Skip to content
Dr Paulina Carriba

Dr Paulina Carriba

Research Associate

School of Biosciences

Email:
carribap@cardiff.ac.uk
Telephone:
+44 (0)29 2087 6878
Location:
Sir Martin Evans Building, Museum Avenue, Cardiff, CF10 3AX

We are interested in the roles of CD40 (TNFRSF5) / CD40L (TNFSR5 or CD154) system in the regulation and elaboration of axons and dendrites in the developing vertebrate nervous system. Using different cellular, molecular and transgenic approaches our aim is to gain insight into how CD40/CD40L regulates neuronal morphology. Brain function depends on a precise but plastic brain architecture. Knowledge of the mechanisms that regulate the growth and morphology of neural processes is essential to understand how the brain is assembled during development and modified by experience, but also how it could be manipulated in pathological conditions.

BSc Biochemistry, Universitat de Barcelona (UB)

PhD Biomedicine, Universitat de Barcelona (UB)

Positions:

2014 - present: Postdoctoral researcher at Cardiff University (UK)

2010 - 2014: Postdoctoral researcher at Hospital Vall d´Hebrón Institut de Recerca (VHIR)

2007 - 2010: Postdoctoral researcher at Institut de Neurociències (INc-UAB)

2002 - 2007: PhD student at Universitat de Barcelona (UB)

Competitive Grants and Scholarships:

2012-2014: Marie Curie Fellow

2002-2006: FPI Fellowship from the Spanish Ministry of Science.

2013

2012

2010

2008

2007

2006

Tumor necrosis factor superfamily (TNFSF) has been extensively characterised in the immune system. In the nervous system, besides their immunological functions, it has been described that some members of this superfamily are potent positive and negative regulators of neural growth. TNFSF are active both as membrane-integrated ligands and as soluble ligands after cleavage from the cell membrane. They bind to one or more members of the TNF receptor superfamily (TNFRSF) triggering forward signalling. Moreover, some TNFRSF members can also act as ligands for the membrane-integrated TNFSF initiating reverse signalling.

My research line is focused in the role of CD40 (TNFRSF5) / CD40L (TNFSR5 or CD154) system in the central nervous system (CNS). Recently, we have described that CD40-activated CD40L reverse signalling is a major physiological regulator of dendrite growth in the CNS, with striking opposite effects on the size and elaboration of dendrite arbors of excitatory hippocampal pyramidal neurons [which are much reduced in Cd40-/- mice] and inhibitory striatal medium spiny neurons (MSN) [which are much larger and exuberant in Cd40-/- mice]. These finding raise new questions such as what is the intracellular mechanism that mediates the opposite effects of CD40L-reverse signalling on dendrite morphology?; is there any phenotypic change in dendrite spines?; are other brain regions regulated by CD40/CD40L? to cite some of them.

Defects in neural processes compromise neuronal networks, producing neurodevelopmental disorders or neurodegenerative diseases. Therefore this knowledge will not only improve our understanding of developmental processes but may also have implications for manipulating morphological changes in neurons occurring in disease or following injury.