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Open Position: Cellular Electrophysiologist

UPDATE 2017-05-29: Position still open. 

We are seeking a talented and enthusiastic researcher with expertise in cellular electrophysiology to advance investigations on the functions and mechanisms of neurotrophic signaling networks in the adult nervous system. The research entails functional assessment of neuronal circuits in the brains of mutant mice lacking different neurotrophic factor receptors in specific subpopulations of neurons.

Candidates will be accepted at the postdoctoral level with a PhD awarded preferably within the last 5 years. Strong and documented expertise in electrophysiological methods as applied to studies of the rodent central nervous system, such as electrophysiological recordings from brain slices, is a requirement for consideration. Experience on calcium imaging would be an advantage.

The successful candidate is expected to be sufficiently independent to set up electrophysiological methods at our laboratory, including supervision of purchase, installation and maintenance of the necessary equipment.

Applications, including CV, list of publications and statement of future interests should be sent to Prof. Carlos Ibanez . Applicants should arrange to have at least two confidential letters of reference sent independently by referees to this email address.

Funding is available for an initial period of 3 to 4 years, starting any time during 2017.

Open Postdoctoral Position: Molecular / Cellular Neurobiologists

UPDATE 2017-05-29: The position has been filled. 

We are seeking a talented and enthusiastic researcher with expertise in molecular and cellular neurobiology to advance investigations on the functions and mechanisms of neurotrophic signaling in the nervous system. The research entails studies of death receptor signaling pathways in cell culture models as well as phenotypic characterisation of mutant mice carrying specific mutations in neurotrophic factor receptors. Please refer to our recent list of publications in this area HERE.

Candidates will be accepted at the postdoctoral level (PhD awarded within the last 5 years). Strong and documented expertise in cellular, molecular and histological methods as applied to studies of the rodent nervous system is a requirement for consideration. Experience with genetically modified mice is highly desirable. The successful candidate is expected to be sufficiently independent to formulate questions, design experiments and perform research.

Our group belongs to a network of laboratories dedicated to different aspects of neuroscience research and provides a strong environment for scientific growth and career development.

Applications, including CV, list of publications and statement of future interests should be sent to Prof. Carlos Ibanez . Applicants should arrange to have at least two confidential letters of reference sent independently by referees to this email address.

Funding is available for an initial period of 3 years, starting any time during 2017.

Deadline for application is March 7, 2017.

Joint retreat of KI and NUS labs in Singapore

Fellows from the KI lab flew to Singapore for a 2 day retreat with the NUS group on 16th and 17th of January 2017. After 4 years of joint lab meetings over Skype, fellows of both groups enjoyed an opportunity to discuss common projects and ideas face to face. We were joined by the NUS and UCSD groups of Prof. Ed Koo and had joint plenary and also parallel sessions, as well as group building activities, as shown in the photo below.

 

New paper shows novel function of the GFRα1 receptor

In this new paper, we show how the GFRα1 receptor regulates Purkinje cell migration independently of GDNF or RET, by limiting the function of NCAM. The paper has just been published in Cell Reports.

During embryonic development of the cerebellum, Purkinje cells (PCs) migrate away from the ventricular zone to form the PC plate. The mechanisms that regulate PC migration are incompletely understood. Here, we report that the neurotrophic receptor GFRα1 is transiently expressed in developing PCs and loss of GFRα1 delays PC migration. Neither GDNF nor RET, the canonical GFRα1 ligand and co-receptor, respectively, contribute to this process. Instead, we found that the neural cell adhesion molecule NCAM is co-expressed and directly interacts with GFRα1 in embryonic PCs. Genetic reduction of NCAM expression enhances wild-type PC migration and restores migration in Gfra1 mutants, indicating that NCAM restricts PC migration in the embryonic cerebellum. In vitro experiments indicated that GFRα1 can function both in cis and trans to counteract NCAM and promote PC migration. Collectively, our studies show that GFRα1 contributes to PC migration by limiting NCAM function.

Read the full paper HERE.

New paper shows how thalamo-cortical axons regulate the radial dispersion of neocortical GABAergic interneurons

In our latest paper, we show how thalamo-cortical axons regulate the radial dispersion of neocortical GABAergic interneurons. The paper has just been published in eLife.

Neocortical GABAergic interneuron migration and thalamo-cortical axon (TCA) pathfinding follow similar trajectories and timing, suggesting they may be interdependent. The mechanisms that regulate the radial dispersion of neocortical interneurons are incompletely understood. In this new study we report that disruption of TCA innervation, or TCA-derived glutamate, affected the laminar distribution of GABAergic interneurons in mouse neocortex, resulting in abnormal accumulation in deep layers of interneurons that failed to switch from tangential to radial orientation. Expression of the KCC2 cotransporter was elevated in interneurons of denervated cortex, and KCC2 deletion restored normal interneuron lamination in the absence of TCAs. Disruption of interneuron NMDA receptors or pharmacological inhibition of calpain also led to increased KCC2 expression and defective radial dispersion of interneurons. Thus, although TCAs are not required to guide the tangential migration of GABAergic interneurons, they provide crucial signals that restrict interneuron KCC2 levels, allowing coordinated neocortical invasion of TCAs and interneurons.

Read the full paper HERE. (Supplemental information 31.6MB)

Swedish Research Council awards new research grant to Carlos Ibanez Lab

The Swedish Research Council (Vetenskapsrådet) has awarded a new grant to our KI group for work on neurotrophic signaling in the adult nervous system and its importance for neuropsychiatric disorders. Tack för förtroendet!

Carlos Ibanez named Weston Visiting Professor at the Weizmann Institute of Science

The Weizmann Institute in Israel has named Carlos Ibanez Weston Visiting Professor in the Faculty of Biochemistry, Department of Biomolecular Sciences for 3 years, starting October 2016 to conduct educational and research activities.

New lab technician joins KI group to help with histology and imaging

Wei Wang has a BSc in Public Health from Medical College of Southeast University, Nanjing, China, and a MSc in Environmental Toxicology from Shanghai Medical College, Fudan University, Shanghai, China. She has worked as Assistant Researcher at the Shanghai Institute of Applied Physics, Shanghai Institutes for Biological Sciences and the University of Gothenburg in Sweden. She joins our group to assist with histological methods and imaging of tissue samples from our mouse models.

New paper demonstrates requirement of p75NTR death domain and transmembrane cysteine for neuronal death in the CNS

In our latest paper, we show how dimers of the p75NTR neurotrophin receptor are indipensable for p75NTR-mediated cell death in the central nervous system. The paper has just been published in the Journal of Neuroscience.

The oligomeric state and activation mechanism that enable p75 NTR to mediate these effects have recently been called into question. In this new study, we have investigated mutant mice lacking the p75NTR death domain (DD) or a highly conserved transmembrane (TM) cysteine residue (Cys 259) implicated in receptor dimerization and activation. Neuronal death induced by proneurotrophins or epileptic seizures was assessed and compared with responses in p75NTR knock-out mice and wild-type animals. Proneurotrophins induced apoptosis of cultured hippocampal and cortical neurons from wild-type mice, but mutant neurons lacking p75NTR, only the p75NTR DD, or just Cys259 were all equally resistant to proneurotrophin-induced neuronal death. Homo-FRET anisotropy experiments demonstrated that both NGF and proNGF induce conformational changes in p75 NTR that are dependent on the TM cysteine. In vivo, neuronal death induced by pilocarpine-mediated seizures was significantly reduced in the hippocampus and somatosensory, piriform, and entorhinal cortices of all three strains of p75 NTR mutant mice. Interestingly, the levels of protection observed in mice lacking the DD or only Cys 259 were identical to those of p75 NTR knock-out mice even though the Cys 259 mutant differed from the wild-type receptor in only one amino acid residue. We conclude that, both in vitro and in vivo, neuronal death induced by p75NTR requires the DD and TM Cys259, supporting the physiological relevance of DD signaling by disulfide-linked dimers of p75NTR in the CNS.

Read the full paper HERE.

Open position: Laboratory technician - Histology

UPDATE 2016-05-25: The position has been filled. 

We are seeking a laboratory technician to help us with histological studies of our lines of mutant mice. The candidates should have documented expertise in histological techniques, including tissue sectioning, immunohistochemistry and microscopy. Experience in histological analysis of nervous tissue is preferred. This is a project employment for a period of up to 2 years.

Application, including CV and reference names of two latest project supervisors should be sent to Prof. Carlos Ibanez

Deadline for application is 29th April, 2016