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The recessive mutant mice bate palmas (bapa) ‐ claps in Portuguese arose from N‐ethyl‐N‐nitrosourea mutagenesis. A single nucleotide, T > C, change in exon 13, leading to a Thr1289Ala substitution, was identified in the lysine (K)‐specific methyltransferase 2D gene (Kmt2d) located on chromosome 15. Mutations with a loss‐of‐function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS). Phenotypic characterization of the bapa mutant was performed using a behavioral test battery to evaluate the parameters related to general activity, the sensory nervous system, the psychomotor system, and the autonomous nervous system, as well as to measure motor function and spatial memory. Relative to BALB/cJ mice, the bapa mutant showed sensory and psychomotor impairments, such as hypotonia denoted by a surface righting reflex impairment and hindquarter fall, and a reduction in the auricular reflex, suggesting hearing impairment. Additionally, the enhanced general activity showed by the increased rearing and grooming frequency, distance traveled and average speed possibly presupposes the presence of hyperactivity of bapa mice compared with the control group. A slight motor coordination dysfunction was showed in bapa mice, which had a longer crossing time on the balance beam compared with BALB/cJ controls. Male bapa mice also showed spatial gait pattern changes, such as a shorter stride length and shorter step length. In conclusion, the bapa mouse may be a valuable animal model to study the mechanisms involved in psychomotor and behavior impairments, such as hypotonia, fine motor coordination and hyperactivity linked to the Kmt2d mutation.

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After analgesic administration, we evaluated general activity in the Open-Field and anxiety-like behavior in the Elevated Plus Maze of vasectomized mice. We divided C57BL/6J male mice into eight groups: saline, three non-operated control groups treated with 10 mg/kg meloxicam, 20 mg/kg tramadol, or both intraperitoneally, and four vasectomized mice groups treated with the same analgesic protocol as the control groups. One group of vasectomized mice received both treatments and an additional 10 mg/kg lidocaine at the incision site. We conducted the vasectomy via scrotal approach under isoflurane inhalation anesthesia and performed behavioral tests after full anesthesia recovery. Mice treated with meloxicam demonstrated low ambulation, spontaneous activity, and rearing frequency. Mice treated with tramadol showed spontaneous behavior compared with the saline control. Due to behavior changes demonstrated by meloxicam controls, we were unable to identify whether meloxicam provided adequate analgesia. Vasectomized mice treated with tramadol showed general activity behavior similar to their control but displayed significantly less rearing, suggesting that they were under potential signs of pain or discomfort. In conclusion, the Open Field test and the Elevated Plus Maze can usefully pre-evaluate analgesic protocols to identify possible interference caused by adverse drug effects. For future directions, an appropriate regimen of meloxicam and tramadol for enhancing mice welfare post vasectomy should be better investigated.