conformational changes in voltage-gated Na+ and K+
channels. These permeability changes bring about a brief reversal of
membrane potential, with Na+ influx causing the rising phase (from
threshold to +30 mV), followed by K+ efflux causing the failing phase
(from peak back to resting). The Na+-K+ pump gradually restores the
ions that moved during propagation of the action potential to their
original location, to maintain the concentration gradients4.
.3.4.
Before an action potential returns to resting, it regenerates an identical
new action potential in the area next to it by means of current flow that
brings the previously inactive area to threshold. This self-perpetuating
cycle continues until the action potential spreads undiminished
throughout the cell membrane4.
There are two types of action potential propagation: (1)
contiguous conduction in unmyelinated fibers, in which the action
potential spreads along every portion of the membrane; and (2) the more
rapid, salutatory conduction in myelinated fibers, in which the impulse
jumps from one node of Ranvier to the next over sections of the fiber
covered with insulating myelin4.
It is impossible to restimulate the portion of the membrane where
impulse has just passed until it has recovered from its refractory period,
ensuring the one-way propagation of action potentials. Action potentials
occurs either maximally in response to stimulation or not at all (all or
none law). Variable strengths of stimuli are coded by varying the
frequency of action potentials, not their magnitude, in an activated nerve
fiber4.
1.1.3.4. Chemical Synaptic and Neurotransmitter Release
Most synapse in the human nervous system are chemicals
synapses at which a chemical messenger transmits information one way

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across a space separating the neurons. A chemical synapse typically
involves a junction between an axon terminal of one neuron, known as
the presynaptic neuron and the dendrites or cell body of a second
neuron, as the postsynaptic neuron. (Pre means before, and post
means after; the presynaptic neuron lies before the synapse and the
postsynaptic lies after the synapse). The dendrites and, to a lesser extent,
the cell body of most neurons receive thousands of synaptic inputs,
which are axon terminals from many other neurons. Some neurons in
the CNS receive as many as 100,000 synaptic inputs4.
The axon terminal of the presynaptic neuron, which conduct its
action potential towards the synapse, ends in a slight swelling, the
synaptic knob. The synaptic knob contains synaptic vesicles, which
store a specific chemical messenger a, neurotransmitter that has been
synthesized and packaged by the presynaptic neuron. The synaptic knob
comes close to, but does not touch the postsynaptic neuron, whose
action potentials are propagated away from the synapse. The space
between the presynaptic and postsynaptic neuron is called the synaptic
cleft4.
The membrane of the presynaptic terminal contains large number
of voltage-gated calcium channels. When an action potential depolarized
the presynaptic membrane, these calcium channels open and allow large
number of calcium ions to flow into the terminal. The quantity of
transmitter substance that is then released from the terminal into the
synaptic cleft is directly related to the number of calcium ions that enter.
The precise mechanism by which the calcium ions cause this release is
not known, but it is believed to be the following3.
When the calcium ions enter the presynaptic terminal, it is
believed that they bind with special protein molecules on the inside
surface of the presynaptic membrane called release sites. This binding in
turn causes the release sites to open through the membrane, allowing a

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few transmitter vesicles to release their transmitter into the cleft after
each single action potential3.

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CHAPTER III
METHODOLOGY

This practicum was done by running the PhysioEx 9.1 Laboratory Simulations
in Physiology application on Exercise 3: Neurophysiology of Nerve Impulses from
Acticity 1 to 9.

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CHAPTER IV
RESULT AND DISCUSSION

4.1. Activity 1: The Resting Membrane Potential


4.2. Activity 2: Receptor Potential
4.3. Activity 3: The Action Potential: Threshold
4.4. Activity 4: The Action Potential: Importance of Voltage-Gated Na+
Channels
4.5. Activity 5: The Action Potential: Measuring Its Absolute and Relative
Refractory Periods
4.6. Activity 6: The Action Potential: Coding for Stimulus Intensity
4.7. Activity 7: The Action Potential: Conductivity Velocity
4.7.1. How Did the Conduction Velocity in the B Fiber Compare with
That in the A Fiber? How Well Did the Results Compared with Your
Prediction?
4.7.2. How Did the Conduction Velocity in the C Fiber Compared with
That in the B Fiber? How Well Did the Results Compared with Your
Prediction?
4.7.3. What is the Effect of Axon Diameter on Conduction Velocity?
4.7.4. What is the Effect of the Amount of Myelination on Conduction
Velocity ?
4.7.5. Why Did the Time Between Stimulation and the Action Potential
at R1 Differ for Each Axon?
4.7.6. Why Did You Need to Change the Timescale on the Oscilloscope
for Each Axon?
4.8. Activity 8: Chemical Synaptic Transmission and Neurotransmitter
Release
4.8.1. When the Stimulus Intensity is Increased, What Changes: the
Number of Synaptic Vesicles or the Amount of Neurotransmitter per
vesicle?
4.8.2. What Happened to the Amount of Neurotransmitter Release
When You Switched from the Control Extracellular Fluid to the
Extracellular Fluid with No Ca2+? How Well the Results Compared
with Your Prediction?
4.8.3. What Happened to the Amount of Neurotransmitter Release
When You Switched from the Extracellular Fluid with No Ca2+ to the

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Extracellular Fluid with Low Ca2+? How Well Did the Results
Compared with Your Prediction?
4.8.4. How Did Neurotransmitter Release in the Mg2+ Extracellular Fluid
Compared to that in the Control Extracellular Fluid? How Well Did
the Results Compared with Your Prediction?
4.8.5. How Does Mg2+ Block the Effect of Extracellular Calcium on
Neurotransmitter Release?
4.9. Activity 9: The Action Potential: Putting It All Together
4.9.1. Why is the Resting Membrane Potential the Same Value in Both
the Sensory Neuron and the Interneuron?
4.9.2. Describe What Happened when You Applied a Very Weak
Stimulus to the Sensory Receptor. How Well Did the Results
Compared with Your Prediction?
4.9.3. Describe What Happened when You Applied a Moderate Stimulus
to the Sensory Receptor. How Well Did the Results Compared with
Your Prediction?
4.9.4. Identify the Type of Membrane Potential (Graded Receptor
Potential or Action Potential) that Occurred at R1, R2, R3, and R4
when You Applied a Moderate Stimulus (View Experiment Results to
View the Response to this Stimulus).
4.9.5. Describe What Happened when You Applied a Strong Stimulus to
the Sensory Receptor. How Well Did the Results Compared with Your
Prediction?

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