Lesion of the sympathetic (noradrenergic) branch of the peripheral autonomic nervous system. Experimental
Neuronal plasticity; Short-term plasticity Definition
In general terms, synaptic plasticity describes a change, persistent or transient, of morphology, composition, or signal transduction efficiency at a neuronal synapse in response to intrinsic or extrinsic signals. ► Long-term potentiation (LTP) and ► long-term depression (LTD) likely represent the most extensively studied forms of synaptic plasticity, which itself is the best characterized form of neuronal plasticity, the cellular substrate for learning and memory.
Physiology and psychopharmacological modulation of LTP and LTD are described in detail elsewhere (see Cross-References). Like these special cases, most other forms of synaptic plasticity are induced by an associative coincidence of signals in space and time, in line with the theory of the so-called "Hebbian plasticity'': A convergence of different second messenger pathways or pre- and post-synaptic activity at the synapse itself. Of note, the term ''synaptic'' could either point to the origin or the affected target of such signals. However, for many phenomena related to drug effects, this distinction cannot be conclusively drawn because a differentiation of cause and effect in neuronal networks is inherently difficult for drugs acting at multiple sites and over a relatively long period of time.
Forms of synaptic plasticity beyond LTP and LTD comprise short-term plasticity (STP) based on presynap-tic transmitter release probability, postsynaptic spine motility, translocation of proteins between extrasynap-ticand synaptic sites, epigenetic, post-transcriptional or post-translational modifications of synaptic proteins, and changes of intra- and extracellular ion concentrations. Some of those changes are described as ''► meta-plasticity'' because they have been shown to change the ability of synapses to undergo classical forms of plasticity like LTP or LTD (Abraham 2008). Common to all those changes is their link to an altered function of synaptic transmission. This could be experimentally shown for some but not all of the above-mentioned examples, and there are certainly more mechanisms to be uncovered by improved and refined approaches and technologies.
The concept of synaptic plasticity was already introduced more than 100 years ago, with W. James, E. Tanzi, E. Lugaro, and D.O. Hebb making milestone contributions in the development of this principle, long before T. Lomo and T.V. Bliss in P. Andersens laboratory could experimentally show in 1973 that specific electric stimuli induce persistent changes in synaptic transmission efficiency, both in vitro and in vivo (see Berlucchi and Buchtel 2009 for a recent review of historical aspects of synaptic plasticity).
For a long time, electrophysiological techniques like extra- or intracellular recordings remained the gold standard to observe synaptic physiology. It is only recently, that optical imaging complemented the functional information with structural data at the level of single synapses in living tissue.
Models of synapses usually show synaptic signal transmission between neurons as a ''static element'' that can be described by a fixed input-output relation: for a single event of chemical signal transmission between neurons, a presynaptic stimulus leads to a defined postsynaptic response. In the most classical case of synaptic transmission, a presynaptic action potential depolarizes the ► presynap-tic bouton, which contains the machinery for vesicular release. A rise of intracellular calcium ([Ca2+]int) induces the release of vesicle-stored neurotransmitters into the synaptic cleft. The transmitter activates postsynaptic receptors that trigger electric or second messenger signals in the postsynaptic cell. When one or several of the contributing synaptic components change their function, the synapse undergoes plastic changes that can last from milliseconds to days or years. More special cases of synaptic signal transmission, like electrical synapses formed by gap junctions, are not described further, as there are to date still very few studies on their structural or functional plasticity. Figure 1
Synaptic Plasticity. Fig. 1. Types of synaptic plasticity across a timescale spanning several orders of magnitude. Depicted is a nonexhaustive selection of mechanisms underlying synaptic plasticity sorted by their approximate time of expression. A common type of classical LTP and LTD is reflected by altered AMPA receptor mediated EPSCs. Cav2 presynaptic, high-voltage activated calcium channels of the Cav2 family; PKC protein kinase type C; NR2 subunit family 2 of the NMDA receptors; AChR acetylcholine receptor; KCC2, potassium-chloride cotransporter type 2; [Cr]int intracellular chloride ion concentration; Gfi/y p/y subunit of trimeric G-protein; EPSC excitatory postsynaptic currents.
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