Role of Cholinergic Synaptic Transmissions in the Development of Retinal Circuits

The precise wiring of neural circuits in the mammalian visual system depends on spontaneous electrical activity in the immature retina. In normal mice, during the first week of postnatal development, this spontaneous activity consists of correlated depolarizations in the developing retina, propagated by cholinergic synaptic transmission. In mutant mice lacking the β-2 subunit for the nicotinic acetylcholine receptor (β2^-/-), retinal waves persist, but are spread by gap junctions instead of cholinergic circuitry. In this study, we use β2^-/- mice to test whether the expression of the neuronal gap junction subunit Connexin 36 (Cx36) is altered due to the lack of cholinergic transmissions. First, we use immunofluorescence to compare the density of cells that express Cx36. Second, we use RT-PCR to determine if β2^-/- mice exhibit altered expression levels of the Cx36 gene. We postulate that β2^-/- mice exhibit higher density of Cx36 expressing cells, and an increase in the mRNA levels of the Cx36 transcript. These experiments will test whether chemical synapses play an influential role in the development of gap junctions.