Hearing loss is the most prevalent sensory disorder effecting humanity and dysfunction in the medial olivocochlear (MOC) system is thought to be involved. The MOC regulates and protects auditory sensitivity by modifying the activity of the outer hair cells in the cochlea. The majority of MOC neurons in mice are present in the ventral nucleus of the trapezoid body (VNTB) in the brainstem. The C57BL/6 (C57) inbred strain of mouse has early-onset hearing loss, preceded by a failure in the efficacy of its MOC system ( Zhu et al., 2007). We examined the neurons of the VNTB in the C57 and compared them with those of a strain which retains auditory sensitivity into old age: the CBA/Ca (CBA). We aimed to determine if differences in excitability in VNTB neurons exist between the strains which could influence MOC function. Mice were decapitated in accordance with the UK Animals (Scientific Procedures) Act 1986 and brainstem slices prepared (Barnes-Davies & Forsythe, 1995). Whole cell recordings were taken from visually identified VNTB cells in pre-hearing onset (P8) and post hearing onset (P16) CBA and C57 mice (Fujino et al., 1997). Prehearing onset, CBA and C57 VNTB cells have similar in current-voltage relationships and action potential (AP) thresholds. Under voltage clamp, cells of both strains display outward currents around -30mV which inactivate rapidly. During a 200ms pulse to -30mV, currents in both strains drop from around 2nA (CBA: 1.77±0.35nA (n=10), C57: 2.36±0.36nA (n=12) to 0.6nA (CBA: 0.75±0.09nA, C57: 0.52±0.08nA). Current clamp recordings indicate that AP thresholds are around -38mV for both strains (CBA:-38.4±2.5mV (n=7), C57:-38.2±1.7mV (n=7). Both strains produce few APs during 200ms current injection of +50pA (CBA: 0.6±0.4, C57: 1.0±1.2). Post-hearing onset, the CBA VNTB neurons develop greater sustained currents at hyperpolarised potentials than in the C57. During a 200ms pulse to -30mV, currents of CBA VNTB cells demonstrate little inactivation (1.73±0.36nA to1.57±0.45nA over 200ms (n=8)). C57 VNTB neurons retain inactivation of low voltage activated currents similar to those present in P8 mice (1.91±0.31nA dropping to 0.49±0.61nA after 200ms(n=7)). Post-hearing onset CBA VNTB neurons also demonstrate greater excitability under current clamp conditions, generating more APs than age matched C57 (CBA: 6.2±1.4 (n=6), C57: 1.5±0.75 (n=4), (P =0.02)) despite having similar thresholds (CBA: -43.6±2.2, C57: 39.5±3.1). These experiments indicate lower excitability of neurons of the VNTB in the C57: a strain of mouse with MOC functional deficits. Decreased activity of MOC neurons in the VNTB would impede efferent control of the sensitivity of the ear and could contribute to the C57 strain’s vulnerability to hearing loss. Data ± SEM. Means compared using unpaired t-tests. P : post natal day.