QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, October 4, 2006, 26(40):10199-10208; doi:10.1523/JNEUROSCI.1223-06.2006

This Article Full Text Full Text (PDF) Supplemental data Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (17) Citing Articles via Google Scholar Google Scholar Articles by Martín-Peña, A. Articles by Ferrús, A. Search for Related Content PubMed PubMed Citation Articles by Martín-Peña, A. Articles by Ferrús, A.

 Previous Article  |  Next Article 

Development/Plasticity/Repair
Age-Independent Synaptogenesis by Phosphoinositide 3 Kinase

Alfonso Martín-Peña,¹ Angel Acebes,¹ José-Rodrigo Rodríguez,¹ Amanda Sorribes,² Gonzalo G. de Polavieja,² Pedro Fernández-Fúnez,^3 * and Alberto Ferrús^1 *

¹Cajal Institute, Consejo Superior de Investigaciones Científicas, 28002 Madrid, Spain, ²Department of Theoretical Physics, Universidad Autónoma, 28049 Madrid, Spain, and ³Department of Neurology, University of Texas Medical Branch, Galveston, Texas 77555

Correspondence should be addressed to Alberto Ferrús, Cajal Institute, Consejo Superior de Investigaciones Científicas, Avenida Dr. Arce 37, 28002 Madrid, Spain. Email: aferrus{at}cajal.csic.es

Synapses are specialized communication points between neurons, and their number is a major determinant of cognitive abilities. These dynamic structures undergo developmental- and activity-dependent changes. During brain aging and certain diseases, synapses are gradually lost, causing mental decline. It is, thus, critical to identify the molecular mechanisms controlling synapse number. We show here that the levels of phosphoinositide 3 kinase (PI3K) regulate synapse number in both Drosophila larval motor neurons and adult brain projection neurons. The supernumerary synapses induced by PI3K overexpression are functional and elicit changes in behavior. Remarkably, PI3K activation induces synaptogenesis in aged adult neurons as well. We demonstrate that persistent PI3K activity is necessary for synapse maintenance. We also report that PI3K controls the expression and localization of synaptic markers in human neuroblastoma cells, suggesting that PI3K synaptogenic activity is conserved in humans. Thus, we propose that PI3K stimulation can be applied to prevent or delay synapse loss in normal aging and in neurological disorders.

Key words: synaptogenesis; Drosophila; PI3K; aging; central complex; locomotion

---

Received March 21, 2006; revised July 26, 2006; accepted Aug. 21, 2006.

Correspondence should be addressed to Alberto Ferrús, Cajal Institute, Consejo Superior de Investigaciones Científicas, Avenida Dr. Arce 37, 28002 Madrid, Spain. Email: aferrus{at}cajal.csic.es

This article has been cited by other articles:

				J. S. King, R. Teo, J. Ryves, J. V. Reddy, O. Peters, B. Orabi, O. Hoeller, R. S. B. Williams, and A. J. Harwood The mood stabiliser lithium suppresses PIP3 signalling in Dictyostelium and human cells Dis. Model. Mech., May 1, 2009; 2(5-6): 306 - 312. [Abstract] [Full Text] [PDF]

				S. D. Buckingham, A. K. Jones, L. A. Brown, and D. B. Sattelle Nicotinic Acetylcholine Receptor Signalling: Roles in Alzheimer's Disease and Amyloid Neuroprotection Pharmacol. Rev., March 1, 2009; 61(1): 39 - 61. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help