Excitation of Skeletal Muscles:

1. Neuromuscular Transmission
starts with AP in the nerve and ends with AP in the muscle
2. Excitation-Contraction Coupling
starts with AP in the muscle and ends with muscular contraction
Synapse
a site where information is transmitted from one cell to another (broad sense)
a junction between two neurons (narrow sense)
consists of the end of a neuron (presynaptic terminal), a small space (synaptic
cleft) and the postsynaptic membrane of another neuron or an effector cell
such as muscle or gland
Information is transmitted by nerve action potential through a succession of
neurons (from one neuron to another). Synapse contains many neurotransmitters
but only one kind for each nerve.
Components of a Synaptic Transmission:
1. Pre-synaptic Neuron first neuron; before the synaptic cleft
has synaptic vesicles (contains neurotransmitter) and mitochondria
neurotransmitter for SKELETAL = acetylcholine
neurotransmitter for SMOOTH/CARDIAC = acetylcholine or
norepinephrine (parasympathetic)
2. Post-synaptic Neuron second neuron; after the synaptic cleft
has receptor proteins, ribosome (protein synthesis)
impulse = action potential = message = conduction = stimulus
1. impulse can be blocked along the way
2. impulse can be replicated if it gets in contact with several neurons resulting to
several outputs
3. integrated with other impulses
Synaptic transmission is complicated compared to neuromuscular
transmission.

TYPES OF SYNAPSES (BROAD SENSE)

In the narrow sense, there is only chemical synapse.

1. Electrical Synapses

allow current to flow/jump from one excitable cell to the next via low
resistance pathways between the cells called gap junctions very small
space
Gap junctions are found in CNS, cardiac muscle and in some types of
smooth muscle and account for the very fast conduction in these tissues
contraction occurs in a coordinated manner
bidirectional

2. Chemical Synapses (Neuromuscular Transmission or Neuromuscular Junction)

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
pre-synaptic membrane (neurotransmitter) ; post-synaptic membrane
(receptor protein)
unidirectional (from presynaptic cell to postsynaptic cell ONLY)
synaptic delay is the time required for the multiple steps in chemical
neurotransmission to occur

The following sequence of events occurs at chemical synapses:

a) An action potential (stimulus) in the presynaptic cell causes opening of
Ca channels
b) An influx of Ca into the presynaptic terminal causes the neurotransmitter,
which is stored in synaptic vesicles, to be released by exocytosis.
c) The neurotransmitter diffuses across the synaptic cleft, binds to receptors
on the postsynaptic membrane and opens channels to a change in membrane
potential on the postsynaptic cell.
2+

2+

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. If the neurotransmitter is excitatory, it
causes depolarization of the postsynaptic cell; if the neurotransmitter is inhibitory, it
causes hyperpolarization of the postsynaptic cell.

Sometimes in a synaptic transmission, when a neurotransmitter combines with

a G-protein receptor, it can perform either (not all):
1. open specific ion channels
2. activate the cyclic AMP (adenosine monophosphate breakdown product of
ATP) or cyclic GMP (guanosine monophosphate) both are second
messengers
3. activate intracellular enzymes
4. alter gene transcription in the nucleus
Components of a G-receptor:
1. alpha
2. beta
3. gamma
Outputs of Synaptic Transmission:
1. Excitation Postsynaptic Potential (EPSP) local depolarization
caused by the opening of sodium channels (depolarization) or depression
of the opening of chloride and potassium channels
summation of EPSPs which reaches threshold causes excitation
2. Inhibitory Postsynaptic Potential (IPSP) local hyperpolarization
opening of potassium or chloride channels (hyperpolarization)
activation of receptor enzymes
summation of IPSPs causes inhibition
Different enzymes that destroy neurotransmitters:
1. acholinesterase (AChase) degrade acetylcholine into acetate and choline
2. Monoamine oxidase (MAO)
3. Cathecol-o-methyltransferase (COMT)

Synthesis of Acetylcholine
choline + acetyl co-enzyme A

acetyltransferase

acetylcholine
acholinesterase

choline

acetate

*other neurotransmitters called catecholamines are degraded by MAO and COMT

Synthesis of Catecholamine:
ECF (pre-synaptic neuron)
Tyrosine Dopa Dopamine Norepinephrine Epinephrine

Reuptake bringing back of the catecholamine by the pre-synaptic neuron

through endocytosis
*those not taken back are destroyed by COMT
*those taken back are destroyed by MAO

Parkinsons disease
dopamine (inhibitory) deficiency leading to over activity of acetylcholine
tx by L-dopa (Livo dopa)
Strychnine
competes with glycine (normal neurotransmitter in the body that generates
IPSP) at postsynaptic receptor
glycine is sometimes exhibitory in different parts of the brain
always excitation
Tetanus Toxin Clostridium tetani
prevents release of GABA (gamma-aminobutyric acid)
GABA is a neurotransmitter that always causes inhibition mostly in the spinal
cord