AHCODA-DB

Experiment name: Tomosyn-2 is required for normal motor performance in mice and sustains neurotransmission at motor endplates. (Geerts 2014)
LSID: http://syli.cz/urn:lsid:public.sylics.com:experiment:24AD-G26D-G6BE

TreatmentAmountAdministration routeAdministration time


Treatment info:
Order of behavioural testing
PhenoTyper Spontaneous Behaviour
PhenoTyper Appetitive Conditioning
PhenoTyper Avoidance Learning

Body Weight
Grip Strength
Vision Test
Nesting
Novel Home Cage Induced Hypophagia
Elevated Plus Maze
Open Field
Novel Object Recognition
T-Maze
Dark/Light Box
Rotorod
Barnes Maze
Fear Conditioning
Acoustic Startle Response and Prepulse Inhibition


Published in Brain Structure and Function 2014:
http://link.springer.com/article/10.1007%2Fs00429-014-0766-0

Tomosyn-2 is required for normal motor performance in mice and sustains neurotransmission at motor endplates
Cornelia J. Geerts1†, Jaap J. Plomp2†, Bastijn Koopmans3, Maarten Loos3, Lizette van der Pijl2, Martin A. van der Valk4, Matthijs Verhage1,5 and Alexander J.A. Groffen1,5
1 Department of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, The Netherlands
2 Department of Molecular Cell Biology, Group Neurophysiology, Research Building, Leiden University Medical Centre, Leiden, The Netherlands
3 Sylics (Synaptologics BV), Amsterdam, The Netherlands
4 Department Experimental Animal Pathology, Antoni van Leeuwenhoek / Netherlands Cancer Institute, Amsterdam, The Netherlands
5 Department of Clinical Genetics, VU Medical Center, Amsterdam, Netherlands
† These authors contributed equally to this work

Abstract
Tomosyn-1 (STXBP5) is a soluble NSF attachment protein receptor complex-binding protein that inhibits vesicle fusion, but the role of tomosyn-2 (STXBP5L) in the mammalian nervous system is still unclear. Here we generated tomosyn-2 null (Tom2KO/KO) mice, which showed impaired motor performance. This was accompanied by synaptic changes at the neuromuscular junction, including enhanced spontaneous acetylcholine release frequency and faster depression of muscle motor endplate potentials during repetitive stimulation. The postsynaptic geometric arrangement and function of acetylcholine receptors were normal. We conclude that tomosyn-2 supports motor performance by regulation of transmitter release willingness to sustain synaptic strength during high-frequency transmission, which makes this gene a candidate for involvement in neuromuscular disorders.


Mouse info:
Mouse ID Strain Coat color Genotype Ear tag Internal ID Sex Date of Birth Sub experiment 1 Sub experiment 2 Sub experiment 3
PH07118 Tom2(null) black hom - 6398 male 20-03-2013
PH07119 Tom2(null) black hom R 6399 male 20-03-2013
PH07120 Tom2(null) black WT L 6400 male 20-03-2013
PH07121 Tom2(null) black hom RL 6401 male 20-03-2013
PH07122 Tom2(null) black WT RR 6402 male 20-03-2013
PH07123 Tom2(null) black WT LL 6403 male 20-03-2013
PH07124 Tom2(null) black hom - 7093 male 05-04-2013
PH07125 Tom2(null) black hom R 7094 male 05-04-2013
PH07126 Tom2(null) black hom L 7095 male 05-04-2013
PH07127 Tom2(null) black WT RL 7096 male 05-04-2013
PH07128 Tom2(null) black WT RR 7097 male 05-04-2013
PH07129 Tom2(null) black WT LL 7098 male 05-04-2013
PH07130 Tom2(null) black hom - 7494 male 11-04-2013
PH07131 Tom2(null) black WT R 7495 male 11-04-2013
PH07132 Tom2(null) black WT L 7496 male 11-04-2013
PH07133 Tom2(null) black WT RL 7497 male 11-04-2013
PH07134 Tom2(null) black hom RR 7498 male 11-04-2013
PH07135 Tom2(null) black hom LL 7499 male 11-04-2013