Inhibition of long-term memory formation by anti-ependymin antisera after active shock-avoidance learning in goldfish.

Ependymins are acidic glycoprotein constituents of goldfish brain cytoplasm and extracellular fluid which are known to participate in biochemical reactions of long-term memory formation. In earlier experiments, anti-ependymin antisera were found to cause amnesia when injected into goldfish brain ventricles after the acquisition of a vestibulomotoric training task. To investigate whether they also inhibit memory consolidation after other learning events the anti-ependymin antisera were injected after an active shock-avoidance learning paradigm, as follows: goldfish were trained in a shuttle-box to cross a barrier in order to avoid electric shocks (unconditioned stimulus) applied shortly after a light signal (conditioned stimulus). Anti-ependymin antisera blocked retention of the learned avoidance when injected 0.5, 4.5 or 24 h after acquisition of the new behavior. They had no effect, however, when injected 72 h after learning. Apparently, long-term memory was already consolidated at this point. Antisera injected 0.5 or 72 h prior to training, also did not influence learning or memory. Thirteen percent of the goldfish fled the light stimulus spontaneously. These fish therefore did not experience the unconditioned stimulus and thus were unable to learn the task. When they were treated with the anti-ependymin antisera and tested 3 days later, the spontaneous escape reaction was not affected (active control group). The ability of anti-ependymin antisera to inhibit memory consolidation and their efficacy after administration at specific time intervals are very similar for the active shock-avoidance learning and for the vestibulomotoric training. We conclude that ependymins are not task-specific, but serve a general function in biochemical reactions essential for long-term memory formation.