Synapses – structure and function, types of synapses

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A synapse' is a specialized functional contact between the membranes of two cells, at least one of which is a neuron. The function of the synapse is transmission of nerve impulse'.

Types of synapses

According to the elements involved, we divide synapses into:

1. interneuronal:
   • axo-dendritic;
   • axo-somatic;
   • dendro-dendritic;
   • axo-axonal;
   • somato-dendritic;
2. neuroeffectors - e.g. neuromuscular plate (contact between axon and muscle fiber);
3. neuroreceptors - between neuron and receptor.

According to the type of signal transmission

1. chemical
2. electrical
3. mixed

Synapses in humans are most often ``chemical synapses, on which the signal is transmitted via a mediator (neurotransmitter). Electrical synapses are rather rare, found for example in the olivary nuclei. Mixed synapses are found in lower animals such as fish.

Structure of an electrical synapse

An electrical synapse allows a direct flow of electrical current and is therefore a very fast (fastest) type of connection. It is formed by ``connexons, composed of six proteins - connexins, which together form a connection of the gap junction type. Flow through an open connection is mostly possible in both directions, with rectified synapses voltage regulation takes place and only one-way conduction occurs. This type of synapse is usually excitatory.

The impulse is transmitted to the postsynaptic membrane only with a slight reduction in amplitude because the cells are connected by narrow connexons, which allows ion flow without opening ion channels. Rarely in mammals (olivary''nucleus, on glia), meaning in cold-blooded animals.

Structure of chemical synapse

Chemical synapses are slow connections, during the process of releasing mediators there is a delay of at least 0.5 ms. They are usually unidirectional and can be both excitatory and inhibitory, depending on the type of mediator released. A synapse is made up of a ``presynaptic structure and a ``postsynaptic structure, between which there is a ``synaptic cleft (the width of the cleft is usually 20−30 nm , inhibitory synapse around 10 nm). The presynaptic structure is either the end of the axon (the so-called terminal bouton) or it is the arching of the axoplasm of the axon during its course (en passant synapse). The presynaptic part is a bag-like extension of the axon that contains synaptic vesicles' (vesicles) and a large number of mitochondria that produce the ATP necessary in the process of neurotransmitter release. Synaptic vesicles contain mediator molecules and accumulate at the synaptic cleft in the so-called active zone of the synapse. The membrane of the postsynaptic structure contains receptors for the mediator.

Transmission of excitation in the synapse

The impulse propagating along the axon reaches the presynaptic structure, causing its depolarization (action potential). Depolarization causes the opening of voltage-gated Ca²⁺ channels' in the presynaptic membrane and an influx of Ca²⁺ into the cell. Calcium ions loosen the bond between the cell's cytoskeleton proteins and synaptic vesicles. Vesicles are moved to the active zone with the help of transport proteins in their membrane (synaptobrevin, synaptotagmin). In the active zone, transport proteins fuse with proteins on the neuron membrane (syntaxin, neurotaxin) and the so-called SNARE complex is formed. The contents of the vesicles are by exocytosis released into the synaptic cleft (the mediator is released in quanta), the mediator binds to the receptor of the postsynaptic membrane, which opens ion channels and generates postsynaptic potentials.

Variants of receptors

The interaction between the receptor and the ion channel can be different. Ion channels in the postsynaptic membrane' that open upon binding of a mediator to a receptor are among the chemically gated ion channels (eg, the nicotinic acetylcholine receptor). The receptor is an immediate part of the channel molecule. Another mode of transmission is coupling of the receptor to G-proteiny. A signaling cascade via adenylate cyclase, second messenger (cAMP) and protein kinase is activated, which results in the opening of the ion channel through phosphorylation.

Removing Mediator

After the interaction of the mediator and the receptor, the mediator must be removed from the synaptic cleft by a specific mechanism. This happens most often in two ways:

• direct breakdown – in the synaptic cleft there are enzymes that break down the mediator (e.g. acetylcholinesterase);
• reuptake - the mediator is taken back into the presynaptic ending and returns to the synaptic vesicles (clathrin and dynamin participation) for reuse (noradrenergic, serotoninergic synapse,...).

Cholinergic synapse

Described as 1. - Otto Loewi:

• nicotinic receptors: ion channel component; influx Na⁺;
• or it can be muscarinic receptors': coupled to G-proteins (metabotropic).

Acetylcholine is broken down by acetylcholinesterase' - anchored on the presynaptic membrane, it represents the regulation of the release of acetylcholine. Subsequently, choline is reuptake by the choline transporter and choline acetyltransferase' and synthesized again in the form of acetylcholine, which is transported into vesicles.

Postsynaptic potentials

File:Postsynaptic potentials.jpg

Scheme of postsynaptic potentials

Postsynaptic potentials depend on the type of mediator and synapse. Two main types of potentials arise in the organism:

1. Excitatory postsynaptic potential (EPSP) is caused by excitatory mediators. In the postsynaptic membrane, Na⁺ (Ca²⁺) channels open and ions enter the cell, causing depolarization. A single EPSP represents a depolarizing change that is deeply subthreshold (2−4 mV). But EPSPs add up (temporal and spatial summation) so that a threshold level (7.5-15 mV) can be reached ), during which an action potential arises in the efferent part of the synapse;
2.  The Inhibitory Postsynaptic Potential' (IPSP) is caused by inhibitory mediators. There is an opening of K⁺ and Cl^- channels and a flow of positive ions out of the cell and negative ions into the cell. The membrane is hyperpolarized by ion movements and the excitability of the neuron decreases. The IPSP value is in the range of 2-5 mV.

Combining EPSPs and IPSPs on the same membrane results in signal summation. If the inhibitory signal sufficiently reduces the excitatory one, no action potential occurs.

Slow postsynaptic potentials' consist only in the regulation of K⁺ channels. An IPSP occurs when channel permeability is increased, an EPSP occurs when channel permeability is decreased. These potentials have a long latency (100-500 ms) and duration (seconds-minutes).

Regulation of excitation transfer

File:Regulation of circuits.jpg

Scheme of regulation of excitation transfer

Presynaptic inhibition can occur in two ways. The first of these is ``axo-axonal inhibition, in which the axon of an inhibitory neuron acts on a presynaptic neuron. "Autoinhibition" consists in binding of the mediator to the receptors of the own presynaptic membrane, from which it is flushed out. Further neurotransmitter release is inhibited, which prevents overstimulation of the postsynaptic membrane.

Postsynaptic inhibition is also possible using an inhibitory neuron, which here, however, acts on a postsynaptic neuron. Autoinhibition can occur afferent collaterally - the collateral from the presynaptic neuron activates an inhibitory interneuron that inhibits the postsynaptic neuron. Efferent collateral connections lead from the postsynaptic neuron through the inhibitory interneuron back to the postsynaptic one.

Presynaptic facilitation and summation occurs especially when two neurons converge to one. Subthreshold stimuli can then trigger an EPSP, and the subsequent summation of these signals will trigger an action potential. Suprathreshold stimuli usually evoke a prolonged action potential.

Occlusion is a special type of summation in which two suprathreshold stimuli evoke a normal action potential (not e.g. prolonged as in presynaptic facilitation and summation).

Links

Related Articles

• Neuron
• Neuromuscular plate
• Reflex

References

• yes. . Lékařská fyziologie. 4. edition. Praha : Grada, 2003. pp. 772. ISBN 80-247-0512-5.
• KITTNAR, Otomar, et al. Lékařská fyziologie. 1. vydání. Praha : Grada, 2011. ISBN 978-80-247-3068-4
• MYSLIVEČEK, Jaromír a A KOL.. Základy neurověd. 2. vydání. Praha : Triton, 2009. 390 s. s. 38. ISBN 978-80-7387-088-1.