The surface morphology of transplants of rat fetal hippocampal tissue, and of cavities formed by aspiration lesion of the adult rat hippocampus and overlying neocortex into which the transplants were placed, was studied by scanning electron microscopy. The surface of lesion cavities was covered by a scar upon which occasional cellular profiles were found. The surface cells resembled supraependymal macrophages. Lesion cavities with a transplant showed similar scarring although the number of supraependymal structures was increased. Polymorphic cells and numerous fiber processes were observed both on the surface and embedded in the scar. Ependymal structures were seen on the non-damaged ventricular surfaces adjacent to the lesion site. These regions, however, also displayed increases in the number and types of supraependymal structures. Scanning electron microscopy demonstrated considerable variability in surface morphology of different transplants and over the surface of individual transplants. A transplant could show regions of scarring, areas covered by cells resembling ependymal cells, and regions covered by a dense matrix of fibers. In many regions the fibers coalesced to form a branching, web-like network over the transplant surface. Transmission electron microscopy indicated that the surface could be covered by ependymal cells or by the scar seen in scanning specimens. Some surface fibers were identified as axons. Cells on the surface of the transplants could be identified as neuronal, glial-like, and phagocytic. The cells and the possible effects of surface morphology on transplant function is discussed.

The purpose of the present study was to determine whether neurochemicals normally found within neuron somata, fibers, and terminals of the hippocampal formation would also be present in transplanted hippocampal tissue that had developed in lesion cavities made in adult rat brains by aspiration of the hippocampus and overlying dorsolateral neocortex. Embryonic Day 15 or 16 rat brain tissue containing hippocampus with some medial pallial anlage was transplanted into the site of hippocampal aspiration lesions in adult male rats. One hundred ten to one hundred thirty-five days later the brains of these rats were sectioned and processed using the avidin-biotin-horseradish peroxidase immunocytochemical procedure to visualize choline acetyltransferase, met-enkephalin (MENK), neurotensin (NT), somatostatin, substance P, tyrosine hydroxylase (TH), or vasoactive intestinal polypeptide. Sections from two brains were stained using the thiocholine technique for visualization of acetylcholinesterase. All of these substances were found within cell bodies and/or fibers in the transplants. However, several abnormalities were noted. In addition to TH-immunoreactive fibers, TH-immunoreactive cell bodies were found in the transplants. Since TH is not expressed in mature hippocampal or cortical neurons this suggests that mechanisms for suppression of manufacture of this enzyme are lacking or inhibited in the transplants. Further, although all of the peptides were present either in fibers or in both cell bodies and fibers, the density of staining for NT and MENK was less than would be expected for normal hippocampus, and none of the cell bodies or fibers reacting for the peptides exhibited any apparent organization resembling that normally observed in hippocampus or cortex. However, some histological organization was present and the cholinergic markers were associated with this organization. These data suggest that some tropic and/or trophic factor such as nerve growth factor is present in the transplants to guide cholinergic innervation.

Embryonic Day 16 or 17 rat tissue containing either hippocampus with some medial pallial anlage or cerebellar/alar plate anlage was transplanted to the site of the ablated hippocampus of otherwise normal adult rats or adult rats previously exposed to the neurotoxin trimethyltin. Ninety to one hundred five days later these rats were compared to control rats in acquisition of passive avoidance and in open field activity. Transplantation of both types of tissue produced behavioral recovery on both tasks in rats with hippocampal lesions that had not been exposed to trimethyltin. Only hippocampal transplants produced recovery of function in rats given trimethyltin. Although transplants of hippocampal tissue had an organotypic structure that was easily differentiated with cell and fiber stains from that of the cerebellar transplants, neither of these routine histological procedures nor immunocytochemical analysis revealed differences between transplants made into normal rats or toxicant-exposed rats. Either of two mechanisms may account for the ability of the transplants to produce behavioral recovery. These are reconstruction of damaged circuitry by the transplant and neurotrophic action of the developing transplant on the host brain. The second mechanism alone may be sufficient to restore function in brain-lesioned but otherwise normal rats. Therefore, either type of transplant is effective. Both mechanisms may be necessary for recovery in brain-lesioned, toxicant-exposed rats. Therefore, only transplants of tissue homotypic to the tissue removed from the brain are effective.

The noradrenergic A5 cell group of the caudal ventrolateral pons has been implicated in regulation of cardiovascular activity. The efferent fibers from this cell group have been established, but the sources of afferents into the region have not. Horseradish peroxidase (HRP) was injected into the A5 region in rabbits, or into regions surrounding A5. The pattern of retrograde labeling indicated that several areas known to have a role in the control of cardiovascular function by the brain send projections to and/or through the A5 region.

The effects of fornix and cingulate lesions on two-way active avoidance, passive avoidance, and tonic immobility were studied in rabbits. Fornix lesions facilitated acquisition of the active avoidance task, impaired acquisition of passive avoidance, and prolonged the duration of tonic immobility. Cingulate lesions impaired the acquisition of the active avoidance task, facilitated acquisition of passive avoidance, and decreased the duration of tonic immobility. The pattern of degeneration produced by these lesions was determined using the Fink-Heimer procedure. In addition to their individual projection patterns, both lesions caused degeneration in the ventral anterior thalamic nucleus and in the area of the zona incerta. We propose that some form of response modulation hypothesis best accounts for the behavioral data and that the ventral anterior thalamus and zona incerta are probable regions where the cingulate gyrus, and structures which contribute to the fornix, directly interface in interactions which influence behavior.

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