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Science Brain and Behavior contiuned 16

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story of how damage to one such neurotransmitter system
results in a specific neurological disorder, beginning with
“Parkinson’s Disease” on page 152.
Structure of Synapses
Loewi’s discovery about the regulation of heart rate by
chemical messengers was the first of two important findings
that form the foundation for current understanding of
how neurons communicate. The second had to wait nearly
30 years, for the invention of the electron microscope,
which enabled scientists to see the structure of a synapse.
The electron microscope, shown on the right in Figure
5-1, uses some of the principles of both an oscilloscope and
a light microscope, shown at the left. The electron microscope
works by projecting a beam of electrons through a
very thin slice of tissue. The varying structure of the tissue
scatters the beam onto a reflective surface where it leaves
an image, or shadow, of the tissue.
The resolution of an electron microscope is much
higher than that of a light microscope because electron
waves are smaller than light waves and so there is much less scatter when the beam
strikes the tissue. If the tissue is stained with substances that reflect electrons, very fine
structural details can be observed. Compare the images at the bottom of Figure 5-1.
The first good electron micrographs, made in the 1950s, revealed the structure of
a synapse for the first time. In the center of the micrograph in Figure 5-2A, the upper
part of the synapse is the axon end terminal; the lower part is the dendrite. Note the
Figure 5-1
Microscopic Advance Whereas a light
microscope (left) can be used to see the
general features of a cell, an electron
microscope (right) can be used to
examine the details of a cell’s organelles.
Organelle that provides
the cell with energy.
Microtubule: Transport
structure that carries
substances to the axon
Synaptic vesicle:
Round granule
that contains
Storage granule:
Large compartment
that holds
synaptic vesicles.
receptor: Site to
which a neurotransmitter
molecule binds.
Postsynaptic membrane:
Contains receptor
molecules that receive
chemical messages.
Presynaptic membrane:
Encloses molecules
that transmit chemical
Synaptic cleft: Small
space separating
presynaptic terminal
and postsynaptic
dendritic spine.
Dendrite of
Glial cell
Figure 5-2
Chemical Synapse (A) Electron photomicrograph
of a synapse. Surrounding the centrally located synapse
are glial cells, axons, dendrites, and other synapses.
(B) Characteristic parts of a synapse. Neurotransmitter,
contained in vesicles, is released from storage granules
and travels to the presynaptic membrane where it is
expelled into the synaptic cleft through the process of
exocytosis. The neurotransmitter then crosses the cleft and
binds to receptor proteins on the postsynaptic membrane.
Electron microscope
Electron gun
Light microscope
R. Roseman/Custom
Medical Stock
Courtesy of Jeffrey Klein
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152 ! CHAPTER 5
Parkinson’s Disease
Focus on Disorders
Case VI: The gentleman . . . is seventy-two years of
age. He has led a life of temperance, and has never
been exposed to any particular situation or circumstance
which he can conceive likely to have occasioned,
or disposed to this complaint: which he
rather seems to regard as incidental on his advanced
age, than as an object of medical attention.
. . . About eleven or twelve, or perhaps more,
years ago, he first perceived weakness in the left
hand and arm, and soon after found the trembling
to commence. In about three years afterwards the
right arm became affected in a similar manner: and
soon afterwards the convulsive motions affected the
whole body and began to interrupt speech. In about
three years from that time the legs became affected.
Of late years the action of the bowels had been very
much retarded. (James Parkinson, 1817/1989)
In his 1817 essay from which this case study is taken, James
Parkinson reported similar symptoms in six patients, some of
whom he observed only in the streets near his clinic. Shaking
was usually the first symptom, and it typically began in
a hand. Over a number of years, the shaking spread to include
the arm and then other parts of the body. As the disease
progressed, patients had a propensity to lean forward
and walk on the forepart of their feet. They also tended to run
forward to prevent themselves from falling.
In the later stages of the disease, patients had difficulty
eating and swallowing. They drooled and their bowel movements
slowed. Eventually, the patients lost all muscular control
and were unable to sleep because of the disruptive
More than 50 years after James Parkinson first described
this debilitating set of symptoms, French neurologist Jean
Charcot named them Parkinson’s disease in recognition of
the accuracy of Parkinson’s observations. Three major findings
have helped researchers understand the neural basis of
Parkinson’s disease.
The first came in 1919 when Constantin Tréatikoff studied
the brains of nine Parkinson patients on autopsy and
found that the substantia nigra (black substance), an area of
the midbrain described in Chapter 2, had degenerated. In the
brain of one patient who had experienced symptoms of
Parkinson’s disease on one side of the body only, the substantia
nigra had degenerated on the side opposite that of the
symptoms. These observations clearly implicated the substantia
nigra in the disorder.
The other two major findings about the neural basis of
Parkinson’s disease came almost half a century later when
methods for analyzing the brain for neurotransmitters had
been developed. One was the discovery that a single neurotransmitter,
dopamine, is related to the disorder, and the
other was that axons containing dopamine connect the substantia
nigra to the basal ganglia.
First, the examination of the brains of six Parkinson patients
during autopsies showed that the dopamine level in
the basal ganglia was reduced to less than 10 percent of normal
(Ehringer & Hornykiewicz, 1960). Confirming the role of
dopamine in this disorder, Urban Ungerstedt found in 1971
that injecting a neurotoxin called 6-hydroxydopamine into
rats selectively destroyed neurons containing dopamine and
produced the symptoms of Parkinson’s disease as well.
The results of these studies and many others, including
anatomical ones, show that (1) the substantia nigra contains
dopamine neurons and (2) the axons of these neurons project
to the basal ganglia. The death of these neurons and the
loss of the neurotransmitter from their terminals create the
symptoms of Parkinson’s disease.
Researchers do not yet know exactly why dopamine
neurons start to die in the substantia nigra of patients who
have the idiopathic form of Parkinson’s disease. (Idiopathic
refers to a condition related to the individual person, not to
some external cause such as a neurotoxin). Discovering why
idiopathic Parkinsonism arises is an important area of ongoing
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round granular substances in the terminal. They are the synaptic vesicles containing
the neurotransmitter.
The dark patches on the dendrite consist mainly of protein receptor molecules that
receive chemical messages. Dark patches on the axon terminal membrane are protein
molecules that serve largely as channels and pumps to release the transmitter or to recapture
it once it is released. The terminal and the dendrite are separated by a small
space, the synaptic cleft.
You can also see on the micrograph that the synapse is sandwiched by many surrounding
structures. These structures include glial cells, other axons and dendritic
processes, and other synapses. The surrounding glia contribute to chemical neurotransmission
in a number of ways—by supplying the building blocks for the synthesis
of neurotransmitters or mopping up excess neurotransmitter molecules, for example.
The drawing in Figure 5-2B details the process of neurotransmission at a chemical
synapse, the junction where messenger molecules are released from one neuron to excite
the next neuron. In this example, the presynaptic membrane forms the axon terminal,
the postsynaptic membrane forms the dendritic spine, and the space between the
two is the synaptic cleft.Within the axon terminal are: specialized structures, including
mitochondria, the organelles that supply the cell’s energy needs; storage granules, large
compartments that hold several synaptic vesicles; and microtubules that transport substances,
including the neurotransmitter, to the terminal.
Chemical synapses are the rule in mammalian nervous systems, but they are not
the only kind of synapse. Rare in mammals but commonly found in other animals, the
electrical synapse (also known as a gap junction) is a fused presynaptic and postsynaptic
membrane that allows an action potential to pass directly from one neuron to
the next. This fusion prevents the brief delay in information flow—about 5 ms per
synapse—of chemical transmission. For example, the crayfish’s electrical synapses activate
its tail flick, a response that allows it to escape quickly from a predator.
Why, if chemical synapses transmit messages more slowly, do mammals depend on
them almost exclusively? The benefits outweigh the drawback of slowed communication.
Probably the greatest benefit is the flexibility that chemical synapses allow in controlling
whether a message is passed from one neuron to the next.
Neurotransmission in Four Steps
The four-step process of chemically transmitting information across a synapse is illustrated
in Figure 5-3 and explained in this section. In brief, the neurotransmitter must be
1. synthesized and stored in the axon terminal;
2. transported to the presynaptic membrane and released in response to an action
3. able to activate the receptors on the target cell membrane located on the postsynaptic
membrane; and
4. inactivated or it will continue to work indefinitely.
Neurotransmitters are derived in two general ways. Some are synthesized in the axon
terminal from building blocks derived from food. Transporters, protein molecules
that pump substances across the cell membrane, absorb the required precursor chemicals
from the blood supply. (Sometimes transporter proteins absorb the neurotransmitter
ready-made.) Mitochondria in the axon terminal provide the energy needed
both to synthesize precursor chemicals into the neurotransmitter and to wrap them in
membranous vesicles.
Dopamine (DA). Amine
neurotransmitter that plays a role in
coordinating movement, in attention and
learning, and in behaviors that are
Synaptic vesicle. Organelle consisting
of a membrane structure that encloses a
quantum of neurotransmitter.
Synaptic cleft. Gap that separates the
presynaptic membrane from the
postsynaptic membrane.
Chemical synapse. Junction where
messenger molecules are released when
stimulated by an action potential.
Presynaptic membrane. Membrane on
the transmitter-output side of a synapse.
Postsynaptic membrane. Membrane
on the transmitter-input side of a synapse.
Storage granule. Membranous
compartment that holds several vesicles
containing a neurotransmitter.
Electrical synapse. Fused presynaptic
and postsynaptic membrane that allows
an action potential to pass directly from
one neuron to the next.
Transporter. Protein molecule that
pumps substances across a membrane
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154 ! CHAPTER 5
Other neurotransmitters, as described in Chapter 3, are synthesized in the cell body
according to instructions contained in the neuron’s DNA, packaged in membranes on
the Golgi bodies, and transported on microtubules to the axon terminal. Cell-derived
neurotransmitters may also be manufactured within the presynaptic terminal from
mRNA that is similarly transported to the terminal.
Regardless of their origin, neurotransmitters in the axon terminal can usually be
found in three locations, depending on the type of neurotransmitter in the terminal.
Some vesicles are warehoused in granules, as mentioned earlier. Other vesicles are attached
to microfilaments in the terminal, and still others are attached to the presynaptic
membrane, ready to release their content into the synaptic cleft.After the contents of
a vesicle have been released from the presynaptic membrane, other vesicles move into
place at that membrane location, ready for release when needed.
When an action potential is propagated on the presynaptic membrane, voltage changes
on the membrane set the release process in motion. Calcium cations (Ca2!) play an
important role. The presynaptic membrane is rich in voltage-sensitive calcium channels,
and the surrounding extracellular fluid is rich in Ca2!.As illustrated in Figure 5-4,
the action potential’s arrival opens these calcium channels, allowing an influx of calcium
ions into the axon terminal.
The incoming Ca2! binds to the protein calmodulin, and the resulting complex takes
part in two chemical reactions: one releases vesicles bound to the presynaptic membrane,
and the other releases vesicles bound to filaments in the axon terminal. The vesicles
released from the presynaptic membrane empty their contents into the synaptic cleft
Synthesis: Building
blocks of a transmitter
substance are imported
into the terminal…
Release: In response
to an action potential,
the transmitter is
released across the
membrane by
Receptor action: The
transmitter crosses
the synaptic cleft and
binds to a receptor.
3 Inactivation: The
transmitter is either
taken back into the
terminal or inactivated
in the synaptic cleft.
… where the
is synthesized and
packaged into
Figure 5-3
Synaptic Transmission
This complex binds to vesicles, releasing
some from filaments and inducing others
to bind to the presynaptic membrane
and to empty their contents.
When an action
potential reaches the
terminal, it opens
calcium channels.
Incoming calcium ions bind to
calmodulin, forming a complex.
Figure 5-4
Neurotransmitter Release
You can use your Foundations of
Behavioral Neuroscience CD to better
visualize the structure and function of the
axon terminal. Go to the section on
synaptic transmission in the neural
communication module and watch the
animation. Note how the internal
components work as a unit to release
neurotransmitter substances across the
synapse. (See the Preface for more
information about this CD.)
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through the process of exocytosis,described in Chapter 3.The vesicles that were formerly
bound to the filaments then migrate to the presynaptic membrane to replace the vesicles
that just emptied their contents.
After the neurotransmitter has been released from vesicles on the presynaptic membrane,
it diffuses across the synaptic cleft and binds to specialized protein molecules
embedded in the postsynaptic membrane. These transmitter-activated receptors have
binding sites for the transmitter substance, or ligand. The postsynaptic cell may be affected
in one of three ways, depending on the type of neurotransmitter and the kind
of receptors on the postsynaptic membrane. The transmitter may
1. depolarize the postsynaptic membrane and so have an excitatory action on the
postsynaptic neuron,
2. hyperpolarize the postsynaptic membrane and so have an inhibitory action on the
postsynaptic neuron, or
3. initiate other chemical reactions that modulate either effect, inhibitory or excitatory,
or that influence other functions of the receiving neuron.
In addition to interacting with the postsynaptic membrane’s receptors, a neurotransmitter
may interact with receptors on the presynaptic membrane. That is, it may
influence the cell that just released it. Presynaptic receptors that a neurotransmitter
may activate are called autoreceptors (self-receptors) to indicate that they receive messages
from their own axon terminals.
How much neurotransmitter is needed to send a message? In the
1950s, Bernard Katz and his colleagues provided an answer. Recording
electrical activity from the postsynaptic membranes of muscles,
they detected small, spontaneous depolarizations they called miniature
postsynaptic potentials. The potentials varied in size, but each size
appeared to be a multiple of the smallest potential.
The researchers concluded that the smallest postsynaptic potential
is produced by releasing the contents of just one synaptic vesicle.
They called this amount of neurotransmitter a quantum. To produce a postsynaptic
potential that is large enough to initiate a postsynaptic action potential requires the simultaneous
release of many quanta from the presynaptic cell.
The results of subsequent experiments show that the number of quanta released
from the presynaptic membrane in response to a single action potential depends on
two factors: (1) the amount of Ca2! that enters the axon terminal in response to the
action potential and (2) the number of vesicles docked at the membrane, waiting to be
released. Both these factors are relevant to synaptic activity during learning, which we
consider at the end of the chapter.
Chemical transmission would not be a very effective messenger system if a neurotransmitter
lingered within the synaptic cleft, continuing to occupy and stimulate receptors.
If this happened, the postsynaptic cell could not respond to other messages
sent by the presynaptic neuron. Therefore, after a neurotransmitter has done its work,
it is quickly removed from receptor sites and from the synaptic cleft.
Deactivation is accomplished in at least four ways. One way is diffusion: some
of the neurotransmitter simply diffuses away from the synaptic cleft and is no longer
available to bind to receptors. The second way is degradation by enzymes in the synaptic
Transmitter-activated receptor.
Protein embedded in the membrane of a
cell that has a binding site for a specific
Autoreceptor. “Self-receptor” in a
neural membrane that responds to the
transmitter that the neuron releases.
Quantum (pl. quanta). Quantity,
equivalent to the contents of a single
synaptic vesicle, that produces a just
observable change in postsynaptic
electric potential.
Bernard Katz
(b. 1911)
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156 ! CHAPTER 5
cleft. In the third way, membrane transporter proteins may bring the transmitter back
into the presynaptic axon terminal for subsequent reuse, a process called reuptake.
The by-products of degradation by enzymes also may be taken back into the terminal to
be used again in the cell. Fourth, some neurotransmitters are taken up by neighboring
glial cells. Potentially, the glial cells can also store transmitter for reexport to the axon
Interestingly, an axon terminal has chemical mechanisms that enable it to respond to
the frequency of its own use. If the terminal is very active, the amount of neurotransmitter
made and stored there increases. If the terminal is not often used, however, enzymes
located within the terminal may break down excess transmitter. The by-products
of this breakdown are then reused or excreted from the neuron.Axon terminals may even
send messages to the neuron’s cell body requesting increased supplies of the neurotransmitter
or the molecules with which to make it.
Varieties of Synapses
So far, we have considered a generic chemical synapse, with features that most synapses
possess. In the nervous system, synapses vary widely, each relatively specialized in location,
structure, function, and target. Figure 5-5 illustrates this diversity on a single
hypothetical neuron.
You have already encountered two kinds of synapses in Chapter 4. One is the axodendritic
synapse detailed in Figure 5-2, in which the axon terminal of a neuron ends
on a dendrite or dendritic spine of another neuron. The other synapse familiar to you
Dendrodendritic: Dendrites
send messages to other
Axodendritic: Axon terminal
of one neuron synapses on
dendritic spine of another.
Axoextracellular: Terminal
with no specific target.
Secretes transmitter into
extracellular fluid.
Axosomatic: Axon terminal
ends on cell body.
Axosynaptic: Axon terminal
ends on another terminal.
Axoaxonic: Axon terminal
ends on another axon.
Axosecretory: Axon terminal
ends on tiny blood vessel
and secretes transmitter
directly into blood.
Figure 5-5
The Versatile Synapse
Reuptake. Deactivation of a
neurotransmitter when membrane
transporter proteins bring the transmitter
back into the presynaptic axon terminal
for subsequent reuse.
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is the axomuscular synapse, in which an axon synapses with a muscle end plate to stimulate
movement (see Figure 4-23B). In addition, Figure 5-5 illustrates the axosomatic
synapse, an axon terminal ending on a cell body; the axoaxonic synapse, an axon terminal
ending on another axon; and the axosynaptic synapse, an axon terminal ending
on another presynaptic terminal—that is, a synapse between some other axon and its
Axoextracellular synapses have no specific targets but instead secrete their transmitter
chemicals into the extracellular fluid. In the axosecretory synapse, a terminal
synapses with a tiny blood vessel called a capillary and secretes its transmitter directly
into the blood. Finally, synapses are not limited to axon terminals. Dendrites also may
send messages to other dendrites through dendrodendritic synapses.
This wide variety of connections makes the synapse a versatile chemical delivery
system. Synapses can deliver transmitters to highly specific sites or to diffuse locales.
Through connections to the dendrites, cell body, or axon of a neuron, transmitters can
control the actions of that neuron in different ways.
Through axosynaptic connections, they can also provide exquisite control over another
neuron’s input to a cell. By excreting transmitters into extracellular fluid or into
the blood, axoextracellular and axosecretory synapses can modulate the function of
large areas of tissue or even of the entire body. Recall that many transmitters secreted
by neurons act as hormones circulating in your blood, with widespread influences on
your body.
Excitatory and Inhibitory Messages
A neurotransmitter can influence the function of a neuron in a remarkable number
of ways. In its direct actions in influencing a neuron’s electrical excitability, however,
a neurotransmitter acts in only one of two ways: either to increase or to decrease the
probability that the cell with which it comes in contact will produce an action potential.
Thus, despite the wide variety of synapses, they all convey messages of only
these two types: excitatory or inhibitory. For simplicity, Type I synapses are excitatory
in their actions, whereas Type II synapses are inhibitory. Each type has a different
appearance and is located on different parts of the neurons under its
As shown in Figure 5-6, Type I synapses are typically located on the
shafts or the spines of dendrites, whereas Type II synapses are typically located
on a cell body. In addition, Type I synapses have round synaptic vesicles,
whereas the vesicles of Type II synapses are flattened. The material on
the presynaptic and postsynaptic membranes is denser in a Type I synapse
than it is in a Type II, and the Type I cleft is wider. Finally, the active zone
on a Type I synapse is larger than that on a Type II synapse.
The different locations of Type I and Type II synapses divide a neuron
into two zones: an excitatory dendritic tree and an inhibitory cell body.
You can think of excitatory and inhibitory messages as interacting from
two different perspectives.
Viewed from an inhibitory perspective, you can picture excitation
coming in over the dendrites and spreading to the axon hillock to trigger
an action potential. If the message is to be stopped, it is best stopped by
applying inhibition on the cell body, close to the axon hillock where the
action potential originates. In this model of excitatory–inhibitory interaction,
inhibition blocks excitation in a “cut ’em off at the pass” strategy.
Type I
Type II
Dendritic shaft
Cell body
Axon hillock
Dense material
on membranes
Sparse material
on membranes
Wide cleft
Narrow cleft
Small active
Large active
Figure 5-6
Excitatory and Inhibitory Zones
Excitatory Type I synapses occupy the
spines and dendritic shafts of the
neuron, and inhibitory Type II synapses
are found on the cell body.
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Another way to conceptualize excitatory–inhibitory interaction is to picture excitation
overcoming inhibition. If the cell body is normally in an inhibited state, the only
way to generate an action potential at the axon hillock is to reduce the cell body’s inhibition.
In this “open the gates” strategy, the excitatory message is like a racehorse
ready to run down the track, but first the inhibitory starting gate must be removed.
In Chapter 2, you met the nineteenth-century English neurologist John Hughlings-
Jackson, who recognized both the role of inhibition and the release of behavior seen in
human neurological disorders when inhibitory messages are blocked. Characteristic
symptoms are “released” when a normal inhibitory influence is lost. The tremors of
Parkinson’s disease, a prime example, must be caused by rhythmically active neurons
that are ordinarily under inhibition. An involuntary unwanted movement such as a
tremor is called a dyskinesia (from the Greek dys, meaning “disordered,” and kinesia,
meaning “movement”).
Evolution of Complex Neurotransmission Systems
Considering all the biochemical steps required for getting a message across a synapse
and the variety of synapses, you may well wonder why—and how—such a complex
communication system ever evolved. This arrangement must make up for its complexity
in the considerable behavioral flexibility that it affords the nervous system. Flexible
behavior is a decided evolutionary advantage.
How did chemical transmitters come to dominate this complex communication
system? If you think about the feeding behaviors of simple single-celled creatures, the
origin of chemical secretions for communication is not that hard to imagine. The earliest
unicellular creatures secreted juices onto bacteria to immobilize and prepare them
for ingestion. These digestive juices were probably expelled from the cell body by exocytosis,
in which a vacuole or vesicle attaches itself to the cell membrane and then
opens into the extracellular fluid to discharge its contents. The prey thus immobilized
is captured through the reverse process of endocytosis.
The mechanism of exocytosis for digestion parallels its use to release a neurotransmitter
for communication. Quite possibly the digestive processes of single-celled
animals were long ago adapted into processes of neural communication in more complex
In Review\ .
In mammals, the principal form of communication between neurons is chemical. Chemical
neurotransmission appears to be an adaptation of processes used by single-celled organisms
to immobilize, ingest, and digest food. When an action potential is propagated
on an axon terminal, a chemical transmitter is released from the presynaptic membrane
into the synaptic cleft. There the transmitter diffuses across the cleft and binds to receptors
on the postsynaptic membrane, after which the transmitter is deactivated. The nervous
system has evolved a variety of synapses, between axon terminals and dendrites, cell
bodies, muscles, other axons, and even other synapses. One variety of synapse releases
chemical transmitters into extracellular fluid or into the bloodstream as hormones, and
still another connects dendrites to other dendrites. Chemical synapses, though slower and
more complex than electrical synapses, more than compensate by greatly increasing behavioral
flexibility. Even though synapses vary in both structure and location, they all do
one of only two things: excite their targets or inhibit them.
158 ! CHAPTER 5
On the Foundations CD, find the area
on synaptic transmission in the neural
communication module. In the sections
on excitatory and inhibitory synapses,
watch the animations to learn more about
excitatory and inhibitory messages.
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Subsequent to the discovery that excitatory and inhibitory chemicals control heart rate,
many researchers of the 1920s thought that the brain must work under much the same
dual-type control. They reasoned that there must be excitatory and inhibitory brain
cells and that norepinephrine and acetylcholine were the transmitters through which
these neurons worked. They could never have imagined what we know today: the
human brain may employ as many as 100 neurotransmitters, which may be excitatory
at one location and inhibitory in another, and more than one neurotransmitter may be
active at a single synapse.
Although neuroscientists are now certain of only about 50 substances that act as
neurotransmitters, discovery in this field continues. Few scientists are willing to put an
upper limit on the eventual number of transmitters that will be found. In this section,
you will learn how neurotransmitters are identified and how they fit within three broad
categories based on their chemical structure. The functional aspects of neurotransmitters
interrelate and are intricate, with no simple one-to-one relation between a single
neurotransmitter and a single behavior.
Identifying Neurotransmitters
Among the many thousands of chemicals in the nervous system, which are neurotransmitters?
Figure 5-7 presents four identifying criteria:
1. The chemical must be synthesized in the neuron or otherwise be present in it.
2. When the neuron is active, the chemical must be released and produce a response
in some target.
3. The same response must be obtained when the chemical is experimentally placed
on the target.
4. A mechanism must exist for removing the chemical from its site of action after its
work is done.
The criteria for identifying a neurotransmitter are fairly easy to apply when examining
the somatic nervous system, especially at an accessible nerve–muscle junction with
only one main neurotransmitter, acetylcholine. But identifying chemical transmitters in
the central nervous system is not so easy. In the brain and spinal cord, thousands of
synapses are packed around every neuron, preventing easy access to a single
synapse and its activities. Consequently, for many of the substances
thought to be CNS neurotransmitters, the four criteria have been met
only to varying degrees. A suspect chemical that has not yet been shown
to meet all the criteria is called a putative (supposed) transmitter.
Researchers trying to identify new CNS neurotransmitters use microelectrodes
to stimulate and record from single neurons. A glass
microelectrode is small enough to be placed on specific targets on a
neuron. It can be filled with a chemical of interest and, when a current
is passed through the electrode, the chemical can be ejected into or onto
the neuron to mimic the release of a neurotransmitter onto the cell.
New staining techniques can identify specific chemicals inside the
cell. Methods have also been developed for preserving nervous system
tissue in a saline bath while experiments are performed to determine
how the neurons in the tissue communicate. The use of “slices of tissue”
simplifies the investigation by allowing the researcher to view a single
neuron through a microscope while stimulating it or recording from it.
Visit the Brain and Behavior Web site
and go to the Chapter 5 Web links for
information about current research on
When released,
chemical must
produce response
in target cell.
Chemical must be
synthesized or
present in neuron.
There must be a mechanism
for removal after chemical’s
work is done.
Same response must 4
be obtained when
chemical is
placed on target.
Figure 5-7
Criteria for Identifying
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Acetylcholine was the first substance identified as a CNS neurotransmitter.
A logical argument that predicted its presence even before
experimental proof was gathered greatly facilitated the process. All the
motor-neuron axons leaving the spinal cord use ACh as a transmitter. Each
of these axons has an axon collateral within the spinal cord that synapses
on a nearby CNS interneuron. The interneuron, in turn, synapses back on
the motor neuron’s cell body. This circular set of connections, called a Renshaw
loop after the researcher who first described it, is shown in Figure 5-8.
Because the main axon to the muscle releases acetylcholine, investigators
suspected that its axon collateral also might release ACh. It seemed
unlikely that two terminals of the same axon would use different transmitters.
Knowing what chemical to look for made it easier to find and obtain
the required proof that ACh is in fact a neurotransmitter in both
locations. The loop made by the axon collateral and the interneuron in the
spinal cord forms a feedback circuit that enables the motor neuron to inhibit
itself from becoming overexcited if it receives a great many excitatory
inputs from other parts of the CNS. Follow the positive and negative signs
in Figure 5-8B to see how the Renshaw loop works.
Today the term “neurotransmitter” is used more broadly than it was
when researchers began to identify these chemicals. The term applies to
substances that carry a message from one neuron to another by influencing
the voltage on the postsynaptic membrane. And chemicals that have
little effect on membrane voltage but rather share a message-carrying
function, such as changing the structure of a synapse, also qualify as neurotransmitters.
Furthermore, neurotransmitters can communicate not only by delivering a message
from the presynaptic to the postsynaptic membrane but by sending messages in
the opposite direction as well. These reverse-direction messages influence the release
or reuptake of transmitters.
The definition of what a transmitter is and the criteria used to identify one have also
become increasingly flexible because neurotransmitters are so diverse and active in such
an array of ways. Different kinds of neurotransmitters typically coexist within the same
synapse, complicating the question of what exactly each contributes in relaying or modulating
a message. To find out, researchers have to apply various transmitter “cocktails”
to the postsynaptic membrane. And some transmitters are gases that act so differently
from a classic neurotransmitter such as acetylcholine that it is hard to compare the two.
Classifying Neurotransmitters
Some order can be imposed on the diversity of neurotransmitters by classifying them
into three groups on the basis of their chemical composition: (1) small-molecule transmitters,
(2) neuropeptides, and (3) transmitter gases.
The first neurotransmitters identified are the quick-acting small-molecule transmitters
such as acetylcholine. Typically, they are synthesized from dietary nutrients and packaged
ready for use in axon terminals.When a small-molecule transmitter has been released
from a terminal button, it can be quickly replaced at the presynaptic membrane.
Because small-molecule transmitters or their main components are derived from
the food that we eat, their level and activity in the body can be influenced by diet.This fact
is important in the design of drugs that act on the nervous system. Many neuroactive
drugs are designed to reach the brain by the same route that small-molecule transmitters
or their precursor chemicals do.
160 ! CHAPTER 5

Motor neuron
Main axon
(Renshaw cell)
Figure 5-8
Renshaw Loop (A) Location of spinalcord
motor neurons that project to the
muscles of the rat’s forelimb. (B) Circular
connections of a motor neuron in a
Renshaw loop, with its main axon going
to a muscle and its axon collateral
remaining in the spinal cord to synapse
with a Renshaw interneuron there. The
terminals of both the main axon and the
collateral contain ACh. The plus and
minus signs indicate that, when the
motor neuron is highly excited, it can
modulate its activity level through the
Renshaw loop.
Small-molecule transmitters. Class of
quick-acting neurotransmitters
synthesized in the axon terminal from
products derived from the diet.

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Kesehatan bagun Pagi dan Meditasi

Dimana saat bangun pagi hari dan melihat sekeliling hidup dimana setelah kedua bola mata ini mulai berkerja untuk melihat sesuatu apa saja,sehingga pikiran mulai bekerja dengan apa yang dilihat,Meditasi dapat dilakukan disaat aktifitas mata dan pikiran mulai bekerja untuk menetukan perbuatan apa yang mau dilakukan oleh pandangan dari kedua bola mata ini,jadi setiap gerakan dari lihatan mata pikiran bekerja untuk menetukan apa langka yang harus di laksanakan baik yah dan baik tidak,manusia itu sendiri yang menentukan apa yang perlu dikalukan,sampai dengan melihat dikala bangun dari tempat tidur dan berdiri untuk langka selajutnya apa,kemudian berjalan kemana yang di inginkan oleh penglihatan bola mata dan diperintakan oleh pikiran yah atau tidak,akan tetapi setiap kehidupan manusia baik wanita dan laki-laki itu sama cuman perbedaan jenis kelamin,coba pola melihat dan pikiran banyak yang menyerupai tidak bedannya dimana manusia itu hidup dalam lingkungan ,akan tetapi setiap mengerakan badan jasmani ini dapat dilihatberupa melihat dan bergerak keselulu penjuruh,Meditasi sangat mendukung dimana prilaku yang kurang sadar apabila manusia disaat mulai bergerak dari aktifitasnya,jadi disaat aktifitas dari setiap gerakan yang tidak sadar itu dapat menjadi sadar apabila di bantu dengan meditasi dan kosentrasi yang tidak sadar menjadi sadar yang muncul dari pikiran manusia itu,kadang-kadang dapat dilihat kesadaran seseorang dapat berkurang akibat banyaknya aktifitas,sibuk,strees,marah,benci,irihati,kawatir,banyak berpikir,menghayal,beragan-agan,ambisi,menagis,tertawa,derita,dan bahagia dan lain-lainnya,

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kurang kesehatan dari jasmani dan rohani antara Meditasi

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sprituality antara biology dan hubungan Meditasi kesadaran

sprituality antara biology dan hubungan Meditasi kesadaran
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kesehatan biology dan Meditasi

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Saya seorang Buddhist yang sedang menjalani kehidupan Spiritual sesuai dengan ajaran Buddha. Akan tetapi saya berusaha dengan tekun untuk manfaat bagi umat Buddha supaya terus melestarikan Buddha, Dharmma, dan Sangha dimana saja, perbuatan karma baik dapat berbuah dalam ketenangan dan kebahagiaan diri sendiri dan semua makhluk hidup di dunia ini. Agama Buddha adalah merupakan Ajaran yang mengajarkan kita untuk melaksanakan Danasikha, sila, samadhi dan Panna. Demikianlah suatu hujud prilaku dan moral etika dapat berjalan dengan baik, didalam kehidupan dimana berada untuk hidup tenang dan Bahagia sewaktu hidup, sebagai umat manusia dimana berada, jalankan kehidupan ini sebaik-baiknya supaya kehidupan dapat mengikuti aturan-aturan kehidupan yang berkeTuhanan Yang Maha Esa.
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