Electrical Synapse or Ephapse

In electrical synapse, there is continuity between presynaptic and postsynaptic neurons. Continuity is provided by gap junction between two neurons. So, there is direct exchange of ions between two neurons. Because of this, action potential reaching presynaptic terminal produces potential change in postsynaptic neuron. Important feature of electrical synapse is that synaptic delay is minimum or even absent because of direct flow of current. If in ephapse fissure between pre- and postsynaptic elements is 2 nm, in chemical ones –50-300 nm. Thus, quicker impulse distribution is in ephapse. Moreover, unlike chemical synapse, impulse can be transmitted in either direction through the electrical synapse thus in 2 directions. They are considered to be only excitatory (due to depolarization development) comparatively to chemical synapses. Postsynaptic current source is presynaptic cell membrane. Chemical mediator is absent and all factors influencing on releasing and action or liquidating of enzymes decomposing mediator (extracellular calcium ions concentration decreasing) do not influence.

Ions transporting electrical currents can not pass through lipid membranes. That is why canal proteins are essential for ions transporting in “membrane contacts” between electrically conjugated cells. Such intercellular contacts are known as nexuses or “ crack contacts ”. There are connexones in every of two neighboring cellular membranes. They are distributed in definite gaps (spaces) and penetrate all membrane thickness. These connexones are located opposite each other in the contact locus and their lumens are located at one and the same level. So, there are 6 subunits. Everyone is 25000 Da. Big molecules (with molecular weight equal to 1000 D and 1,5 nm in diameter) come through them.

Nexuses form functional syncitium:

– in non-vertebrata;

– in vertebrata CNS;

– in vertebrata myocardium;

– in vertebrata smooth musculature.

Also all stages at embryonic stage and all epitheliocytes (particularly of lens) contain them.

Crack contacts are highly-regulated.

Closage is caused by: pH reducing, calcium ions level increasing.

Closage reasons:

– cells deep injury;

– metabolism disorder.

Closage role:

– injured places isolation and restriction (for example, at myocardial infarction);

– exchange with signal molecules (for example, with secondary messengers) which in turn is essential for regulation of:

– metabolism;

– mitosis;

– meiosis;

– cells migration during specific protection (immunity) as well as non-specific one (phagocytosis);

– regeneration;

– reparation;

– hemopoiesis;

– cells death.

Chemical synapses are dominant in CNS (comparatively to electrical ones) because:

– they are more specific (regulated by chemicals particularly medicines);

– provide bigger possibility to be regulated in intercellular communications.

Chemical Synapse

Chemical synapse is the junction between a nerve fiber and a muscle fiber or between two nerve fibers, through which signals are transmitted by release of chemical transmitter. In chemical synapse, there is no continuity between presynaptic and postsynaptic neurons because of presence of a space called synaptic cleft between two neurons. Action potential reaching presynaptic terminal causes release of neurotransmitter from vesicles of terminal. Neurotransmitter reaches postsynaptic neuron through synaptic cleft and causes production of potential change. The structure and functions of the chemical synapse are given below.

EXCITATORY FUNCTION

When action potential reaches presynaptic axon terminal, voltage gated calcium channels at presynaptic membrane are opened. Now calcium ions enter axon terminal from extracellular fluid (Fig.15).

Calcium ions cause fusion of synaptic vesicles with cell membrane and release of neurotransmitter substance from vesicles by means of exocytosis.

   

Presy­naptic neuron	Arrive of action potential in axon terminal
	Opening of calcium channels in presynaptic membrane
	Influx of calcium ions from ECF into the axon terminal
	Opening of vesicles and release of Ach