Faulty plasticity: A common thread connecting neurological diseases

Document Type

Article

Publication Date

12-1-2012

Abstract

Plastic processes, in particular Long Term Potentiation (LTP) and Long Term Depression (LTD), seem to play a role in the development of certain neurological disorders. Both physiological processes are defined by long lasting changes in synaptic transmission and are commonly studied in the hippocampus, although there is evidence of their occurrence in some other brain areas, particularly cortico-striatal networks. It is well known that plasticity is affected in Alzheimer's disease due to a deficiency in N-Methyl-D-Asparte (NMDA) receptors, one of the central elements on which the induction of LTP hinges. The present chapter focuses, however, on recent developments in animal and human studies that associate LTP to other conditions such as Huntington's, Parkinson's, and dystonia. In most cases, plasticity, as indexed by LTP or LTD manipulations, is impaired. In some instances, NMDA receptors are involved together with other neurotransmitters systems. We point out that a unified view of the role of plasticity in disease has not been developed. However, recent models of homeostatic plasticity (a negative feedback mechanism, present in neural populations, that offset excessive excitation or inhibition by adjusting the limits of synaptic strength) may be useful to understand and predict some of the observed effects. We argue that future research has to establish plasticity's contribution, either as a promoter of a given disorder or as a side-effect resulting from other physiological processes. © 2012 by Nova Science Publishers, Inc. All rights reserved.

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