Homozygous mutant mice die at birth from respiratory failure. At embryonic day 17.5 to 18.5 homozygous embryos appear smaller and do not display spontaneous movement or sensorimotor reflexes. Dilated vascular channels in subcutaneous tissues give the embryos an external blotchy appearance. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue from homozygous animals. Histological analysis of fetal diaphragm tissue reveals a dispersed pattern of innervation and fewer layers of muscle fibers. Thin, disarrayed intercostal and anterior chestwall muscles are also observed. Spontaneous miniature endplate potential (mEPP) activity is detected in the diaphragm phrenic nerve, but no evoked endplate potentials (EPP), evoked neurotransmitter release or muscle contraction is detected with stimulation of the neuromuscular junction (NMJ). Mutant NMJs exhibit larger endplate diameters and lower levels of acetylcholinesterase. Tetrodotoxin (TTX) resistant miniature excitatory postsynaptic currents (mEPSCs), but not evoked, action-potential dependent responses are detected from mutant central nervous system (CNS) synapses. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Thismutant mouse strain may be useful in studies of neuroexocytosis and neurotransmitter release in the developing nervous system.

Homozygous <i> Snap25</i> knock-out mice exhibit neonatal lethality. Late embryos lack spontaneous movement or sensorimotor reflexes, and abnormal innervation and muscle fiber development is observed.



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