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B A Black

Publications and source records attributed to B A Black.

4 recordsLinked to original sources
PubMed1992

Transplantation of fetal cholinergic neurons into the hippocampus attenuates the cognitive and neurochemical deficits induced by AF64A.

The present experiments examined whether transplanted fetal cholinergic neurons would attenuate the behavioral and neurochemical deficits induced by the cholinotoxin AF64A (ethylcholine aziridinium ion). Bilateral injections of AF64A (3 nmol) into the lateral ventricles produced significant learning and memory impairments together with decreases in hippocampal high-affinity choline uptake (HAChU). AF64A-treated rats were impaired on both a standard radial arm maze (RAM) task and a working memory version in which a one-hour delay was imposed between the fourth and fifth arm choices. Transplantation of embryonic day E-17 septal/diagonal band tissue into the hippocampus (HPC) promoted recovery of performance on the standard version of the RAM task. However, this recovery was not observed when the animals were tested on the more difficult delay version of the task. Neurochemical analysis indicated that AF64A produced a significant (31%) decrease in hippocampal HAChU that was attenuated (14%) by transplantation of fetal cholinergic neurons. Histological analysis revealed that the transplants survived and innervated the HPC. There was no apparent relationship between fiber ingrowth into the HPC and behavioral recovery. These data indicate that transplant-induced behavioral recovery may be related to and limited by the cognitive demands of the testing situation. Generalized increases in cholinergic activity, transplant-mediated release of trophic factors, or a combination of both may underlie the behavioral recovery observed in the present studies.

Analysis of Variance↗
PubMed1985

Effects of acid on the basal lamina of the rat stomach and duodenum.

Rapid restitution of the gastric and intestinal epithelium after acute injury involves emigration of cells from the gastric glands and basal half of the intestinal villi. An intact basal lamina is prerequisite to the restitution process. The present study was performed to determine the effects of acid on the rat gastric and duodenal basal lamina. The basal lamina was denuded in vitro by ultrasonic vibration. The tissue was then immersed in 0.2 M mannitol (control) or in HCl (5-50 mM) for 10 min. Samples of the tissues were examined by transmission and scanning electron microscopy. Some samples were stained with ruthenium red to demonstrate glycosaminoglycans. The lower concentrations of acid (5 and 10 mM) had little or no effect on the structure of the basal lamina. However, exposure to 20 and 50 mM HCl caused extensive damage to the basal lamina and exposed the underlying connective tissue matrix of the lamina propria. Ruthenium red staining demonstrated differences in size and location of glycosaminoglycans within the basal laminae of stomach and intestine. Exposure to acid at concentrations of 20 or 50 mM caused total loss of ruthenium red staining in both intestinal and gastric basal laminae. Exposure to 10 mM acid resulted in loss of the outermost (luminal) layer of anionic sites from the gastric basal lamina. These studies demonstrate that brief exposure to acid, in concentrations which are necessary for the formation of hemorrhagic erosions in the stomach, caused damage to the basal lamina. This damage may impair epithelial restitution and thus account, in part, for the role of acid in ulcerogenesis.

Animals↗