Erratum Phosphorylation of synapsin domain A is required for post-tetanic potentiation

نویسندگان

  • Ferdinando Fiumara
  • Chiara Milanese
  • Anna Corradi
  • Silvia Giovedi
  • Gerd Leitinger
  • Andrea Menegon
  • Pier Giorgio Montarolo
  • Fabio Benfenati
  • Mirella Ghirardi
چکیده

We apologise for an error that occurred in the e-press version of this article. The print and online version of this article are correct. The last sentence of the first paragraph of the section 'Post-tetanic potentiation at C1-B2 synapses requires phosphorylation of synapsin domain A', is incorrect. The correct sentence is shown below. A statistical comparison of these four groups using two-way ANOVA for repeated measures revealed a significant effect of the treatment, i.e. Introduction Post-tetanic potentiation (PTP) is a widespread form of homosynaptic plasticity that, together with other forms of short-term synaptic enhancement (STE), is considered as one of the neural substrates of short-term memory and synaptic computation (Fisher et al. Even though PTP – and other forms of STE – are generally thought to depend on the activity-dependent increase of Ca 2+ concentration in presynaptic terminals, the downstream molecular effectors of Ca

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Phosphorylation of synapsin domain A is required for post-tetanic potentiation.

Post-tetanic potentiation (PTP) is a form of homosynaptic plasticity important for information processing and short-term memory in the nervous system. The synapsins, a family of synaptic vesicle (SV)-associated phosphoproteins, have been implicated in PTP. Although several synapsin functions are known to be regulated by phosphorylation by multiple protein kinases, the role of individual phospho...

متن کامل

Site-specific synapsin I phosphorylation participates in the expression of post-tetanic potentiation and its enhancement by BDNF.

A large amount of experimental evidence has highlighted the rapid changes in synaptic efficacy induced by high-frequency stimulation and BDNF at central excitatory synapses. We clarified the quantal mechanisms and the involvement of Synapsin I (SynI) phosphorylation in the expression of post-tetanic potentiation (PTP) and in its modulation by BDNF in mouse glutamatergic autapses. We found that ...

متن کامل

Synapsin controls both reserve and releasable synaptic vesicle pools during neuronal activity and short-term plasticity in Aplysia.

Neurotransmitter release is a highly efficient secretory process exhibiting resistance to fatigue and plasticity attributable to the existence of distinct pools of synaptic vesicles (SVs), namely a readily releasable pool and a reserve pool from which vesicles can be recruited after activity. Synaptic vesicles in the reserve pool are thought to be reversibly tethered to the actin-based cytoskel...

متن کامل

MAPK/Erk-dependent phosphorylation of synapsin mediates formation of functional synapses and short-term homosynaptic plasticity.

MAPK/Erk is a protein kinase activated by neurotrophic factors involved in synapse formation and plasticity, which acts at both the nuclear and cytoplasmic level. Synapsin proteins are synaptic-vesicle-associated proteins that are well known to be MAPK/Erk substrates at phylogenetically conserved sites. However, the physiological role of MAPK/Erk-dependent synapsin phosphorylation in regulating...

متن کامل

Pentylenetetrazol-Induced Epileptiform Activity Affects Basal Synaptic Transmission and Short-Term Plasticity in Monosynaptic Connections

Epileptic activity is generally induced in experimental models by local application of epileptogenic drugs, including pentylenetetrazol (PTZ), widely used on both vertebrate and invertebrate neurons. Despite the high prevalence of this neurological disorder and the extensive research on it, the cellular and molecular mechanisms underlying epileptogenesis still remain unclear. In this work, we e...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2007