To determine whether central communication of retinal signals is neces
sary for the development of an experimentally induced myopia, tree shr
ews were exposed to monocular deprivation (MD) while the action potent
ials of retinal cells in the deprived eye were blocked with intravitre
ally injected tetrodotoxin (TTX-MD animals). TTX injections (0.6 mu g
in 3 mu L) and MD began about 15 days after eye opening, at the start
of the susceptible period for the development of lid-suture myopia. Si
x injections were given, one every second day to produce 12 days of MD
and TTX-blockade. Control TTX animals (TTX-open) received TTX in one
eye, but not MD, on the same injection schedule and were always found
to be behaviorally unresponsive to visual stimuli through the injected
eye indicating that TTX blocked central communication of action poten
tials. Other control animals received intravitreally injected saline i
n either an open eye (saline-open), or an MD eye (saline-MD). A sham-i
njected group (sham-inj-MD) received MD and an anesthetic and surgical
manipulations except for penetration of the sclera. In all groups, on
e eye in each animal was an untreated control. Two effects were found.
Air MD groups, including the TTX-MD animals, developed a significant
vitreous chamber elongation in the deprived eye, indicating that an ex
perimental myopia developed despite ganglion cell blockade. Thus, reti
nal mechanisms in tree shrew can detect the presence of a degraded vis
ual image and produce an experimental myopia that does not depend on t
he receipt of visual messages by central neural structures. In additio
n, eyes in which the sclera was punctured had smaller vitreous chamber
depths than comparable uninjected eyes, indicating that puncturing th
e sclera reduced the normal elongation. These data suggest that forces
within the eye normally contribute to its expansion and may be resist
ed by the choroid and/or the sclera.