The development of the central nervous system is dependent on spontane
ous action potentials and changes in [Ca2+](i) occurring in neurons [1
-4], In the mammalian retina, waves of spontaneous electrical activity
spread between retinal neurons, raising [Ca2+](i) as they pass [5-7],
In the ferret retina, the first spontaneous Ca2+ waves have been repo
rted at postnatal day 2 and are thought to result from the Ca2+ influx
associated with bursts of action potentials seen in ganglion cells at
this time [5-7], These waves depend on depolarisation produced by vol
tage-gated sodium channels, but their initiation and/or propagation al
so depends upon nicotinic cholinergic synaptic transmission between am
acrine cells and ganglion cells [8]. Here, we report contrasting resul
ts for the chick retina where Ca2+ transients are seen at times before
retinal synapse formation but when there are extensive networks of ga
p junctions, These Ca2+ transients do not require nicotinic cholinergi
c transmission but are modulated by acetylcholine (ACh), dopamine and
glycine, Furthermore, they propagate into the depth of the retina, sug
gesting that they are not restricted to ganglion and amacrine cells, T
he transients are abolished by the gap-junctional blocker octanol, Thu
s, the Ca2+ transients seen early in chick retinal development are tri
ggered and propagate in the absence of synapses by a mechanism that in
volves several neurotransmitters and gap junctions.