The study will be published in the Journal of Neuroscience (February 28, 2007 issue). They had opportunity to determine activity-dependent plasticity – a cellular process, in which the connections between individual brain cells get stronger the more often they are used, such as during learning - in the hippocampus of freely moving mouse mutants. Recording in vivo techniques were developed last year by the group of Drs. J.M. Delgado-García and A. Gruart (see Gruart et al., 26: 1077-1087, 2006), and allow determining the explicit relation between the learning process and the physiological synaptic enhancement in the hippocampus.
Neurotrophins and their receptors might serve as feedback regulators for the efficacy of synaptic transmission. As recently shown in vivo by some of us, the BDNF-TrkB system is well known for its importance in synaptic plasticity and long-term potentiation (LTP) in the hippocampus (see Gruart et al., Learn. Mem., 4: 54-62, 2007). However, until now, the role of other neurotrophin systems in mediating synaptic modulation remained to be elucidated. In their study, the groups of Drs. M. Dierssen, and J.M. Delgado-García and A. Gruart used transgenic mice overexpressing TrkC to test the hypothesis that in vivo overexpression of the TrkC receptor could produce an increase in survival and/or neuronal induction or promotion in the hippocampus, with some putative consequences for learning and synaptic plasticity in adult mice. In their experiments, the activity-dependent strength of the hippocampal CA3-CA1 synapse –a brain region involved in learning- was recorded in behaving mice, while animals were being trained to the classical conditioning of eyelid responses.
For the first time, the work clearly provides evidence for a direct, causal role for the NT-3-TrkC cascade in the physiological potentiation of field excitatory post-synaptic potentials (fEPSP) evoked at the CA3-CA1 synapse during the acquisition of an associative learning task, as well as in early and late maintenance of experimentally induced LTP. Interestingly, overexpression of TrkC seems to reduce the efficiency of conditioned learning, an effect that has previously been observed after LTP ‘saturation’ induced experimentally in behaving mice (Gruart et al., 26: 1077-1087, 2006). It is thus possible that TrkC overexpression enhances too much hippocampal synaptic activity, which then occludes normal associative learning.
This paper shows for the first time the dissociation between the ability to learn a task and the changes in synaptic plasticity seen during synaptic potentiation in behaving mice and suggests that it is the combination of different neurotrophin systems what leads to the proper balance of learning abilities in mammals.
Gloria Lligadas | alfa
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