There are mechanisms to avoid Vit.d3 toxicity. In it's most active form (1,25 dihydroxy d3) is a potent stimulator of intestinal calcium absorption and bone mineral reabsorption; the net effect of which is to increase serum calcium concentrations in conjunction with parathyroid hormone (PTH). However, to reach this active form d3 (formed by a UV photoreaction) must first undergo two enzymatic reactions in the liver and kidney resp. These processes are subject to feedback inhibition and thus are downregulated if too much 1,25 d3, calcium or phosphate is present in the serum. In addition, if these mechanisms are bypassed, there is an additional level of control to prevent toxicity. Namely, 1,25 d3 is converted to the vastly less active forms 24,25 d3 and 25,26 d3. If this fails, calcitonin can be released to sequester calcium back into the bone and cause increased renal excretion of calcium.
To induce toxicity, one must ingest truly stupendous quantities of d3 for a long period of time. The only case I've ever heard of was in a man who took between 200,000 and 2,000,000 IU per day for a period of two years before toxicity symptoms began to show (hypercalcemia and osteomalacia).
To put it in perspective, the recommended intake of d3 per day is 600IU. By spending 30 minutes out in the sun with exposed skin you generate 15,000IU of d3. If there were not a control mechanism highly sun exposed people would have brittle bones and arrhythmias from all the calcium in their blood.
d3 is fat soluble, which for all practical purposes means it has to be taken with a fatty meal to be absorbed properly (e.g. it requires bile secretion for solubilization and uptake in the intestine).
It's debatable whether d3 and calcium supplements are necessary in animals which consume mammals for a living and are for the most part nocturnally active. But, it couldn't hurt unless you were packing the entire mouse full of the stuff before feeding and probably not even then. The only tangible risk is calcium stones in the animal's renal system.