Synaptic augmentation

Last updated February 26, 2019

Augmentation is one of four components of short-term synaptic plasticity that increases the probability of releasing synaptic vesicles during and after repetitive stimulation such that

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity.

A(t)=[{\rm {TransmitterRelease}}(t)/{\rm {TransmitterRelease}}(0)]-1,

when all the other components of enhancement and depression are zero, where $A$ is augmentation at time $t$ and 0 refers to the baseline response to a single stimulus. The increase in the number of synaptic vesicles that release their transmitter leads to enhancement of the post synaptic response. Augmentation can be differentiated from the other components of enhancement by its kinetics of decay and by pharmacology. Augmentation selectively decays with a time constant of about 7 seconds and its magnitude is enhanced in the presence of barium. All four components are thought to be associated with or triggered by increases in internal calcium ions that build up and decay during repetitive stimulation.

In physiology, a stimulus is a detectable change in the internal or external environment. The ability of an organism or organ to respond to external stimuli is called sensitivity. When a stimulus is applied to a sensory receptor, it normally elicits or influences a reflex via stimulus transduction. These sensory receptors can receive information from outside the body, as in touch receptors found in the skin or light receptors in the eye, as well as from inside the body, as in chemoreceptors and mechanoreceptors. An internal stimulus is often the first component of a homeostatic control system. External stimuli are capable of producing systemic responses throughout the body, as in the fight-or-flight response. In order for a stimulus to be detected with high probability, its level must exceed the absolute threshold; if a signal does reach threshold, the information is transmitted to the central nervous system (CNS), where it is integrated and a decision on how to react is made. Although stimuli commonly cause the body to respond, it is the CNS that finally determines whether a signal causes a reaction or not.

Barium is a chemical element with symbol Ba and atomic number 56. It is the fifth element in group 2 and is a soft, silvery alkaline earth metal. Because of its high chemical reactivity, barium is never found in nature as a free element. Its hydroxide, known in pre-modern times as baryta, does not occur as a mineral, but can be prepared by heating barium carbonate.

Calcium is a chemical element with symbol Ca and atomic number 20. As an alkaline earth metal, calcium is a reactive metal that forms a dark oxide-nitride layer when exposed to air. Its physical and chemical properties are most similar to its heavier homologues strontium and barium. It is the fifth most abundant element in Earth's crust and the third most abundant metal, after iron and aluminium. The most common calcium compound on Earth is calcium carbonate, found in limestone and the fossilised remnants of early sea life; gypsum, anhydrite, fluorite, and apatite are also sources of calcium. The name derives from Latin calx "lime", which was obtained from heating limestone.

During a train of impulses the enhancement of synaptic strength due to the underlying component $A^{*}$ that gives rise to augmentation can be described by

{\frac {dA^{*}}{dt}}=J(t)a^{*}-k_{A^{*}}A^{*}

where $J(t)$ is the unit impulse function at the time of stimulation, $a^{*}$ is the incremental increase in $A^{*}$ with each impulse, and $k_{A^{*}}$ is the rate constant for the loss of $A^{*}$ . During a stimulus train the magnitude of augmentation added by each impulse, a*, can increase during the train such that

a^{*}=a_{0}^{*}Z^{ST}

where $a_{0}^{*}$ is the increment added by the first impulse of the train, $Z$ is a constant that determines the increase in $a^{*}$ with each impulse, $S$ is the stimulation rate, and $T$ is the duration of stimulation.

Augmentation is differentiated from the three other components of enhancement by its time constant of decay. This is shown in Table 1 where the first and second components of facilitation, F1 and F2, decay with time constants of about 50 and 300 ms, and potentiation, P, decays with a time constant than ranges from tens of seconds to minutes depending on the duration of stimulation. Also included in the table are two components of depression D1 and D2, along with their associated decay time constants of recovery decay back to normal. Depression at some synapses may arise from depletion of synaptic vesicles available for release. Depression of synaptic vesicle release may mask augmentation because of overlapping time courses. Also included in the table is the fraction change in transmitter release arising from one impulse. A magnitude of 0.8 would increase transmitter release 80%.

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.

	Decay constant	Magnitude/Impulse
F1	50 ms	0.8
F2	300 ms	0.12
A	7 s	0.01^†
P	20 s to minutes^‡	0.01

D1	5 to 6 s	-0.15
D2	minutes	-0.001

^†The magnitude of augmentation added by each impulse can increase during the train. ^‡The time constant of P can increase with repetitive stimulation.

The balance between various components of enhancement and depression at the mammalian synapse is affected by temperature so that maintenance of the components of enhancement is greatly reduced at temperatures lower than physiological. During repetitive stimulation at 23 °C components of depression dominate synaptic release, whereas at 33–38 °C synaptic strength increases due to a shift towards components of enhancement.

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The active zone or synaptic active zone is a term first used by Couteaux and Pecot-Dechavassinein in 1970 to define the site of neurotransmitter release. Two neurons make near contact through structures called synapses allowing them to communicate with each other. As shown in the adjacent diagram, a synapse consists of the presynaptic bouton of one neuron which stores vesicles containing neurotransmitter, and a second, postsynaptic neuron which bears receptors for the neurotransmitter, together with a gap between the two called the synaptic cleft. When an action potential reaches the presynaptic bouton, the contents of the vesicles are released into the synaptic cleft and the released neurotransmitter travels across the cleft to the postsynaptic neuron and activates the receptors on the postsynaptic membrane.

Synaptic fatigue, or short-term synaptic depression, is an activity-dependent form of short term synaptic plasticity that results in the temporary inability of neurons to fire and therefore transmit an input signal. It is thought to be a form of negative feedback in order to physiologically control particular forms of nervous system activity.

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