Neuroplasticity is classically accepted as the capacity of neurons to change the shape of their connection tree. This ability is made possible by messenger pathways that mediate signal transduction in the brain. The short- and long-term modulatory effects that neurotransmitters exert on their target neurons via regulation of intracellular messenger pathways can be viewed as the basis of neural plasticity. Besides the brain's intracellular messenger pathways are themselves targets of long-term regulation and contribute prominently to drug-induced neural plasticity.There are three general types of mechanisms by which a drug could alter levels of a protein: regulation of gene transcription, regulation of RNA translation and turnover, or regulation of protein turnover. Studies of drug regulation of gene expression to date have focused almost exclusively on two families of transcription factors: CREB (cAMP response element binding protein) and related proteins mediate many of the effects of cAMP and probably Ca2+ on gene expression. CREB's transcriptional activity is regulated primarily via its phosphorylation by cAMP-dependent and Ca2+-dependent protein kinases. Increasing evidence demonstrates that psychotropic drug treatments can regulate CREB function in the brain, presumably by influencing these intracellular pathways.c-Fos, c-Jun, and products of related immediate early genes (IEGs) are regulated in the brain by diverse types of stimuli, including numerous drug and other treatments. Extracellular stimuli are thought to regulate these transcription factors primarily by regulating their expression, possibly mediated via the cAMP- or Ca2+-dependent phosphorylation of CREB or CREB-like proteins. However, Fos- and Jun-like proteins are also known to be phosphorylated by many protein kinases, and this serves to further regulate their transcriptional activity.On the basis of these studies is evident that neuroplasticity may be present even in the elderly. In order to evaluate the neuroplasticity in older people, the purpose of this chapter was to study the effects of an antioxidant agent (Q-TER®) in the treatment of presbyacusis.

New drugs to improve the neuroplasticity of the central auditory pathway

GUASTINI, LUCA
2011-01-01

Abstract

Neuroplasticity is classically accepted as the capacity of neurons to change the shape of their connection tree. This ability is made possible by messenger pathways that mediate signal transduction in the brain. The short- and long-term modulatory effects that neurotransmitters exert on their target neurons via regulation of intracellular messenger pathways can be viewed as the basis of neural plasticity. Besides the brain's intracellular messenger pathways are themselves targets of long-term regulation and contribute prominently to drug-induced neural plasticity.There are three general types of mechanisms by which a drug could alter levels of a protein: regulation of gene transcription, regulation of RNA translation and turnover, or regulation of protein turnover. Studies of drug regulation of gene expression to date have focused almost exclusively on two families of transcription factors: CREB (cAMP response element binding protein) and related proteins mediate many of the effects of cAMP and probably Ca2+ on gene expression. CREB's transcriptional activity is regulated primarily via its phosphorylation by cAMP-dependent and Ca2+-dependent protein kinases. Increasing evidence demonstrates that psychotropic drug treatments can regulate CREB function in the brain, presumably by influencing these intracellular pathways.c-Fos, c-Jun, and products of related immediate early genes (IEGs) are regulated in the brain by diverse types of stimuli, including numerous drug and other treatments. Extracellular stimuli are thought to regulate these transcription factors primarily by regulating their expression, possibly mediated via the cAMP- or Ca2+-dependent phosphorylation of CREB or CREB-like proteins. However, Fos- and Jun-like proteins are also known to be phosphorylated by many protein kinases, and this serves to further regulate their transcriptional activity.On the basis of these studies is evident that neuroplasticity may be present even in the elderly. In order to evaluate the neuroplasticity in older people, the purpose of this chapter was to study the effects of an antioxidant agent (Q-TER®) in the treatment of presbyacusis.
2011
978-161761949-6
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11567/842337
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 0
  • ???jsp.display-item.citation.isi??? ND
social impact