Research Report Localization of GABA (g-aminobutyric acid) markers in the turtle’s basal optic nucleus John Martin a,b , Michael Ariel c, * a Center for Anatomical Science and Education, Saint Louis University School of Medicine, St. Louis, MO 63104, USA b Department of Surgery, Saint Louis University School of Medicine, St. Louis, MO 63104, USA c Department of Pharmacological and Physiological Science, Saint Louis University, 1402 S. Grand Blvd., St. Louis, MO 63104, USA Accepted 15 October 2005 Available online 9 November 2005 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, Journal of Neurophysiology 86 (2001) 2919 – 2930. [6], N. Kogo, T.X. Fan, M. Ariel, Synaptic pharmacology in the turtle accessory optic system, Experimental Brain Research 147 (2002) 464 – 472. [23]]. In the present study, the inhibitory neurotransmitter g-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. D 2005 Elsevier B.V. All rights reserved. Theme: Sensory systems Topic: Subcortical visual pathways Keywords: Accessory optic system; GAD; Ultrastructure; Synapse; Retinal slip; Brainstem; Direction-sensitive 1. Introduction The turtle’s accessory optic system (the basal optic nucleus, BON) is a collection of neurons in the ventrolateral mesencephalon. It has been shown that neurons in the BON receive excitatory inputs from direction-sensitive retinal ganglion cells distributed across the entire contralateral retina [23,43]. The convergence of these inputs onto BON neurons forms an average, full-field motion signal, called retinal slip, which is relayed to vestibular and oculomotor pathways for the control of eye and head movements that compensate for movements of the visual field. Neurons in the BON also receive non-retinal inputs [24]. Retinal application of lidocaine increased the frequency of spontaneous BON inhibitory events, suggesting that a tonic retinal output normally blocks inhibitory pathways to the BON from within the brainstem. One possible source of this inhibition 0006-8993/$ - see front matter D 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.brainres.2005.10.040 * Corresponding author. Fax: +1 314 977 5127. E-mail address: ARIELM@SLU.EDU (M. Ariel). Brain Research 1066 (2005) 109 – 119 www.elsevier.com/locate/brainres