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DTSTART:20151025T020000
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DTSTAMP:20260430T145243Z
UID:5548861af1858251382440@ist.ac.at
DTSTART:20151005T124500
DTEND:20151005T140000
DESCRIPTION:Speaker: Yves Barde\nAbstract: Neurotrophins are small dimeric 
 proteins encoded by 4 genes in mouse and human. They signal either through
  ligand-specific tyrosine kinase receptors or the pan-neurotrophin recepto
 r p75\, a member of the tumour necrosis receptor family. As no closely rel
 ated genes have been identified in short lived species typically used by g
 eneticists\, progress has been quite slow in elucidating neurotrophin sign
 alling. Indeed\, it is only recently that 2 of the long known neurotrophin
  tyrosine kinase receptors\, TrkA and TrkC\, were discovered to kill neuro
 ns in the absence of their respective ligands NGF and NT3. These results e
 xplain at long last the NGF dependency for survival of TrkA-expressing neu
 rons. In addition\, it is becoming clear that BDNF\, by far the most wides
 pread neurotrophin in the brain\, is not a significant survival factor in 
 the CNS in the absence of lesion\, in line with the finding that its recep
 tor TrkB does not kill neurons in the absence of BDNF. This neurotrophin i
 s localized pre- and not post-synaptically and is stored in large dense co
 re vesicles of excitatory neurons as revealed by light and electron micros
 copy. These results are in line with numerous studies indicating a “feed 
 forward” mechanism that is readily apparent in the striatum\, with the co
 rtical afferents delivering BDNF onto medium-sized spiny neurons. This mec
 hanism is of special relevance to diseases such as Huntington’s and it ap
 pears that GABA-ergic neurons need BDNF to reach\, possibly also to keep t
 heir normal size including the extent of dendritic arborisation and spine 
 numbers. In mice lacking Mecp2\, the gene associated with most cases of Re
 tt Syndrome\, the levels of BDNF are markedly reduced in some brain areas\
 , including the cerebral cortex and the size of their striatum is signific
 antly decreased. In an attempt to increase BDNF levels with substances dif
 fusing into the CNS\, we found that fingolimod\, a drug used for the treat
 ment of multiple sclerosis\, restored the size of the striatum to a volume
  close to normal. It also markedly improved the loco-motor activity of ani
 mals lacking MeCP2. Fingolimod turned out to increase BDNF levels in areas
  such as the cerebral cortex and the striatum but not in others such as th
 e cerebellum. These results formed the basis for an exploratory clinical t
 rial with Rett syndrome patients.
LOCATION:Raiffeisen Lecture Hall\, Central Building\, ISTA
ORGANIZER:aeller@ist.ac.at
SUMMARY:Yves Barde: The Institute Colloquium: Neurotrophins in development 
 and disease
URL:https://talks-calendar.ista.ac.at/events/549
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