To the Editor: In the complex organization of neural cells of the retina, there are five different cell types. One of them is the horizontal cell, which is connected laterally with the synaptic bodies of the rods and cones, as well as with the dendrites of the bipolar cells.1 Most researchers claim that the outputs of the horizontal cells are always inhibitory and provide the "lateral inhibition" by sending feedback to cones negatively,2 which is important in all sensory systems and helps to ensure the transmission of sensory patterns with proper contrast. However, it seems that more studies are needed to clarify the exact role of horizontal cells.
On the other hand, chaos synchronization in physical and biological systems has been widely studied over the last few years. Chaos, which is a universal phenomenon in nonlinear dynamics, exists in a variety of neural systems ranging from the simple to the complex. Chaotic oscillations of individual neurons may be responsible for many regular regimes of operation. Researchers have developed many neuronal models to simulate chaos of real neurons and obtained many significant results. In addition, experimental evidence demonstrates that synchronous neuronal oscillations underlie many cortical processes. Ensembles of neurons can synchronize in order to accomplish critical functional goals, such as the biological information processing or the production of regular rhythmical activity.3,4 To achieve chaos synchronization of neuronal systems, many control methods, such as feedback control, have been developed.4
As a clue for synchronization in vertebrate retina, it can be emphasized that such a process has been seen in the inner plexiform layer of retina, where amacrine cells, bipolar cells, and ganglion cells have synapses, and it has been shown that amacrine cells play a synchronization role by giving feedback on ganglion cells for generating spontaneous activity in developing vertebrate retina.5
In the physiological view of human retina, such a synapse exists in outer plexiform layer between photoreceptors, horizontal cells, and bipolar cells. We hypothesize that horizontal cells’ functional role is synchronizing. This organizational role is obtained by hyperpolarization which generates a feedback signal to the phtotoreceptors.2
For instance, in a flash light stimulation of the retina, a simplified biphasic waveform response is recorded: an a-wave is the first large negative component, followed by the b-wave, which is the corneal positive and usually larger amplitude wave. Most studies state that a-wave originates from the photoreceptor layer and b-wave originates from the bipolar cells. We suggest that horizontal cells, by their long and bushy dendrites, may synchronize photoreceptors and give bipolar cells the burst of firing. It means that horizontal cells interact with the photoreceptors in the outer plexiform layer of the retina and create a possibility for bipolar cells to burst. More explicitly, if two, or a lattice, of chaotic photoreceptors are arranged together with no interactions (i.e., no horizontal cell in this example), the outcome of such a summative system is random with zero mean, which means that the output of one photoreceptor will be inhibited by the output of the other ones. In contrast, if we assume interconnections between photoreceptor cells by horizontal cells, synchronization will occur and a negative a-wave will be produced. This negative hyperpolarized a-wave will cause depolarization of bipolar cells.
By claiming such a hypothesis, it seems that horizontal cells play a key role in transferring data from outer plexiform to inner plexiform. In disease states, which result in decreasing a-wave amplitudes and increasing latency, malfunctioning of horizontal cells may be the cause of delay in the synchronization process.
In this context we demonstrated the role of horizontal cells as synchronizer based on chaos synchronization, which is an organizational role in complex systems and exists in a variety of neural systems ranging from the simple to the complex.6 We are able to explain some diseases which affect the full-field electroretinogram components more precisely.