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Nicoletta Berardi

Cortical plasticity during development and in the adult

S. Capsoni, G. Ugolini, A. Comparini, F. Ruberti, N. Berardi, A. Cattaneo. Alzheimer-like neurodegeneration in aged antinerve growth factor transgenic mice. Proc. Natl. Acad. Sci. USA, 97(12), Jun 6, pg. 6826-6831 (2000)

G. DiCristo, N. Berardi, L. Cancedda,  T. Pizzorusso, E. Putignano, G.M. Ratto, L. Maffei. (2001) Requirement of ERK activation for visual cortical plasticity. Science, 292, pg. 2337-2340

Pizzorusso T, Medini P, Berardi N, Chierzi S, Fawcett JW, Maffei L. Reactivation of ocular dominance plasticity in the adult visual cortex. Science. 2002 Nov 8;298(5596):1248-51.

Berardi N, Pizzorusso T, Ratto GM, Maffei L. Molecular basis of plasticity in the visual cortex. Trends Neurosci. 2003 Jul;26(7):369-78.

 

 

 

 

 

 

 


My field of interest is the study of visual cortical plasticity and of its molecular basis, both during development and in the adult. Presently, two main research lines are pursued:

1) Determinants of the critical period for monocular deprivation.

During restricted windows in development called critical periods cortical circuits are particularly sensitive to experience. Subsequently, cortical plasticity declines with age. The possibility to reactivate plasticity in the adult visual cortex would be important also to favour brain repair in the adult CNS. We have found that the removal of chondroitin-sulphate proteoglycans from the extracellular matrix of the adult visual cortex or the decrease of GABAergic inhibition in the visual cortex reactivates ocular dominance plasticity. We are currently investigating the molecular mechanisms underlying these effects and their possible exploitation for recovery from experimental amblyopia. Recently, we have also started to investigate the role of the environment in visual cortical development and plasticity in dark rearing, a procedure which is known to delay visual cortical development and the closure of the critical period.

2) Visual recognition memory and spatial memory in a murine model for Alzheimer disease.

Recently, a new mouse model for sporadic Alzheimer disease (AD) has been developed by A. Cattaneo (SISSA) which shows all the hallmarks of human AD, including extensive and progressive neurodegeneration, neurofibrillary tangles, plaques and cholinergic deficit. We have first demonstrated that visual acuity is normal in AD11 mice. We have then characterized the progression of the cognitive deficits in these mice in a visual  recognition memory task and in a spatial memory task, finding a very good correlation with the progression of the Alzheimer-like neurodegeneration. We are currently investigating the effectiveness of pharmacological treatment and of environment in ameliorating the memory deficits and the neurodegeneration in AD11 mice.

Electrophysiological (in vivo), behavioural, and anatomical techniques are used in combination in our researches.