The excitatory postsynaptic potential is an excitatory potential in the postsynaptic membrane of neurons. The individual potentials are summed spatially and temporally and can give rise to an action potential. Transmission disorders such as myasthenia gravis or other myasthenias disrupt these processes.
What is the excitatory postsynaptic potential?
The excitatory postsynaptic potential is an excitatory potential in the postsynaptic membrane of neurons. Neurons are separated by a 20- to 30-nm gap, also known as the synaptic cleft. It is the minimal gap between the presynaptic membrane region of a neuron and the postsynaptic membrane region of the downstream neuron. Neurons transmit excitation. Therefore, their synaptic cleft is bridged by the release of biochemical messengers, also known as neurotransmitters. This creates an excitatory postsynaptic potential at the membrane region of the downstream cell. This is a localized change in the postsynaptic membrane potential. This gradual change in potential triggers an action potential in the postsynaptic element. The excitatory postsynaptic potential is thus a part of neuronal excitatory conduction and arises during depolarization of the downstream cell membrane. The excitatory postsynaptic potentials are received and processed by the downstream neuron by summing them spatially and temporally. When the threshold potential of the cell is exceeded, a newly formed action potential is propagated away from the axon. The opposite of the excitatory postsynaptic potential is the inhibitory postsynaptic potential. Here, hyperpolarization occurs at the postsynaptic membrane, preventing the initiation of an action potential.
Function and task
The excitatory postsynaptic potential and the inhibitory postsynaptic potential affect all neurons. When their threshold potential is exceeded, neurons depolarize. They respond to this depolarization by releasing excitatory neurotransmitters. A certain amount of these substances activates transmitter-sensitive ion channels in the neuron. These channels are permeable to potassium and sodium ions. Local and graduated potentials in the sense of an excitatory potential thus depolarize the postsynaptic membrane of the neuron. When the membrane potential is derived intracellularly, the excitatory postsynaptic potential is the depolarization of the soma membrane. This depolarization occurs as a result of passive propagation. Summation of individual potentials occurs. The amount of neurotransmitter released and the magnitude of the predominant membrane potential determine the magnitude of the excitatory postsynaptic potential. The higher the pre-depolarization of the membrane, the lower the excitatory postsynaptic potential. If the membrane is pre-depolarized beyond its resting potential, then the postsynaptic excitatory potential decreases and may reach zero. In this case, the reversal potential of the excitatory potential is reached. If the pre-depolarization turns out to be even higher, a potential with opposite sign is produced. Thus, the excitatory postsynaptic potential is not always equivalent to depolarization. It rather moves the membrane towards a certain equilibrium potential, which often remains below the respective resting membrane potential. The action of a complex ionic mechanism plays a role in this. At the excitatory postsynaptic potential, an increased membrane permeability for potassium and sodium ions can be observed. On the other hand, potentials with decreased conductance for sodium and potassium ions may also occur. In this context, the ion channel mechanism is thought to trigger the closure of all leaky potassium ion channels. The inhibitory postsynaptic potential is the opposite of the excitatory postsynaptic potential. Again, the membrane potential changes locally at the postsynaptic membrane of neurons. At the synapse, there is hyperpolarization of the cell membrane, which inhibits the initiation of action potentials under the excitatory postsynaptic potential. The neurotransmitters at the inhibitory synapse trigger a cell response.Thus, the channels of the postsynaptic membrane open and allow potassium or chloride ions to pass through. The resulting potassium ion outflow and chloride ion influx evokes local hyperpolarization in the postsynaptic membrane.
Diseases and disorders
Several diseases interfere with communication between individual synapses and thus with signal transduction at the chemical synapse. One example is the neuromuscular disease myasthenia gravis, which affects the muscle end plate. It is an autoimmune disease of as yet unknown cause. In this disease, the body produces autoantibodies against the body’s own tissues. In muscle disease, these antibodies are directed against the postsynaptic membrane on neuromuscular endplates. Most commonly, the autoantibodies in this disease are acetylcholine receptor antibodies. They attack the nicotinic acetylcholine receptors at the junctions between nerves and muscles. The resulting immunological inflammation destroys the local tissue. As a consequence, the communication between nerve and muscle is disturbed because the interaction between acetylcholine and its receptor is impeded or even prevented by the acetylcholine receptor antibodies. The action potential can therefore no longer pass from the nerve to the muscle. The muscle is therefore no longer excitable. The sum of all acetylcholine receptors decreases at the same time as the receptors are destroyed by the immune activity. The subsynaptic membranes disintegrate and endocytosis gives rise to an autophagosome. Transport vesicles fuse with the autophagosomes and the acetylcholine receptors change due to this immune reaction. With these changes, the entire motor end plate changes. The synaptic cleft widens. For this reason, acetylcholine diffuses out of the synaptic cleft or is hydrolyzed without binding to the receptor. Other myasthenias show similar effects on the synaptic cleft and excitatory postsynaptic potential.
