MORPHOLOGICAL CORRELATES OF NEURAL REGENERATION IN THE FEEDING SYSTEMOF APLYSIA-CALIFORNICA AFTER CENTRAL-NERVOUS-SYSTEM LESIONS

Morphological techniques were used to study regeneration of central ne ural pathways involved in feeding behavior following bilateral crushes of the cerebral-buccal connectives (CBCs). Electron microscopic analy sis revealed that CBC crushes completely transect axons within the ner ve core while leaving a remnant of the nerve sheath intact. Changes in the ultrastructure of the CBCs at the crush site were determined for 1, 7, 14, 21, and 50 days postlesion. At 1 day postlesion, the crush s ite was no longer compressed, and the nerve core had assumed a circula r shape. In addition, several small axon profiles were evident, and la rge areas of tissue debris and prominent microglial cells were observe d. Membranous debris and hemocytes were also present in sinuses that a ppeared in the sheath adjacent to the crush site. From 7 to 50 days po stlesion, the core of the nerve at the crush site increased in size du e to the addition of small diameter axons. Initially, the sheath surro unding the crush site exhibited hyperplasia and contained a few small bundles of processes, apparently due to newly sprouted axons that had strayed from the nerve core. By 50 days postlesion, the crush site app eared nearly normal; the nerve core was reacquiring the normal radial pattern of axon profiles with some medium-sized axon profiles covered with glial sheath and exhibiting invaginations typical of the intact C BC. However, there was still a distinct lack of large diameter axons. Cobalt backfills across the crush site revealed neurons in the cerebra l ganglion by postlesion day 9. Positions of stained cell bodies were consistent with those observed in controls, although the numbers of st ained neurons did not recover to control levels even by postlesion day 63. The changes in the crush site and return of cell body staining wi th time postlesion are correlated with the recovery of consummatory fe eding. (C) 1997 Wiley-Liss, Inc.