RT Journal Article SR Electronic T1 Role for Reelin in Neurotransmitter Release JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 2352 OP 2360 DO 10.1523/JNEUROSCI.3984-10.2011 VO 31 IS 7 A1 Sabine Hellwig A1 Iris Hack A1 Janina Kowalski A1 Bianka Brunne A1 Joel Jarowyj A1 Andreas Unger A1 Hans H. Bock A1 Dirk Junghans A1 Michael Frotscher YR 2011 UL http://www.jneurosci.org/content/31/7/2352.abstract AB The extracellular matrix molecule Reelin is known to control neuronal migration during development. Recent evidence suggests that it also plays a role in the maturation of postsynaptic dendrites and spines as well as in synaptic plasticity. Here, we aimed to address the question whether Reelin plays a role in presynaptic structural organization and function. Quantitative electron microscopic analysis of the number of presynaptic boutons in the stratum radiatum of hippocampal region CA1 did not reveal differences between wild-type animals and Reelin-deficient reeler mutant mice. However, additional detailed analysis showed that the number of presynaptic vesicles was significantly increased in CA1 synapses of reeler mutants. To test the hypothesis that vesicle fusion is altered in reeler, we studied proteins known to control transmitter release. SNAP25, a protein of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, was found to be significantly reduced in reeler mutants, whereas other SNARE complex proteins remained unaltered. Addition of recombinant Reelin to organotypic slice cultures of reeler hippocampi substantially rescued not only SNAP25 protein expression levels but also the number of vesicles per bouton area indicating a role for Reelin in presynaptic functions. Next, we analyzed paired-pulse facilitation, a presynaptic mechanism associated with transmitter release, and observed a significant decrease at CA1 synapses of reeler mutants when compared with wild-type animals. Together, these novel findings suggest a role for Reelin in modulating presynaptic release mechanisms.