Synaptic plasticity

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For the general concept of brain plasticity, see Neuroplasticity.

In neuroscience, synaptic plasticity is the ability of the connection, or synapse, between two neurons to change in strength. There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the amount of neurotransmitter released into a synapse and changes in how effectively cells respond to those neurotransmitters (Gaiarsa et al., 2002). Since memories are postulated to be stored in synapses of the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory (see Hebbian theory).

Two known molecular mechanisms for synaptic plasticity were revealed by research in laboratories such as that of Eric Kandel. The first mechanism involves modification of existing synaptic proteins (typically protein kinases) resulting in altered synaptic function (Shi et al., 1999). The second mechanism depends on second messenger neurotransmitters regulating gene transcription and changes in the levels of key proteins at synapses. This second mechanism can be triggered by protein phosphorylation but takes longer and lasts longer, providing the mechanism for long-lasting memory storage. Long-lasting changes in synaptic connectivity (long-term potentiation, or LTP), between two neurons can involve the making and breaking of synaptic contacts.

A synapse's strength also depends on the number of ion channels it has (Debanne et al., 2003). Several facts suggest that neurons change the density of receptors on their postsynaptic membranes as a mechanism for changing their own excitability in response to stimuli. In a dynamic process that is maintained in equilibrium, NMDA and AMPA receptors are added to the membrane by exocytosis and removed by endocytosis (Shi et al., 1999; Song and Huganir, 2002; Pérez-Otaño and Ehlers, 2005). These processes, and by extension the number of receptors on the membrane, can be altered by synaptic activity (Shi et al., 1999; Pérez-Otaño and Ehlers, 2005). Experiments have shown that AMPA receptors are delivered to the membrane due to repetitive NMDAR activation (Shi et al., 1999; Song and Huganir, 2002).

If the strength of a synapse is only reinforced by stimulation or weakened by its lack, a positive feedback loop will develop, leading some cells never to fire and some to fire too much. But two regulatory forms of plasticity, called scaling and metaplasticity, also exist to provide negative feedback (Pérez-Otaño and Ehlers, 2005). Synaptic scaling serves to maintain the strengths of synapses relative to each other, lowering amplitudes of small excitatory postsynaptic potentials in response to continual excitation and raising them after prolonged blockage or inhibition (Pérez-Otaño and Ehlers, 2005). This effect occurs gradually over hours or days, by changing the numbers of NMDA receptors at the synapse (Pérez-Otaño and Ehlers, 2005). Metaplasticity, another form of negative feedback, reduces the effects of plasticity over time (Pérez-Otaño and Ehlers, 2005). Thus, if a cell has been affected by a lot of plasticity in the past, metaplasticity makes future plasticity less effective. Since LTP and LTD (long-term depression) rely on the influx of Ca2+ through NMDA channels, metaplasticity may be due to changes in NMDA receptors, for example changes in their subunits to allow the concentration of Ca2+ in the cell to be lowered more quickly (Pérez-Otaño and Ehlers, 2005).

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