Py. Burgi et Nm. Grzywacz, MODEL FOR THE PHARMACOLOGICAL BASIS OF SPONTANEOUS SYNCHRONOUS ACTIVITY IN DEVELOPING RETINAS, The Journal of neuroscience, 14(12), 1994, pp. 7426-7439
Spontaneous waves of bursts of action potentials propagate across the
ganglion-cell surface of developing retinas. A recent biophysical mode
l postulated that this propagation is mediated by an increase in extra
cellular K+, following its ejection from ganglion cells during action
potentials. Moreover, the model hypothesized that bursts might termina
te due to the accumulation of intracellular Ca2+ and the subsequent ac
tivation of a Ca2+-dependent K+ conductance in the cells' dendrites. F
inally, the model proposed that an excitatory synaptic drive causes a
neuromodulation of the waves' properties. To test the feasibility of t
he model, we performed computer simulations of the network of developi
ng ganglion cells under control and pharmacological-manipulation condi
tions. In particular, we simulated the effects of neostigmine, Cs+ and
TEA, low Ca2+ concentrations, and Co2+. A comparison of the simulatio
ns with electrophysiological and pharmacological experimental data rec
ently obtained in turtles (Sernagor and Grzywacz, 1993a), and cats and
ferrets (Meister et al., 1991; Wong et al., 1993), showed that the mo
del for the most part is consistent with the behavior of developing re
tinas. Moreover, modifications of the model to allow for GABAergic inp
uts onto ganglion cells (Sernagor and Grzywacz, 1994) and poor [K+](ou
t) buffering (Conners et al., 1982) improved the model's fits. These r
esults lent further support to important roles of extracellular K+ con
centration and synaptic drive for the propagation of waves.