“Changes in plasticity during postnatal development. Opening and closing plasticity Windows”

“Ventanas de plasticidad durante el desarrollo cerebral”

Speaker: Prof. Antonio Rodríguez-Moreno. Catedrático de Fisiología.
Institution: Universidad Pablo de Olavide. Sevilla
Place: CIPF conference room

Abstract: The mammalian brain has the ability to change in response to experience, a property termed plasticity. Plasticity involves the re-organization of cortical maps during development, and is fundamental for learning and memory. Throughout development, activity sensory-dependent plastic changes occur during permissive and critical periods of plasticity, with environmental influences subsequently shaping brain circuits further, reordering and refining neural connections into the definitive adult circuits. The closing of such permissive windows is associated with the loss of plasticity at particular synapses, producing specific functional effects. Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are the two best-known forms of plasticity. Spike timing-dependent plasticity (STDP) is a Hebbian form of long-term synaptic plasticity detected in all species examined to date, from insects to humans. This process is a strong candidate to underlie circuit remodelling during development, as well as that in subsequent learning and memory. In STDP, the order and relative millisecond timing of pre-and postsynaptic action potentials (APs, spikes) determines the direction and magnitude of synaptic changes. Thus, timing-dependent LTP (t-LTP) occurs when a presynaptic spike is followed by a postsynaptic spike, whereas timing-dependent LTD (t[1]LTD) is induced when this order is inverted, although exceptions exist. A presynaptic form of t-LTD that requires the activation of presynaptic NMDA receptors (preNMDARs) has been described in the hippocampus and in the visual and somatosensory cortices. These presynaptic forms of t-LTD disappear in the first weeks of development, by the fourth week of postnatal development in the mouse hippocampus, although how this loss is brought about is not known. Moreover, it is unclear whether the closing of this window of plasticity in the fourth week of development is reversible or not. Determining the mechanisms that produce the closure of plasticity windows is important when studying the brain responses to experience and injury. Indeed, defining such processes may have important implications for brain repair, sensorial recovery, the treatment of neurodevelopmental disorders and even, for educational policy