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Acetylcholine (ACh) has been recognized for a long time as a major neurotransmitter in the retina, however, little is known about the contribution of acetylcholine receptors in synaptic processing. Moreover, even less information is available concerning their role during development. To address this question further, we examined the physiological and pharmacological properties of neuronal nicotinic acetylcholine receptors (nAChRs) in retinal ganglion cells from embryonic (E) 12-18-day-old Leghorn chicks. Patch-clamp recordings in whole-cell configuration revealed that at E12 approximately 21% of the ganglion cells responded to acetylcholine pulses with inward currents. The number of responsive cells progressively increased to 57% at E15 to reach up to 15 positive cells out of 15 cells tested at E18. Acetylcholine-evoked responses could be subdivided, according to their time course, into fast and slowly desensitizing. Taking advantage of the selectivity of the frog toxin epibatidine (Epi), that preferentially activates heteromeric neuronal nicotinic acetylcholine receptors, we compared the currents evoked by this toxin vs. the effects of acetylcholine. A further characterization of the receptor diversity during development was to assess their sensitivity to the alpha-conotoxin MII (alpha-CTX-MII), which has been shown to preferentially block alpha6- and alpha3beta2-containing receptors. These data demonstrate that ganglion cells of the chick retina express multiple receptor subtypes that progressively develop as a function of retina maturation.

Motion blindness (MB) is defined as the selective disturbance of visual motion perception despite intact perception of other features of the visual scene. MB is characterized by a pandirectional deficit of motion direction discrimination and is assumed to result from damage to the visual motion pathway, especially area MT/V5. However, the most characteristic feature of primate MT/V5 neurons is not their motion selectivity but their preference for one direction of motion (direction selectivity), which changes incrementally at neighbouring columns. In addition to this microscopic directional organization, studies in nonhuman and human primates suggest that single directions of motion are also coded at a more macroscopic level. We thus hypothesized that if MB in humans results from damage to direction-selective neurons in the visual motion pathway, posterior brain damage might cause MB which is direction selective, not pandirectional. The present study investigated motion direction discrimination in patients with posterior unilateral brain damage and determined separate psychophysical thresholds for the four cardinal directions. In addition, we analysed whether the direction of erroneous motion perception (i.e. the perception of right motion for upward motion) was random or showed a directional bias. We report three principal findings. First, motion direction discrimination was severely impaired in one or two directions while it was normal in the other directions. This constituted direction-selective MB. Second, MB was characterized not only by a quantitative direction-selective increase in psychophysical thresholds but also by a qualitative impairment of perceiving motion direction systematically in wrong directions. Both findings suggest that the cortical modules specialized for the perception of a single direction of motion might be larger than previously thought. Third, lesion analysis showed that unilateral damage, not only the human homologue of MT/V5 but also to parieto-occipital cortex, leads to MB.

Motion blindness (MB) or akinetopsia is the selective disturbance of visual motion perception while other features of the visual scene such as colour and shape are normally perceived. Chronic and transient forms of MB are characterized by a global deficit of direction discrimination (pandirectional), which is generally assumed to result from damage to, or interference with, the motion complex MT+/V5. However, the most characteristic feature of primate MT-neurons is not their motion specificity, but their preference for one direction of motion (direction specificity). Here, we report that focal electrical stimulation in the human posterior temporal lobe selectively impaired the perception of motion in one direction while the perception of motion in other directions was completely normal (unidirectional MB). In addition, the direction of MB was found to depend on the brain area stimulated. It is argued that direction specificity for visual motion is not only represented at the single neuron level, but also in much larger cortical units.