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

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, March 2, 2005, 25(9):2267-2276; doi:10.1523/JNEUROSCI.4053-04.2005

This Article Full Text Full Text (PDF) 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 (6) Citing Articles via Google Scholar Google Scholar Articles by Ster, J. Articles by Hussy, N. Search for Related Content PubMed PubMed Citation Articles by Ster, J. Articles by Hussy, N.

 Previous Article  |  Next Article 

Cellular/Molecular
Insulin-Like Growth Factor-1 Inhibits Adult Supraoptic Neurons via Complementary Modulation of Mechanoreceptors and Glycine Receptors

Jeanne Ster, ^* Claude Colomer, ^* Cécile Monzo, Anne Duvoid-Guillou, Françoise Moos, Gérard Alonso, and Nicolas Hussy

Biologie des Neurones Endocrines, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche 5101, Centre CNRS Institut National de la Santé et de la Recherche Médicale de Pharmacologie et d'Endocrinologie, 34094 Montpellier Cedex 5, France

In the CNS, insulin-like growth factor-1 (IGF-1) is mainly known for its trophic effect both during development and in adulthood. Here, we show than in adult rat supraoptic nucleus (SON), IGF-1 receptor immunoreactivity is present in neurons, whereas IGF-1 immunoreactivity is found principally in astrocytes and more moderately in neurons. In vivo application of IGF-1 within the SON acutely inhibits the activity of both vasopressin and oxytocin neurons, the two populations of SON neuroendocrine cells. Recordings of acutely isolated SON neurons showed that this inhibition occurs through two rapid and reversible mechanisms, both involving the neuronal IGF-1 receptor but different intracellular messengers. IGF-1 inhibits Gd³⁺-sensitive and osmosensitive mechanoreceptor cation current via phosphatidylinositol-3 (PI3) kinase activation. IGF-1 also potentiates taurine-activated glycine receptor (GlyR) Cl^- currents by increasing the agonist sensitivity through a extremely rapid (within a second) PI3 kinase-independent mechanism. Both mechanoreceptor channels and GlyR, which form the excitatory and inhibitory components of SON neuron osmosensitivity, are active at rest, and their respective inhibition and potentiation will both be inhibitory, leading to strong decrease in neuronal activity. It will be of interest to determine whether IGF-1 is released by neurons, thus participating in an inhibitory autocontrol, or astrocytes, then joining the growing family of glia-to-neuron transmitters that modulate neuronal and synaptic activity. Through the opposite and complementary acute regulation of mechanoreceptors and GlyR, IGF-1 appears as a new important neuromodulator in the adult CNS, participating in the complex integration of neural messages that regulates the level of neuronal excitability.

Key words: insulin-like growth factor 1; taurine; mechanoreceptor; osmoregulation; astrocyte; neuroendocrine cells

---

Received Sep 30, 2004; revised January 11, 2005; accepted January 13, 2005.

This article has been cited by other articles:

				V. B. Caraiscos, R. P. Bonin, J. G. Newell, E. Czerwinska, J. F. Macdonald, and B. A. Orser Insulin Increases the Potency of Glycine at Ionotropic Glycine Receptors Mol. Pharmacol., May 1, 2007; 71(5): 1277 - 1287. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help