The behavioral tagging hypothesis postulates that learning induces the synthesis of plasticity-related proteins (PRPs) that will be captured at tagged synapses (those activated during training), to stabilize the mnemonic trace. This mechanism can be observed by the interaction of two learning tasks: a weak task “B”, which only induces the tag at activated synapses, and a strong task “A”, which induces the s...
The behavioral tagging hypothesis postulates that learning induces the synthesis of plasticity-related proteins (PRPs) that will be captured at tagged synapses (those activated during training), to stabilize the mnemonic trace. This mechanism can be observed by the interaction of two learning tasks: a weak task “B”, which only induces the tag at activated synapses, and a strong task “A”, which induces the synthesis of PRPs that can be captured by the synapses tagged by B. So, what are the requirements for A to cooperate with B? A should provide new proteins around the space and time of B´s tag. Moreover, A should not impair or erase the B´s tag, nor compete for the PRPs (Fonseca et al, 2004; Young et al, 2006).
The molecular species and the kinetics of the tag and the PRPs probably depend on the properties and characteristics of the tasks. We reason, as proposed by Lu et al (2007), that one candidate to play a role of PRPs provided by A could be the neurotrophic factor BDNF.
Although direct evidence for the existence of the tag and capture processes is still pending, the behavioral tagging hypothesis is a good and versatile model that explains any interaction between two behavioral tasks experienced by an animal during a close time window.
References
Fonseca R, Nägerl UV, Morris RG, Bonhoeffer T. (2004) Competing for memory: hippocampal LTP under regimes of reduced protein synthesis. Neuron 44(6):1011-20.
Lu Y, Christian K, Lu B. (2007) BDNF: A key regulator for protein synthesis-dependent LTP and long-term memory? Neurobiol Learn Mem. In press.
Young JZ, Isiegas C, Abel T, Nguyen PV. (2006) Metaplasticity of the late-phase of long-term potentiation: a critical role for protein kinase A in synaptic tagging. Eur J Neurosci. 23(7):1784-94.