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Behavioral and immune changes in v-Ha-ras transgenic mice
L L Colombo1, A Stazzone, G J Chen
1Arizona Prevention Center, College of Medicine, University of Arizona, Tucson 85724, USA.
Immunopharmacology and Immunotoxicology
|August 22, 2000
Summary
Transgenic mice with an activated v-Ha-ras oncogene showed decreased activity and altered immune markers. Increased Interleukin-1 alpha (IL-1α) levels were linked to reduced open field behavior, suggesting a role in oncogene-induced changes.
Area of Science:
- Oncology
- Immunology
- Neuroscience
Background:
- Transgenic mice (Oncomice) expressing an activated v-Ha-ras oncogene develop mammary tumors.
- The study investigated potential links between oncogene expression, behavioral changes, and immune system alterations.
Purpose of the Study:
- To assess if v-Ha-ras oncogene expression impacts mouse behavior.
- To explore associations between behavioral changes and immune system markers, specifically Interleukin-2 (IL-2) and Interleukin-1 alpha (IL-1α).
Main Methods:
- Behavioral activity was measured using an open field test, recording line crossings and rears.
- Immune markers were quantified in spleen and thymus cell supernatants and serum.
- Mice were subjected to dietary changes (Lieber-DeCarli diet) and pharmacological treatment (cocaine).
Main Results:
- Oncomice exhibited significantly lower activity levels in the open field test compared to control FVB mice.
- Lieber-DeCarli diet reduced activity in both Oncomice and FVB mice.
- Cocaine treatment increased line crossings in both mouse strains.
- Oncomice showed elevated levels of IL-2 in spleen and thymus supernatants and higher IL-1α in serum.
- A negative correlation was observed between IL-1α levels and open field activity.
Conclusions:
- Increased IL-1α levels are directly associated with reduced open field activity in Oncomice.
- Elevated IL-1α may play a crucial role in mediating oncogene-induced immune and behavioral modifications.
- IL-1α could be a necessary factor facilitating the transforming activity of oncogenes.