Flash applied 0.4 s before the electrical stimulation of VIIIth nerves significantly increased the amplitude of both synaptic components (p < 0.001; Figures 5C–5E). Thus, a preceding visual stimulus increases the S/N ratio of sound-evoked spiking

activity in the VIIIth nerve ( Figure 4) and the efficacy of synapses made by the VIIIth nerve on the M-cell ( Figure 5), leading to facilitated sound detection in the M-cell. GSK1349572 datasheet In teleosts, exogenous DA elevates the firing threshold of VIIIth nerves (Curti and Pereda, 2010), and the activation of D1Rs increases the efficacy of VIIIth nerve-Mauthner cell synapses (Pereda et al., 1992, 1994). We therefore examined the role of the DA receptor in the visual enhancement of audiomotor functions, including sound-evoked M-cell response and C-start behavior. Using focal application of pharmacological agents in the vicinity of M-cell lateral dendrites (Figure 6A), which are innervated by VIIIth nerves (Eaton et al., 1977; Korn and Faber, 2005), we found that the total integrated charge of a-CSCs in M-cells was reduced by the D1R antagonist SCH-23390 (p < 0.001), and increased by the DA receptor Fasudil supplier agonist apomorphine (p < 0.05). Importantly, the preceding

flash-induced enhancement of a-CSCs in M-cells was largely impaired by SCH-23390 application (Figure 6B), and was totally occluded by apomorphine application (Figure 6C). These findings indicate that D1R activation is required for the visual modulation of auditory responses in Mauthner cells. We then examined whether D1Rs mediate flash-induced increases in both the S/N ratio of VIIIth nerves and the efficacy of VIIIth nerve-Mauthner cell synapses. SCH-23390 application prevented flash-induced

increase in the S/N ratio of out VIIIth nerves (Figure 6D), whereas apomorphine application mimicked the flash-induced effects as it significantly suppressed the spontaneous spiking activity of VIIIth nerves (p < 0.01; Figure S3A1) and increased the S/N ratio (p < 0.01; Figure S3A2). Furthermore, local application of the persistent sodium channel blocker riluzole largely suppressed the spontaneous spiking activity of VIIIth nerves (p < 0.05; Figure S3B1) and prevented SCH-23390-induced increase in the spontaneous spiking activity of VIIIth nerves (Figure S3B2). These results suggest that D1R activation mediates visual modulation of the S/N ratio of VIIIth nerves possibly through suppressing persistent sodium channels (see also Curti and Pereda, 2010).