Recently, the T-type calcium current was shown to be part of the machinery of mechanotransduction of low threshold sensory neurons, the Down hair neurons (Shin et al. 2003). Identification of D-hair neurons, in vitro, led us to analyse the molecular mechanisms involving T-type I_Ca in mechanotransduction (Dubreuil et al. 2004). Biophysical properties of T-type I_Ca supported the hypothesis that it could confer excitability to peripheral GABAergic receptors. Intracellular Ca²⁺ measurements were performed on dissociated D-hair neurons, loaded with Fura 2, and identified by their rosette-like growth after treatment with NT-4. The emission fluorescence from the soma was acquired with a PM tube and the resulting (340/380nm) emission ratio was converted into [Ca²⁺]. In D-hair cells isolated from adult mice, GABA (100µM) induced a 47 ± 15% increase in [Ca²⁺]_i relative to basal values (n=4), while it was unable to modify [Ca²⁺]_i in non D-hair neurons. SR-95531 (20µM) blocked GABA-induced [Ca²⁺]_i increase, suggesting that the receptor involved in the GABA stimulation was the GABA_A receptor. Muscimol (20µM), a specific GABA_A receptor agonist, also produced a 47 ± 5% increase in [Ca²⁺]_i (n=8). When the second peak of the response to muscimol was expressed as a percentage of the first muscimol-induced [Ca²⁺]_i increase, nickel (50µM) and mibefradil (10µM), two known blockers of T-type calcium channels, inhibited this response by 89 ± 2% (n=8) and 92.5 ± 4% (n=3), respectively. TTX (100nM-500nM) inhibited muscimol-induced [Ca²⁺]_i increase by 49 ± 7% (n= 9). Using a video-imaging system, nickel-sensitive muscimol-induced increase in [Ca²⁺]_i was also found to be in neurites, suggesting a functional co-localisation of the GABA_A receptors and the T-Type [Ca²⁺]channels in this subcellular compartment.