Valproate reopens critical-period learning of absolute pitch

This paper reviews 10 principles of experience-dependent neural plasticity and considerations in applying them to the damaged brain. Neuroscience research using a variety of models of learning, neurological disease, and trauma are reviewed from the perspective of basic neuroscientists but in a manner intended to be useful for the development of more effective clinical rehabilitation interventions. Neural plasticity is believed to be the basis for both learning in the intact brain and relearning in the damaged brain that occurs through physical rehabilitation. Neuroscience research has made significant advances in understanding experience-dependent neural plasticity, and these findings are beginning to be integrated with research on the degenerative and regenerative effects of brain damage. The qualities and constraints of experience-dependent neural plasticity are likely to be of major relevance to rehabilitation efforts in humans with brain damage. However, some research topics need much more attention in order to enhance the translation of this area of neuroscience to clinical research and practice. The growing understanding of the nature of brain plasticity raises optimism that this knowledge can be capitalized upon to improve rehabilitation efforts and to optimize functional outcome.

Background Typically, randomization software should allow users to exert control over the different aspects of randomization including block design, provision of unique identifiers and control over the format and type of program output. While some of these characteristics have been addressed by available software, none of them have all of these capabilities integrated into one package. The main objective of the Random Allocation Software project was to enhance the user's control over different aspects of randomization in parallel group trials, including output type and format, structure and ordering of generated unique identifiers and enabling users to specify group names for more than two groups. Results The program has different settings for: simple and blocked randomizations; length, format and ordering of generated unique identifiers; type and format of program output; and saving sessions for future use. A formatted random list generated by this program can be used directly (without further formatting) by the coordinator of the research team to prepare and encode different drugs or instruments necessary for the parallel group trial. Conclusions Random Allocation Software enables users to control different attributes of the random allocation sequence and produce qualified lists for parallel group trials.

Neuronal circuits across several systems display remarkable plasticity to sensory input during postnatal development. Experience-dependent refinements are often restricted to well-defined critical periods in early life, but how these are established remains mostly unknown. A representative example is the loss of responsiveness in neocortex to an eye deprived of vision. Here we show that the potential for plasticity is retained throughout life until an inhibitory threshold is attained. In mice of all ages lacking an isoform of GABA (gamma-aminobutyric acid) synthetic enzyme (GAD65), as well as in immature wild-type animals before the onset of their natural critical period, benzodiazepines selectively reduced a prolonged discharge phenotype to unmask plasticity. Enhancing GABA-mediated transmission early in life rendered mutant animals insensitive to monocular deprivation as adults, similar to normal wild-type mice. Short-term presynaptic dynamics reflected a synaptic reorganization in GAD65 knockout mice after chronic diazepam treatment. A threshold level of inhibition within the visual cortex may thus trigger, once in life, an experience-dependent critical period for circuit consolidation, which may otherwise lie dormant.