HCN PAIN

Role of HCN ion channels in somatic sensation and pain

Coordinatore	more  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Prof. Nome: Peter Anthony Cognome: Mcnaughton Email: send email Telefono: +44 1223 334012 Fax: +44 1223 334100
Nazionalità Coordinatore	Non specificata
Totale costo	178˙874 €
EC contributo	178˙874 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-02-15   -   2010-02-14

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE  Organization address address: The Old Schools, Trinity Lane city: CAMBRIDGE postcode: CB2 1TN contact info Titolo: Prof. Nome: Peter Anthony Cognome: Mcnaughton Email: send email Telefono: +44 1223 334012 Fax: +44 1223 334100	UK (CAMBRIDGE)	coordinator	0.00

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 Obiettivo del progetto (Objective)

'Pain arises when a stimulus activates a pain-specific nerve fibre by opening an ion channel, causing a depolarisation (positive change in membrane potential) and triggering action potentials that propagate to the central nervous system to elicit a sensation of pain. The rate of depolarisation between action potentials determines their frequency, and thus the pain intensity. An important modulator of this rate is the hyperpolarisation-activated inward current, Ih. Ih ion channels are made up from combinations of four different subunits, HCN1-4. We have shown that the fast HCN1 subunits are expressed in large neurones sensing light touch, and the slower HCN2 in small pain-sensitive neurones. We aim to find out more about which subunits are expressed in which types of sensory neurones, and how their behaviour is modulated by inflammatory mediators. Neuropathic pain, an anomalous pain state characterised by ongoing pain and hypersensitivity, is not well understood and causes a substantial reduction in quality of life for those who suffer from it. There is evidence that Ih is involved in neuropathic pain, but which subunit is important and how it enhances neuropathic pain is unknown. We will tackle these and other questions by the use of mice in which each HCN subunit has been genetically deleted. We will record electrical responses from neurones in cell culture, where their behaviour can more readily be investigated. We will study the response of wild-type and HCN knockout mice to a mild painful stimulus. These studies will advance our understanding of the role of HCN subunits in pain, and if particular subunits have crucial roles in some aspects of pain (e.g. in neuropathic pain) the work will act as a stimulus to the development of novel drugs aimed at specifically blocking those subunits.'