SYNAPSE & NEUROTRANSMISSION

Lecture 3
Dr. Suroor Mohamed

1 Define the synapse?

2what are the type of synapse & its different ?
3- How are the post synaptic action done?
4- What is mean by Neurotramsmitter?

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⦁ Synapses – specialized junction where an axon terminal
contacts another neuron or cell type , by which excitable
cells communicate with one another where information is
transmitted from between them. As Nerve to nerve
synapse, nerve to muscle - neuromuscular junction, and
nerve to gland - neuroglandular junction

⦁ synapse: is the functional connection between a neuron

and a second cell . In the CNS, this other cell is also
neuron In the PNS, the other cell may be either a neuron
or an effecter cell within a muscle or gland.

WHAT A R E THE COMPONENTS OF A SYNAPSE ?

⦁ Synaptic knob of the pre-synaptic cell ( contains transmitter )

฀ (2) Synaptic cleft (space ) contains enzyme that destroys the
transmitter
⦁ (3) Post-synaptic membrane ( contains receptors for the transmitter )

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⦁There are two general types of synapses
Electrical Synapses (Gap Junctions)
Chemical Synapses (Neurological)
⦁ Types of Synapses Electrical Synapses
Electrical synapses allow current to flow from one excitable cell to
the next via low resistance pathways between the cells called gap
junctions which are account for the very fast conduction in these
tissues. Like in cardiac ventricular muscle, in the uterus, and in the
bladder, allowing cells in these tissues to be activated simultaneously
and ensuring that contraction occurs in a coordinated manner.
Chemical Synapses Transmission across the majority of synapses in
the nervous system is one-way, and occurs through the release of
chemical neurotransmitters from pre synaptic cells. There is a gap
between the presynaptic cell membrane and the postsynaptic cell
membrane, known as the synaptic cleft.
⦁ Information is transmitted across the synaptic cleft via a
neurotransmitter, a substance that is released from the
presynaptic terminal and binds to receptors on the postsynaptic
terminal.

⦁ The following sequence of events occurs at chemical synapses:

⦁ An action potential in the presynaptic cell causes Ca2+ channels to
open. An influx of Ca2+ into the presynaptic terminal causes the
neurotransmitter, which is stored in synaptic vesicles, to be released
by exocytosis. The neurotransmitter diffuses across the synaptic
cleft, binds to receptors on the postsynaptic membrane, and produces
a change in membrane potential on the postsynaptic cell. The change in
membrane potential on the postsynaptic cell membrane can be either
excitatory or inhibitory, depending on the nature of the
neurotransmitter released from the presynaptic nerve terminal.
Opening of ion channels often produces either depolarization the
inside of the post synaptic membrane called( excitatory post synaptic
potential)(EPSP). In other cases, causing hyper polarization inside the
post synaptic membrane( more negative) called inhibitory post
synaptic potential(IPSP).
If the neurotransmitter is excitatory, it causes depolarization of the
postsynaptic cell;
if the neurotransmitter is inhibitory, it causes hyperpolarization of the
postsynaptic cell.
**In contrast to electrical synapses, neurotransmission across chemical
synapses is unidirectional (from presynaptic cell to postsynaptic cell).

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 RESPONSE OF THE POSTSYNAPTIC NEURON?
⦁ If the membrane potential is depolarized and brought closer or to threshold, then
it is called an Excitatory PostSynaptic Potential (EPSP). For example, if Na+ ions
enter the cell - the inside of the cell becomes more positive, and the RMP of -70
mV gets moved closer to threshold (-55 mV).
⦁ If the membrane potential is hyperpolarized and moved further away from
threshold, then it is called an Inhibitory PostSynaptic Potential (IPSP). For
example, if K+ ions leave or CI- ions enter the cell, the inside becomes more
negative, and the RMP of -70 mV gets moved further away from threshold, making
the cell less likely to reach threshold.
Synaptic Input—Excitatory and Inhibitory Postsynaptic Potentials
The inputs being either excitatory or inhibitory , if the sum of the inputs is sufficient to
bring the postsynaptic cell to threshold, it will then fire an action potential.
⦁ Excitatory Postsynaptic Potentials (EPSPs) are synaptic inputs that depolarize the
postsynaptic cell, bringing the membrane potential closer to threshold and closer to
firing an action potential. EPSPs are produced by opening Na+ and K+ channels, similar to
the nicotinic ACh receptor. The membrane potential is driven to a value approximately
halfway between the equilibrium potentials for Na+ and K+, or 0 mV, which is a
depolarized state.
Excitatory neurotransmitters include ACh, norepinephrine, epinephrine, dopamine,
glutamate, and serotonin.
⦁ Inhibitory Postsynaptic Potentials (IPSPs) are synaptic inputs that hyperpolarize the
postsynaptic cell, taking the membrane potential away from threshold and farther from
firing an action potential. IPSPs are produced by opening Cl− channels. The membrane
potential is driven toward the Cl− equilibrium potential (approximately −90 mV), which is
a hyperpolarized state.
⦁ Inhibitory neurotransmitters are γ-aminobutyric acid (GABA) and glycine.

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 AP ACTION OTENTIAL IS NOT PRODUCED AT
THE SYNAPSE ?
⦁ a. change in membrane potential is conducted electronically (local
graded response) across the soma
⦁ b. membrane threshold is lower at axon hillock
⦁ c. AP will be generated IF the sum of all inputs to the cell causes
the membrane potential to reach threshold

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Neurotransmitter
Neurotransmitters are signal molecules that are released from
neurons depending on the location of neuron and type of effector
(target) cell it acts on , that s allow the transmission of signals
from one neuron to the next across synapses
They are also found at the axon endings of motor neurons, where
they stimulate the muscle fibers.
Neurotransmitters function by changing the permeability of the cell
membrane to various ions such as sodium and potassium. If an
excess of sodium ions flow into the nerve cell, an impulse is
generated. If an excess of potassium ions flow out, the impulse is
inhibited.

Neurotransmitters are divided into two groups depending on the rate of

action
A. Small-molecule - rapidly acting transmitters (usually open ion channels)
⦁ 1. Acetylcholine

⦁ 2. Amines

⦁ 3. Amino acids

⦁ 4. NO

B. Neuropeptides - action is slow (usually act on DNA or through second

messenger systems) - Released in very small quantities but effect is very
potent
⦁ 1. Opioids

⦁ 2. peptides

⦁ 3. Hypothalamic and pituitary peptides

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⦁ The following criteria are used to formally designate a
substance as a neurotransmitter:
⦁ The substance must be synthesized in the presynaptic cell;
the substance must be released by the presynaptic cell on
stimulation; and, if the substance is applied exogenously to the
postsynaptic membrane at physiologic concentration, the
response of the postsynaptic cell must mimic the in vivo
response.

Fate of released neurotransmitters

⦁ a. Neuropeptides - diffusion and enzymatic hydrolysis
⦁ b. Small molecule transmitters
⦁ 1) diffusion
⦁ 2) enzymatic hydrolysis
⦁ 3) re-uptake into the presynaptic terminal
⦁ 4) Bind to receptor than degradation (enzymatic hydrolysis)

A) Excitatory NT

⦁ 1) Glutamate - accounts for approximately 75% of all excitatory

transmission in the brain, so it is the most common excitatory NT in the
brain. It is released in cerebral cortex, brain stem. Involved in learning and
memory. Also called glutamic acid.
⦁ 2) Aspartate - similar to glutamate but found mostly in the spinal cord for
excitation. (aspartic acid)

B) Inhibitory NT

⦁ 3) GABA - Gamma AminoButyric Acid (GABA) is the most common inhibitory

NT in the brain. Released in thalamus, hypothalamus, cerebellum, occipital
lobe and retina.
⦁ 4) Glycine - is the simplest amino acid and is the most common inhibitory NT
in the spinal cord. It is also released in the brain and retina.

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 ⦁ Acetylcholine was the first neurotransmitter to be discovered.
฀ It is responsible for much of the stimulation of muscles, including the muscles of
the gastro-intestinal system.
⦁ It is also found in sensory neurons and in the autonomic nervous system, and has a
part in scheduling REM (dream) sleep.
⦁ Acetylcholine is transmitted within cholinergic pathways that are concentrated
mainly in specific regions of the brainstem and are thought to be involved in
cognitive functions, especially memory. Severe damage to these pathways is the
probable cause of Alzheimer’s disease.
⦁ The plant poisons curare cause paralysis by blocking the acetylcholine receptor
sites of muscle cells. The well-known poison botulin works by preventing the
vesicles in the axon ending from releasing acetylcholine, causing paralysis.
⦁ ACh binds to two types of receptors, 1) nicotinic and 2) muscarinic.

⦁ In the PNS, ACh is the sole NT used by the Somatic nervous system
(SNS): at the NMJ ACh binds to nicotinic receptors on skeletal muscle
and causes excitation (contraction) of skeletal muscle.
⦁ In the Autonomic nervous system (ANS), it is release by all neurons at
the ganglia and binds to nicotinic receptors on postgalionic neurons. It is
also released by parasympathetic postgalionic neurons and binds with
muscarinic receptors on effector tissue (cardiac muscle, smooth muscle
and glands).
⦁ In general terms, nicotinic receptors are always excitatory (in that when
stimulated they cause an EPSP) and muscarinic receptors are generally
inhibitory (in that when stimulated they usually cause an IPSP).

⦁ Botox = a neurotoxin produced by a bacterium Chlostridium botuninum , It causes food

poisoning (botulism)
⦁ The toxin blocks the release of acetyl choline neurotransmitter to muscles , Causes
muscle paralysis
⦁ Cosmetically used to smooth lines and creases
⦁ Medically used to relax muscles that causing illnesses such as spasms and strabismus
(cross-eyed).
⦁ Botulinum toxin binds to pre-synaptic membranes at neuromuscular junctions, enters
the neuron, and then a component of the toxin interferes with the release of
neurotransmitter.
Release of acetylcholine is blocked.
⦁ No acetylcholine? No muscular contraction. (flaccid paralysis)

after botox

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