Synapse and Neurotransmission

Question 1

Structure of Synapse and Synaptic Transmission (explain)

Answer 1

Nerve cells communicate by passing on electrical signals known as action potentials.

We call the cell in which the signal originates the
presynaptic cell, and the cell which receives it the postsynaptic cell.

The presynaptic cell is a neurone but the postsynaptic cell can be a neurone or muscle cell.

When an action potential reaches the end of an axon it must then influence the adjacent nerve / effector cell if the signal is to be passed on.

The potential problem with using action potentials to
allow intercellular communication is that electrical activity can’t jump the gap between one cell and the next.

To get round this nerve cells use a structure called the synapse.

Transmission of the signal from the nerve to the corresponding cell depends on the release of a messenger molecule called a neurotransmitter from the nerve terminal, and this affects the adjacent cell, tending to
either excite it or inhibit it. This is an example of chemical
transmission!

Question 2

How are Neurotransmitters released?

Answer 2

➢ When the wave of depolarization reaches the end bulb it opens voltage dependent Ca2+ channels
➢ Ca2+ enters the cell in accordance with it’s
concentration gradient.
➢ The influx of Ca2+ causes exocytosis of the vesicle containing neurotransmitter
➢ The neurotransmitter (Ach) is released from the presynaptic membrane.
➢ It enters the gap between the cells (the synaptic cleft) and reaches the receptors in the post synaptic membrane of the next cell along
➢ Ach interacts with a ligand gated ion channel permeable to Na+, when it interacts with the channel it opens it and Na+ flows into the cell, down it’s concentration gradient.
> The effect is therefore is to depolarize or excite the postsynaptic cell. Some synapses however are inhibitory in nature.

Question 3

Ionotropic or metabotropic receptors (explain)

Answer 3

Several neurotransmitter molecules such as noradrenaline (NA), acetylcholine (ACh), glutamate, serotonin (5-hydroxytryptamine [5-HT], gamma-aminobutyric acid (GABA) and glycine serve as ligands (agonists) for both types of receptors.

The binding of neurotransmitters to receptors on the post-synaptic cell membrane can transduce information by two
molecular mechanisms;

➢ Some receptors are ligand gated channels and are known as ionotropic receptors – which cause a rapid opening of
ion channels resulting in depolarisation or hyperpolarisation of the postsynaptic cell membrane mediating fast ionic synaptic responses that occur within a millisecond;

➢ Some receptors are G-protein coupled receptors in which the receptor is coupled to G-proteins are known as
metabotropic receptors which result in the production of α and β subunits and GTP resulting in the initiation of a
wide variety of cellular responses mediating slow, biochemically mediated synaptic responses which can occur within seconds to minutes

Question 4

Two receptors that ACh utilises (explain)

Answer 4

1) The ACh receptor at the neuromuscular junction of skeletal muscle is an ionotropic receptor known as the nicotinic
receptor. Once the nicotinic receptor is activated in skeletal muscle there is a transient increase in the permeability of
Na+ and K+ causing depolarisation and stimulation (activation) of the muscle fibre.

2) The ACh receptors at the neuromuscular junction of cardiac muscle is a metabotropic receptor known as the muscarinic receptor. Once the muscarinic receptor is activated in cardiac muscle it ultimately causes the activation
of a type of K+ channel which results in the expulsion of K+ from the cell and membrane hyperpolarisation which
inhibits cardiac excitation.

Whilst ACh stimulates skeletal muscle it inhibits cardiac muscle due to the receptors present in the cells of the tissue

(NOTE: The nicotinic versus and muscarinic nomenclature is pharmacological and based on whether the ACh receptor is
activated by nicotine or muscarine, two natural products that behave like agonists).

Question 5

Excitatory and Inhibitory Post-synaptic Potentials (explain)

Answer 5

A change in membrane potential (Vm) caused by the flow of charge is called a postsynaptic potential (PSP) if it is generated at the postsynaptic membrane by a neurotransmitter (a receptor potential is generated at a sensory nerve ending by an external stimulus).

If the neurotransmitter is excitatory and produces a depolarising PSP it is referred to as an excitatory postsynaptic potential (EPSP)

If the neurotransmitter is inhibitory and produces a
hyperpolarising PSP it is referred to as an inhibitory postsynaptic potential (IPSP).

In all cases the stimulus produces a membrane potential that may be graded depending on the strength or quantity of the input signal.

Whether or not the effect of synaptic transmission is excitatory or inhibitory in nature depends on whether the neurotransmitter opens ion channels which cause a depolarization or hyperpolarization respectively

Question 6

Two types of Summation (explain)

Answer 6

A combination or summation of EPSPs can evoke an action potential.

Summation may occur in two ways;

1. Temporal summation: Temporal summation occurs when EPSPs arrive rapidly in succession. This occurs when an EPSP is evoked before the previous one has decayed, a subsequent EPSP tends to add its amplitude to the residual of
   the preceding EPSP meaning that the postsynaptic cell is brought even closer to the threshold potential and is more likely to fire an action potential.
2. Spatial summation:
   Spatial summation occurs when the postsynaptic cell is stimulated by more than one synaptic end bulb at once. The combination of these EPSPs arriving from numerous dendrites can lead to EPSPs that are substantially larger than those generated by any single synapse. Again this means that the postsynaptic cell is more likely to fire an action potential, since the EPSPs evoked by each cell adds up.

Question 7

Signal Termination (explain)

Answer 7

Effective transmission across chemical synapses not only requires the release of neurotransmitters and activation of receptors, but also the rapid and efficient removal of the transmitter.

It is important that the neurotransmitter does not
persist in the cleft so that it doesn’t interfere with incoming signals.

There are three ways in which neurotransmitter can be
removed from the cleft;

1. The most common mechanism - the neurotransmitter is taken back up into the presynaptic cell (referred to as re-uptake). This is mediated by specific transport systems located in the presynaptic plasma membrane.
2. Enzymes may also degrade the neurotransmitter. At the neuromuscular junction and other cholinergic synapses, the termination of the signal is accomplished by the action of enzymes i.e. acetylcholinesterase
   breaks down acetylcholine into it’s constituent parts, choline and actetate.
3. Finally, neurotransmitter may simply diffuse away.