LEUVEN RESEARCH INSTITUTE FOR NEUROSCIENCE & DISEASE
DETLEF BALSCHUN, PROF. DR. RER.NAT. HABIL
Contact address:
Laboratory of Biological Psychology, KU Leuven
Tiensestraat 102
3000 Leuven
Tel: +32 16 325 816
Fax: +32 16 326 099
E-mail: detlef.balschun@ppw.kuleuven.be
Web:
http://ppw.kuleuven.be/home/english/research/lbp/lbpMembers/00049654
EDUCATION AND PROFESSIONAL TRAINING
1979
1984
2002
Master (Diploma), Martin-Luther-University Halle-Wittenberg, Germany
PhD, Martin-Luther-University Halle-Wittenberg, Germany
DSc (Habilitation), Otto-von-Guericke-University Magdeburg, Germany
RESEARCH TOPICS
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Synaptic plasticity (Long-term potentiation, Long-term depression)
Cellular and molecular mechanisms of learning and memory
Aging and Neurodegeneration
RESEARCH AREAS
Our research group is interested in the molecular and cellular mechanisms that underlie
learning & memory and their deterioration during neurodegenerative diseases (e.g. Alzheimer’s
disease (AD)). To approach these topics, we take advantage of cellular models of synaptic plasticity
such as long-term potentiation (LTP), a long-lasting increase of synaptic transmission that is observed
after high-frequency stimulation of afferent inputs. LTP was first described by Bliss and Lomo in 1973
and developed thereafter into the most extensively investigated cellular correlate of learning. We
also established robust protocols to achieve long-term depression (LTD), a lasting depression of
synaptic transmission, which represents the physiological counterpart of LTP.
Since the two major groups of AD symptoms, cognitive decline and psychiatric symptoms
converge on synaptic processes, it is tempting to use readouts of synaptic function as early markers
for the onset of AD pathology. Over the past decade, long-term potentiation (LTP) has developed into
a prime tool for this purpose, because it has been proven being a sensitive indicator of early AD
onset and its mechanisms are well explored which facilitates causal conclusions. While LTP has been
extensively studied in animals models of AD, LTD, the physiological counterpart of LTP, was largely
neglected even though recent evidence indicates that LTD is crucial for some types of hippocampusdependent learning. Therefore, LTD is likely to be affected by the progression of neurodegenerative
diseases, both in human subjects and in mouse models of these diseases.
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LEUVEN RESEARCH INSTITUTE FOR NEUROSCIENCE & DISEASE
In addition to the hippocampus, which has a pivotal role in declarative and configural types of
learning, we are interested in the prefrontal cortex (PFC), a brain region that participates in several
higher order processes such as working memory, novelty detection (familiarity discrimination),
decision making, associative types of memory and their extinction. Most of our work is done on brain
slices (extracellular, patch-clamp and multielectrode array recordings), but we introduced recently
also in-vivo recording techniques with conventional and multi-array electrodes to strengthen the
links to behaviour.
SELECTED PUBLICATIONS
1. Trovo L, Ahmed T, Callaerts-Vegh Z, Buzzi A, Bagni C, Chuah M, Vandendriessche T, D'Hooge R,
Balschun D, Dotti CG (2013) Low hippocampal PI(4,5)P(2) contributes to reduced cognition in
old mice as a result of loss of MARCKS. Nat Neurosci 16:449-55.
2. Van der Jeugd A, Ahmed T, Burnouf S, Belarbi K, Hamdame M, Grosjean ME, Humez S, Balschun
D, Blum D, Buee L, D'Hooge R (2011) Hippocampal tauopathy in tau transgenic mice coincides
with impaired hippocampus-dependent learning and memory, and attenuated late-phase longterm depression of synaptic transmission. Neurobiol Learn Mem 95:296-304.
3. Schmeisser,M.J., Ey,E., Wegener,S., Bockmann,J., Stempel,A.V., Kuebler,A., Janssen,A.L.,
Udvardi,P.T., Shiban,E., Spilker,C., Balschun,D., Skryabin,B.V., Dieck,S., Smalla,K.H., Montag,D.,
Leblond,C.S., Faure,P., Torquet,N., Le Sourd,A.M., Toro,R., Grabrucker,A.M., Shoichet,S.A.,
Schmitz,D., Kreutz,M.R., Bourgeron,T., Gundelfinger,E.D., & Boeckers,T.M. et al. (2012)
Autistic-like behaviours and hyperactivity in mice lacking ProSAP1/Shank2. Nature 486:256260.
4. Van der Jeugd A, Hochgrafe K, Ahmed T, Decker JM, Sydow A, Hofmann A, Wu D, Messing L,
Balschun D, D'Hooge R, Mandelkow EM (2012) Cognitive defects are reversible in inducible
mice expressing pro-aggregant full-length human Tau. Acta Neuropathol 123:787-805.
5. Koch,D., Spiwoks-Becker,I., Sabanov,V., Sinning,A., Dugladze,T., Stellmacher,A., Ahuja,R.,
Grimm,J., Schuler,S., Muller,A., Angenstein,F., Ahmed,T., Diesler,A., Moser,M., tom,D.S.,
Spessert,R., Boeckers,T.M., Fassler,R., Hubner,C.A., Balschun,D., Gloveli,T., Kessels,M.M., &
Qualmann,B. et al. (2011) Proper synaptic vesicle formation and neuronal network activity
critically rely on syndapin I. EMBO J 30:4955-4969.
6. Balschun D, Moechars D, Callaerts-Vegh Z, Vermaercke B, Van Acker N, Andries L, D'Hooge R
(2010) Vesicular glutamate transporter VGLUT1 has a role in hippocampal long-term
potentiation and spatial reversal learning. Cereb Cortex 20:684-693.
7. Denayer E, Ahmed T, Brems H, Van Woerden G, Borgesius NZ, Callaerts-Vegh Z, Yoshimura A,
Hartmann D, Elgersma Y, D'Hooge R, Legius E, Balschun D (2008) Spred1 is required for synaptic
plasticity and hippocampus-dependent learning. J Neurosci 28:14443-14449.
8. Huang KP, Huang FL, Jager T, Li J, Reymann KG, Balschun D (2004) Neurogranin/RC3 enhances
long-term potentiation and learning by promoting calcium-mediated signaling. J Neurosci
24:10660-10669.
9. Balschun D, Wolfer DP, Gass P, Mantamadiotis T, Welzl H, Schutz G, Frey JU, Lipp HP (2003)
Does cAMP response element-binding protein have a pivotal role in hippocampal synaptic
plasticity and hippocampus-dependent memory? J Neurosci 23:6304-6314.
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