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Coloboma hyperactive mutant exhibits delayed neurobehavioral developmental milestones
C J Heyser1, M C Wilson, L H Gold
1Department of Neuropharmacology, Scripps Research Institute, La Jolla, CA 92037, USA.
Brain Research. Developmental Brain Research
|November 21, 1995
Summary
The coloboma mutation in mice causes developmental delays and behavioral changes, including hyperactivity and head bobbing. Early identification of these synaptic vesicle protein gene alterations can reveal developmental impacts.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- The coloboma mutation (Cm) is a gene deletion on mouse chromosome 2, affecting the synaptosomal-associated protein of 25 kDa (SNAP-25) gene.
- This semi-dominant mutation leads to hyperactivity, head bobbing, and eye abnormalities in heterozygotes.
Purpose of the Study:
- To investigate the onset and progression of the coloboma behavioral phenotype during postnatal development.
- To correlate changes in SNAP-25 isoform expression with neurobehavioral milestones.
Main Methods:
- Examination of neurobehavioral developmental milestones in coloboma mutant mice during the first postnatal week.
- Assessment of motor skills, body weight, and sensory responses.
Main Results:
- Coloboma mutants exhibited delayed attainment of motor skills like righting reflex and bar holding.
- Early signs included body weight differences (day 7), hyperreactivity to touch (day 11), and head bobbing (day 14).
Conclusions:
- The coloboma mutation disrupts the normal timeline of developmental milestone acquisition in mice.
- These findings support the link between altered SNAP gene expression and functional behavioral consequences during development.