Abstract
Transgenic mice overexpressing bcl-2,
due to inhibition of naturally occurring cell death, have
much larger brains and optic nerves as compared to wild-type
mice. Since developmental cell death is believed to exert
a crucial role in establishing the mature neural circuitry
and function, we asked the question of whether basic aspects
of vision were altered in bcl-2 mice. Local visually
evoked potentials (VEPs) in response to patterned stimuli
were recorded from the primary visual cortex. The representation
of the vertical meridian was displaced by about 15% in
the bcl-2 mouse, accounting for brain expansion.
However, visual acuity, contrast threshold, and response
latency were normal, indicating that compensatory mechanisms
can ensure normal basic properties of vision in spite of
marked neuronal redundancy.
