Skeletal muscle atrophy is a serious concern for the patients afflicted by limb restriction due to surgery (e.g. arthrodesis), several articular pathologies (e.g. arthralgia), or simply following cast immobilization. To study the molecular events involved in this immobilization-induced debilitating condition, a convenient mouse model for atrophy is lacking. Here we provide a new immobilization procedure exploiting the normal flexion of the mouse hindlimb using a surgical staple to fix the ventral part of the foot to the distal part of the calf. Histological analysis revealed that our approach induced significant skeletal muscle atrophy by reducing the myofibre size of the tibialis anterior (TA) muscle by 36%, compared to the untreated contralateral TA within a few days post-immobilization. Two molecular markers for atrophy, atrogin-1/MAFbx and MuRF-1 mRNAs were significantly up-regulated by 1.9 and 5.9 fold, respectively. Interestingly, our model also revealed the presence of an early inflammatory process during atrophy, characterized by the mRNA up-regulation of TNF, IL-1 and IL-6 (1.9, 2.4 and 3.4 fold, respectively) simultaneously with the up-regulation of the common leukocyte marker CD45 (6.1 fold). Moreover, muscle rapidly recovered upon remobilization, an event associated with significantly increased levels of UCP-3 and PGC-1 mRNA, key components of pro-oxidative muscle metabolism. This model offers unexpected new insights into the molecular events involved in immobilization atrophy.