SYNAPTIC

TRANSMISSION

By :Yana Asv
21232PSY054
What is Synapse?
In the late 1800s, Ramón y Cajal anatomically demonstrated a narrow gap separating
one neuron from another. In 1906, Charles Scott Sherrington physiologically
demonstrated that communication between one neuron and the next differs from
communication along a single axon. He inferred a specialized gap between neurons and
introduced the term synapse to describe it.
It can be defined as :
“A synapse is a small gap at the end of a neuron that allows a signal to pass from one
neuron to the next. Neurons are cells that transmit information between your brain and
other parts of the central nervous system. Synapses are found where neurons connect
with other neurons.”
Sherrington’s study: A brief
summary
Sherrington strapped a dog into a harness above the ground and pinched one of the
dog's feet. After a fraction of a second, the dog flexed (raised) the pinched leg and
extended the other legs. Sherrington found the same reflexive movements after he made
a cut that disconnected the spinal cord from the brain. Evidently, the spinal cord
controlled the flex- ion and extension reflexes. In fact, the movements were more
consistent after he separated the spinal cord from the brain. In an intact animal,
messages descending from the brain modify the reflexes, making them stronger at some
times and weaker at others.
 Properties of Synapse
 Speed of a Reflex and Delayed transmission at the Synapse : Sherrington found that the speed of
conduction through the reflex arc varied but was never more than about 15 meters per second (m/s). In
contrast, previous research had measured action potential velocities along sensory or motor nerves at
about 40 m/s. Sherrington concluded that some process must be slowing conduction through the reflex,
and he inferred that the delay occurs where one neuron communicates with another. This idea is critical,
as it established the existence of synapses. Sherrington, in fact, introduced the term synapse.
 Temporal Summation: Sherrington found that repeated stimuli within a brief time have a cumulative
effect. He referred to this phenomenon as temporal summation, meaning summation over time. A light
pinch of the dog’s foot did not evoke a reflex, but a few rapidly repeated pinches did. Sherrington
surmised that a single pinch did not reach the threshold of excitation for the next neuron.
 Spatial Summation: Sherrington also found that synapses have the property of spatial summation-that
is, summation over space. Synap- tic inputs from separate locations combine their effects on a neuron.
Sequence of Chemical Events at a
Synapse
1. The neuron synthesizes chemicals that serve as neurotransmitters. It synthesizes the smaller neurotransmitters in the
axon terminals and synthesizes neuropeptides in the cell body.
2. Action potentials travel down the axon. At the presynaptic terminal, an action potential enables calcium to enter the
cell. Calcium releases neurotransmitters from the terminals and into the synaptic cleft, the space between the
presynaptic and postsynaptic neurons.
3. The released molecules diffuse across the narrow cleft, attach to receptors, and alter the activity of the postsynaptic
neuron. Mechanisms vary for altering that activity.
4. The neurotransmitter molecules separate from their receptors.
5. The neurotransmitter molecules may be taken back into the presynaptic neuron for recycling or they may diffuse
away.
6. Some postsynaptic cells send reverse messages to control the further release of neurotransmitter by presynaptic cells.
Figure: Some major events in
transmission at a synapse
Neurotransmitters
At a synapse, a neuron releases chemicals that affect another neuron. Those chemicals
are known as neurotransmitters.
Neurons synthesize nearly all neurotransmitters from amino ac- ids, which the body
obtains from proteins in the diet.
Examples : Acetylcholine , Dopamine , Serotonin, Glutamate , GABA , etc.
Hence Neurotransmitters can be defined as : Chemical messengers that carry, boost, and
balance signals between neurons (also known as nerve cells) and target cells throughout
the body are called neurotransmitters. These target cells may be in glands, muscles, or
other neurons.
Storage of Neurotransmitters
• Most neurotransmitters are synthesized in the presynaptic terminal, near the point of release. The
presynaptic terminal stores high concentrations of neurotransmitter molecules in vesicles, tiny nearly
spherical packets.
• Nitric oxide is an exception to this rule. Neurons release nitric oxide as soon as they form it instead of
storing it.
• The presynaptic terminal also maintains much neurotransmitter outside the vesicles.
• Neurons that release serotonin, dopamine, or norepinephrine contain an enzyme, MAO (monoamine
oxidase), that breaks down these transmitters into inactive chemicals, thereby preventing the transmit-
ters to accumulate to harmful levels. The first antidepressant drugs that psychiatrists discovered were
MAO inhibitors. By blocking MAO, they increase the brain’s supply of sero- tonin, dopamine, and
norepinephrine.
Release and Diffusion of
Neurotransmitters
• At the end of an axon, an action potential itself does not release the neurotransmitter.
Rather, depolarization opens voltage- dependent calcium gates in the presynaptic
terminal. Within 1 or 2 milliseconds (ms) after calcium enters the terminal, it causes
exocytosis-bursts of release of neurotransmitter from the presynaptic neuron.
• After its release from the presynaptic cell, the neurotransmitter diffuses across the
synaptic cleft to the postsynaptic membrane, where it attaches to a receptor. The
neurotransmitter takes no more than 0.01 ms to diffuse across the cleft, which is only
20 to 30 nanometers (nm) wide.
 Activating Receptors of the Postsynaptic
Cell
The effect of a neurotransmitter depends on its receptor on the postsynaptic cell. When the neurotransmitter attaches to its
receptor, the receptor may open a channel—exerting an ionotropic effect—or it may produce a slower but longer effect-a
metabotropic effect.
• IONOTROPIC EFFECT : When the neurotransmitter binds to an ionotropic recep- tor, it twists the receptor just enough to
open its central channel, which has a shape that lets a particular type of ion pass through. In contrast to the sodium and
potassium channels along an axon, which are voltage-gated, the channels controlled by a neurotransmitter are transmitter-
gated or ligand-gated channels. (A ligand is a chemical that binds to something.) That is, when the neurotransmitter attaches,
it opens a channel. Ionotropic effects begin quickly, sometimes within less than a millisecond after the transmitter attaches.
The effects decay with a half-life of about 5 ms.
• METABOTROPIC EFFECT : When a neurotransmitter attaches to a metabotropic receptor, it bends the receptor protein
that goes through the membrane of the cell. The other side of that receptor is attached to a G protein-that is, a protein coupled
to guanosine triphosphate (GTP), an energy- storing molecule. Bending the receptor protein detaches that G protein, which is
then free to take its energy elsewhere in cell, a is increased concentration of a second messenger, such as cyclic adenosine
monophosphate (cyclic AMP), inside the cell. Just as the “first messenger” (the neurotransmitter) carries information to the
postsynaptic cell, the second messenger communicates to areas within the cell. It may open or close ion channels in the
membrane or activate a portion of a chromosome.
Inactivation and Reuptake of Neurotransmitters
A neurotransmitter does not linger at the postsynaptic membrane, where it might continue exciting or inhibiting
the receptor. Various neurotransmitters are inactivated in different ways.
1. After Acetylcholine activates a receptor, the enzyme ace- holinesterase (a-SEE-til-ko-lih-NES-the-raze)
breaks it into two fragments: acetate and choline. The choline diffuses back to the presynaptic neuron,
which takes it up and recon- nects it with acetate already in the cell to form acetylcholine again.
2. Serotonin and the catecholamines (dopamine, norepi- tive fragments at the postsynaptic membrane. They
simply detach from the receptor. At that point, the next step var- ies. The presynaptic neuron takes up much
or most of the released neurotransmitter molecules intact and reuses them. This process, called reuptake,
occurs through special mem- brane proteins called transporters.
The activity of trans- porters varies among individuals another. Any transmitter molecules that the transporters
do not take will instead break down by an enzyme called COMT. The breakdown products wash away and
eventually show p h the bod and urine.
Negative Feedback from the
Postsynaptic Cell
• A couple of mechanisms in the nervous system serve that function.
• First, many presynaptic terminals have receptors sensitive to the same transmitter
they release. These receptors are known as auto-receptors- receptors that respond to
the released transmitter by inhibiting further synthesis and release. That is, they
provide negative feedback.
• Second, some postsynaptic neurons respond to stimulation by releasing chemicals
that travel back to the pre-synaptic terminal to inhibit further release of transmitter.
Figure: Inactivation
and Reuptake of
Neurotransmitters
Electrical Synapses
A few special- purpose synapses do operate electrically. Because electrical transmission is faster than
even the fastest chemical trans- mission, electrical synapses have evolved in cases where ex- act
synchrony between two cells is important. For example, some of the cells that control your rhythmic
breathing are synchronized by electrical synapses.
At an electrical synapse, the membrane of one neuron comes into direct contact with the membrane of
another. This contact is called a gap junction.
Fairly large pores of the membrane of one neuron line up pre- cisely with similar pores in the membrane
of the other cell. These pores are large enough for sodium and other ions to pass readily, and unlike the
other membrane channels we have considered, these pores remain open constantly. Therefore, whenever
one of the neurons is depolarized, sodium ions from that cell can pass immediately into the other neuron
and de- polarize it, too. As a result, the two neurons act as if they were a single neuron.
Figure: A gap
junction for an
electrical synapse