SV2A/B Double Knockout Mouse

Introduction Synaptic vesicle protein 2 (SV2) is a membrane glycoprotein found only in the secretory vesicles of neural and endocrine cells. It appears to be unique to vertebrates, suggesting that it evolved as a part of complex signaling systems. In mammals, there are three SV2 genes denoted A, B, and C. The molecular mechanism by which these proteins regulate secretion is not clear. It has been proposed that the SV2s perform a redundant function, an argument supported by the apparent co-localization of SV2A and SV2B on synaptic vesicles, however, several findings suggest that the isoforms differ in their functions. SV2 enhances low-frequency neurotransmission by increasing the resting readily releasable pool (RRP) and thus release probability in quiescent neurons. Technology description Dr Sandra Bajjalieh’s laboratory has generated SV2A/B double knockout (KO) mice. SV2B KOs were bred with animals heterozygous for the SV2A gene disruption to produce SV2A+/-SV2B-/- breeders, which were used to generate SV2A/B KOs. All animals are 99.99% C57BL/6. Similar to SV2A KOs, SV2A/B KOs exhibit a severe seizure phenotype which supports the interpretation that SV2 can influence mechanisms of seizure generation or propagation. Hippocampal neurons cultured from mice lacking both SV2A and SV2B demonstrate altered activity-dependent synaptic depression. These examples of altered neurotransmission were all observed in the absence of changes in either synapse or synaptic vesicle density or morphology. This transgenic model is an essential tool to investigate how the loss of SV2 affects neural signaling in brain networks. Related Publication(s)
Proc Natl Acad Sci U S A 101(26): 9861-6, 2004. The Journal of Neuroscience 26(4): 1303-1313, 2006.

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