PRESSBIRTH

Arginine vasopressin and ion transporters in the modulation of brain excitability during birth and birth asphyxia seizures

 Coordinatore HELSINGIN YLIOPISTO 

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 Nazionalità Coordinatore Finland [FI]
 Totale costo 2˙497˙419 €
 EC contributo 2˙497˙419 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2013-ADG
 Funding Scheme ERC-AG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-02-01   -   2019-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    HELSINGIN YLIOPISTO

 Organization address address: YLIOPISTONKATU 4
city: HELSINGIN YLIOPISTO
postcode: 14

contact info
Titolo: Dr.
Nome: Katri
Cognome: Wegelius
Email: send email
Telefono: +358 9 191 59859

FI (HELSINGIN YLIOPISTO) hostInstitution 2˙497˙419.00
2    HELSINGIN YLIOPISTO

 Organization address address: YLIOPISTONKATU 4
city: HELSINGIN YLIOPISTO
postcode: 14

contact info
Titolo: Prof.
Nome: Kai Kalervo
Cognome: Kaila
Email: send email
Telefono: 358919000000
Fax: 358407000000

FI (HELSINGIN YLIOPISTO) hostInstitution 2˙497˙419.00

Mappa


 Word cloud

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receptor    regulation    mechanisms    copeptin    data    excitability    newborn    cl    graded    alkalosis    pilot    blood    restoration    birth    our    normal    asphyxia    exchange    avp    seizures    triggers    neonatal    cotransporter    indicate    actions       na    brain    bbb    acting   

 Obiettivo del progetto (Objective)

'A transient period of asphyxia in the newborn is an obligatory part of normal parturition. A more prolonged disturbance in cerebral blood supply is a major cause of neonatal seizures. Current therapies of birth asphyxia seizures are ineffective and the underlying mechanisms are unknown. Our recent landmark work on a rat model of birth asphyxia showed that asphyxia is followed by brain alkalosis, which triggers seizures. The brain-confined alkalosis is generated by activation of Na/H exchange in the blood-brain barrier (BBB). Both alkalosis and the consequent seizures can be suppressed by graded restoration of the high CO2 level after asphyxia and with blockers of Na/H exchange. Our pilot data indicate that arginine vasopressin (AVP) triggers the post-asphyxia seizures by activating the BBB-located luminal V1a receptor-coupled Na/H exchanger. Akin to human infants, a very high level of plasma copeptin (a part of pro-AVP) is seen following asphyxia but, notably, the copeptin levels remain low with graded restoration of normocapnia. Moreover, intravenous AVP V1a receptor antagonists, acting on the BBB, block the generation of seizures. In striking contrast, AVP suppresses network excitability when acting on V1aRs in the neonate hippocampus. Thus, I hypothesize that AVP acts on the BBB to promote neonatal seizures, and that this effect is paralleled by a central anticonvulsant action. Next to nothing is known about AVP actions on ionic regulation in the brain. Our pilot data indicate that AVP inhibits the Na-K-2Cl cotransporter NKCC1 and activates the K-Cl cotransporter KCC2 in a manner consistent with reduction of excitability. My laboratory has an internationally leading role in work on neuronal pH and Cl- regulation and on functions of the immature brain. Understanding the mechanisms of AVP actions during normal birth and birth asphyxia will provide novel insights on the control of the excitability of the newborn brain. This work has a high translational impact.'

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