Based on our measurements of the MVL thresholds, with and without GVD compensation, we conclude that the visible lesion thresholds produced by 44 fs pulses in rhesus eyes are increased in energy due to GVD. The MVL ED50 was reduced by one third when the pulse was pre-chirped to compensate for GVD in the eye. This reduction in amplitude also holds true in the artificial eye for the LIB ED50 bubble thresholds and the LDP ED50 plasma channels, when using pre-chirped pulses versus non-chirped pulses. We also conclude from the data presented that low-density plasmas, and not LIB cavitation bubbles, are the probable mediating factor at the visible lesion thresholds observed within live eyes, for pulse durations at and below 50 fs. Therefore, the plasma channel created by LDPs is the major damage mechanism, if not the only damage mechanism, at MVL threshold energies for these pulse durations.