## 1 Introduction
In brief, the specific stage II development of waves induced by SACs and mediated by the neurotransmitter acetylcholine is made of a transitory network of autonomous busters that improve the opportunistic local synchrony via \begin{table}
\begin{tabular}{c c c c} \hline \hline
**Synaptic Transmission** & **Main Action** & **Mediated By** & **Effect** \\ \hline \multirow{2}{*}{Gap junctions} & Activity-dependent & Electrical synapse coding & Dynamic interactions \\  & regulation and plasticity & ON–OFF directionally & between electrical and \\  & & selective ganglion cells & chemical synapses \\ \hline \multirow{4}{*}{Acetylcholine} & To held under a current & Transient network & \\  & clamp (I\({}_{\text{h}}\) = 0) when a & neuron with an E\({}_{\text{Cl}}\) (–70 \\  & voltage is pulsed from & mV) manipulation, and & \\  & \(-\)70 mV to 15 mV. & A\({}_{2}\)AR up-regulate SACs’ & \\  & & presynaptic waves. & \\ \hline \multirow{2}{*}{ Glutamate} & Ultra-fast response of & \multirow{2}{*}{P8 and P22 retinas} & \multirow{2}{*}{Restores bursting activity} \\  & photoreceptors synapse & & \\ \hline \hline \end{tabular}  
* I\({}_{\text{h}}\): holding cation current, E\({}_{\text{Cl}}\): membrane potential, A\({}_{2}\)AR: adenosine A(2A) receptor, SACs: starburst amacrine cells, P8/P22: postnatal days.  
\end{table} 
Table 1: Impact of the junctions and synaptic transmission on retinal networking. cholinergic coupling, which can improve wave propagation, depending on the conditions. However, it must be noted that some of these parameters can be pharmacologically controlled [25]. In stage III, the later waves appear to be spatially bound and more localized than stage II waves. These localized activity patterns could potentially have a link to how receptive fields are formed before vision becomes functional [24; 26]. The light adaptation phenomenon allows the cone response to dominate over rod responses at high illumination. Then, dark-adaptation and light-adaptation processes are related to the rate of regeneration of photopgiments and the intracellular concentration of calcium. The photoreceptor synapse, in turn, exhibits a high basal release of glutamate from its axon terminal and affects the activity of the bipolar and horizontal cells. Then, the bipolar cells form a synapse with amacrine and retinal ganglion cells. However, the glutamate-mediated synaptic activity of the retinal bipolar and ganglion cells affects the transmission of visual information via the ganglion cells. [PERSON] et al. showed that bursting activity in the photoreceptor synapse can be reinitiated pharmacologically in postnatal day P8 (stage III) and postnatal day P22 retinas with chemical agents upon blocking all synaptic connections by applying an antagonist [21; 27]. In the developing retina, waves evolve in consecutive stages based on different types of synaptic transmission (gap junctions (stage I), acetylcholine (stage II), and glutamate (stage III)), and are mediated by transient networks of specific cell types [28]. SACs have a special asymmetric synaptic distribution of excitatory and inhibitory synapses, and therefore they are involved in steering the selectivity in the mature retina but they have a different role during early development [29]. Due to autonomous intrinsic cellular mechanisms, these cells exhibit a spontaneous rupture behavior and trigger stage II retinal waves but this activity disappears with maturation [21]. SACs are made of a transitory network of autonomous busters that produce opportunistic local synchrony via cholinergic coupling during stage II, which can form to propagate waves depending on the conditions. There is a great deal of theoretical information and experimental modeling studies that are available regarding stage II retinal waves but there are still crucial issues that are not addressed in these studies [20]. The models studied so far do not explain the influence of biophysical parameters (conductance) on the activity of SACs during this stage.