A Synapse is a close functional contact between the membranes of an axon terminal and another nerve cell, and a site of cellular communication.
There are some similarities between central synapses and the neuromuscular junction (NMJ) - the motor end plate - particularly in the mechanisms by which transmitters are released. At most central synapses there may be some thickening but no repeated folding of the post-synaptic membrane comparable to that at the NMJ.
The commonest transmitters in the CNS are glutamate (excitatory) and GABA (Gamma-Amino-Butyric Acid, inhibitory), and a single afferent impulse arriving at a synapse usually produces only subthreshold changes in the post-synaptic membrane potential. Excitatory transmitters depolarise and inhibitory transmitters hyperpolarise the membrane.
The generation of action potentials depends on the algebraic sum of sub-threshold depolarisations and hyperpolarisations; when the axon hillock reaches threshold, and only then does the axon fire action potentials.
Synapses on neurones can occur on the dendrites or the soma (and called axo-dendritic and axo-somatic synapses); most synapses are on the dendrites. The diagram shows synapses on the surface of a motoneurone some of which are red and others green, representing different functions - excitation and inhibition. Note the Axon Hillock - the small area at the start of the axons whose function is the generate action potentials when the cell body becomes depolarised and reaches threshold.
Synapses are areas of close contact between the axon terminal of one neurone and another cell, where neurotransmitters (ligands) are released, diffuse across the synaptic gap and act on ligand-gated ion channels and other receptors in the post-synaptic membrane.
Synapses on neurones can occur on the dendrites or the soma (and called axo-dendritic and axo-somatic synapses); most synapses are on the dendrites.
The release of transmitter at nerve endings often depends on changes in intracellular calcium levels in the terminal. Calcium ions enter the terminal when it is depolarised, such as on the arrival of the action potential. The change in intracellular calcium causes release of vesicles containing neurotransmitter.
Excitatory synapses release a neurotransmitter such as glutamate that produces a transient depolarisation of the membrane - an Excitatory Post-Synaptic Potential (EPSP). Current flows into the post-synaptic cell as a result of a neurotransmitter acting on a ligand-gated ion channel in the post-synaptic membrane.
There is a short synaptic delay - a fraction of a millisecond - between the arrival of a nerve impulse at the pre-synaptic terminal, and the start of the EPSP. The synaptic delay is the time taken for transmitter to be released, diffuse across the synaptic gap, act on the post-synaptic receptor, and for the ion channel to open.
Image source: classes.midlandstech.edu
Algebraic summation of subthreshold Post-Synaptic Potentials (PSPs)
Central synapses on motoneurones differ from the nerve-muscle junction (NMJ) in that there are many synapses on the neuronal body and dendrites.
Whereas at the NMJ, one action potential in the nerve ending causes one action potential in the muscle cell. In contrast, in the motoneurone, single action potentials arriving at synapses cause sub-threshold events, the EPSP and IPSP.
If excitatory events exceed inhibitory influences and the membrane potential at the axon hillock reaches threshold, the axon fires a train of action potentials, the frequency of which is related to the level of depolarisation.
EPSPs and IPSPs
During the EPSP, the membrane becomes permeable to sodium and potassium ions simultaneously for a fraction of a millisecond. The equilibrium potential of the EPSP is around 0 mV (roughly half way between the equilibrium potentials of sodium and potassium). As a result the ion movements during the EPSP depolarise the post-synaptic membrane. The electrotonic properties of the membrane cause the EPSP to return to the baseline resting potential within about 12 msec.
Inhibitory synapses release an inhibitory neurotransmitter that produces a transient hyperpolarisation called an Inhibitory Post-Synaptic Potential (IPSP). The mechanism is not dissimilar to that described above, except that the neurotransmitter acts on a different ligand-gated channel that opens the channel to potassium and/or chloride ions. The equilibrium potential of the IPSP is between -70 and -90 mV. As a result, when the membrane is already depolarised, the ion movements hyperpolarise the post-synaptic membrane.
Each synaptic contact either depolarises or hyperpolarises the cell membrane, and when they are simulataneously active, the of numerous synaptic inputs to the neurone summate algebraically; the resultant changes in the membrane potential at the initial segment of the axon are crucial for the generation of action potentials.
These are rapid events and the balance of excitatory and inhibitory inputs on a short timescale (literally millisecond by millisecond) accounts for the speed of reflexes and reaction times.
Chemical Neurotransmission in the CNS
Glutamate is the main excitatory transmitter in the CNS and, by acting on the post-synaptic AMPA receptor, is responsible for the EPSP. When Glutamate binds to the AMPA receptor the membrane becomes permeable to sodium and potassium ions, which results in depolarisation.
Glycine is the inhibitory neurotransmitter responsible for the IPSP seen in motoneurones and commonly within the spinal cord and brainstem. When glycine binds to its receptor, it makes the membrane more permeable to potassium, and hyperpolarises the cell.
GABA is the commonest inhibitory transmitter in the brain, including the cortex, basal ganglia and cerebellum. It operates by opening the GABAA ion channel which makes the membrane more permeable to chloride ions: this results in a hyperpolarisation of the cell.