Abstract
Recent physiological data have demonstrated that retinal slip, the sensory code of global visual pattern motion, results from complex interactions of excitatory and inhibitory visual inputs to neurons in the turtle's accessory optic system (the basal optic nucleus, BON) [M. Ariel, N. Kogo, Direction tuning of inhibitory inputs to the turtle accessory optic system, J. Neurophysiol. 86 (2001) 2919–2930. [6], N. Kogo, T.X. Fan, M. Ariel, Synaptic pharmacology in the turtle accessory optic system, Exp. Brain Res. 147 (2002) 464–472. [23]]. In the present study, the inhibitory neurotransmitter γ-aminobutyric acid (GABA), its synthetic enzyme, glutamic acid decarboxylase (GAD-67) and its receptor subtypes GABA A and GABA B receptors were localized within the BON. GABA antibodies revealed cell bodies and processes, whereas antibodies against GAD revealed a moderate density of immunoreactive puncta throughout the BON. GAD in situ hybridization labeled BON cell bodies, indicating a possible source of inhibition intrinsic to the nucleus. Ultrastructural analysis revealed terminals positive for GAD that exhibit symmetric synaptic specializations, mainly at neuronal processes having small diameters. Neurons exhibiting immunoreactivity for GABA A receptors were diffusely labeled throughout the BON, with neuronal processes exhibiting more labeling than cell bodies. In contrast, GABA B-receptor-immunoreactive neurons exhibited strong labeling at the cell body and proximal neuronal processes. Both these receptor subtypes are functional, as evidenced by changes of visual responses of BON neurons during application to the brainstem of selective receptor agonists and antagonists. Therefore, GABA may be synthesized by BON neurons, released by terminals within its neuropil and stimulate both receptor subtypes, supporting its role in mediating visually evoked inhibition contributing to modulation of the retinal slip signals in the turtle accessory optic system.
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