Abstract

The Mauthner cells are pair of identifiable hindbrain neurons that participate in the escape response of fishes. Membrane excitability in these cells is regulated by inhibitory neurons that use glycine as a transmitter. We examined the possibility that the inhibitory transmitter gamma-amino butyric acid (GABA) may also act on the Mauthner cells. We used immunocytochemical methods involving an antibody against glutamic acid decarboxylase (GAD), the synthesizing enzyme for GABA. Our study revealed dense GAD immunoreactive terminals surrounding the Mauthner cells. Puncta counts showed that the distribution of GAD immunoreactivity was densest at the distal lateral dendrite of the Mauthner cells; the distribution of puncta tapers gradually in regions closer to the soma. The axon cap was devoid of GABAergic immunoreactivity. We also performed unilateral lesions of the octaval nuclei to evaluate the origin of the GAD immunoreactive terminals. Following the lesions, we found marked decreases in GAD immunoreactive terminals on the proximal lateral dendrite, soma, and proximal ventral dendrite of both Mauthner cells. These results suggest that the octaval region contributes to bilateral inhibition of the Mauthner cells. The distal lateral dendrite of the ipsilateral Mauthner cell also showed a reduction in GAD immunoreactive terminals. This suggests that GABA mediates remote dendritic inhibition of this cell. GAD immunoreactive puncta also surrounded other large reticulospinal neurons, some of which are serially reiterated along the anterior-posterior axis of the hindbrain. Thus, GABA may also exert an influence not only on the Mauthner cells, but also on other reticulospinal neurons.

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