PubMed Health⌕ Search

Biomedical subjects

S H Pearlman

Publications and source records attributed to S H Pearlman.

5 recordsLinked to original sources
PubMed1991

Striatal implants protect the host striatum against quinolinic acid toxicity.

Quinolinic acid (QA) and related excitotoxins produce a pattern of neuronal loss and neurochemical changes in the rat striatum similar to that of patients suffering from Huntington's disease, suggesting neurotoxicity is important in the etiology of that disease. Thus, strategies for limiting excitotoxin-induced striatal damage, like that caused by QA, may be of great benefit to these individuals. Accordingly, we tested the ability of both neural and non-neural tissue implants to protect the rat striatum against a subsequent QA challenge. Our results demonstrated that recipients of fetal striatal grafts were significantly less affected by striatal injections of QA than non-grafted animals. In contrast to the latter, fetal striatal tissue recipients did not exhibit apomorphine-induced rotation behavior and showed a sparing of cholinergic and enkephalinergic systems normally lost following QA injections. Animals grafted with adult rat sciatic nerve, adrenal medulla or adipose tissue all showed a less dramatic behavioral protection and sparing of cholinergic and enkephalinergic systems. These results suggest that fetal striatal tissue exerts an optimal, and perhaps specific protective influence on the host brain.

Adrenal Medulla↗
PubMed1991

[Protective effect of intrastriatal grafts in an experimental model of Huntington's disease. Behavioral and morphological correlation].

The intrastriatal injection of the excitotoxin quinolinic acid (Q.A.) in rats produces neuroanatomical and neurochemical changes mimicking those appearing in the striatum in Huntington's disease (H.D.). Although its cause is unknown, it has been hypothesized that the neurodegenerative changes seen in H.D. may result from the action of an endogenous toxin. Therefore, the development of new strategies for limiting or preventing Q.A.-or other neurotoxic-induced degeneration may be of therapeutic interest for neurodegenerative disorders. Accordingly, we tested the ability of various tissue transplants to protect the rat striatum against a subsequent Q.A. insult. Using a "unilateral model", i.e. unilateral intrastriatal grafts followed by an ipsilateral intrastriatal injection of Q.A., we were able to quantify a behavioral protective effect of the grafts in recording the apomorphine-induced rotational behavior that normally appears after the striatal Q.A.-induced lesion. Our results show that one of the tested tissue, fetal striatum, protects the recipients against the lesioned-induced rotational behavior that appeared in non-grafted lesioned animals. The other grafted tissues (adrenal medulla, peripheral nerve, adipose tissue) seemed to provide a less dramatic protection than fetal striatum; however, this difference did not reach significance. Quantification of the striatal neuronal loss showed that the behavioral protection is significantly correlated with a better neuronal survival in the grafted animals. These results suggest that intracerebral grafts can protect the host brain against a toxin-induced damage, like the one resulting from Q.A. intrastriatal injection. Though fetal striatal grafts seem to exert an optimal protection, this protective effect may at least partially result from a host-mediated response to the transplantation procedure. The mechanism underlying this protective effect is unclear, but the present data suggest that it might be related to a transplantation-induced astroglial reaction resulting in an increased neuronotrophic activity that could protect against the toxic effect of Q.A. The results of this study also support the concept that the effect of transplantations could occur through processes other than a direct restoration of deficient transmitters or a reconstruction of damaged pathways. Further characterization of the factors implicated in the present paradigm might conceivably open avenues for possible therapeutic preventive interventions in neurodegenerative disorders.

Animals↗
PubMed1990

Fetal hypothalamic transplants into brain irradiated rats: graft morphometry and host behavioral responses.

This study was designed to test the hypothesis that neural implants can ameliorate or prevent some of the long-term changes associated with CNS irradiation. Using a rat model, the initial study focused on establishing motor, regulatory, and morphological changes associated with brain radiation treatments. Secondly, fetal hypothalamic tissue grafts were placed into the third ventricle of rats which had been previously irradiated. Adult male Long Evans rats received one of three radiation doses (15, 22.5, & 30 Gy) or no radiation. Three days after irradiation, 7 animals in each dose group received an embryonic day 17 hypothalamic graft into the third ventricle while the remaining 8-9 animals in each group received injections of vehicle solution (sham). Few changes were observed in the 15 and 22.5 Gy animals, however rats in the 30 Gy treatment group showed stereotypic and ambulatory behavioral hyperactivity 32 weeks after irradiation. Regulatory changes in the high dose group included decreased growth rate and decreased urine osmolalities, but these measures were extremely variable among animals. Morphological results demonstrated that 30 Gy irradiated animals showed extensive necrosis primarily in the fimbria, which extended into the internal capsule, optic nerve, hippocampus, and thalamus. Hemorrhages were found in the hippocampus, thalamus, and fimbria. Defects in the blood brain barrier also were evident by entry of intravascularly injected horseradish peroxidase into the parenchyma of the brain. Animals in the 30 Gy grafted group showed fewer behavioral changes and less brain damage than their sham grafted counterparts. Specifically, activity measures were comparable to normal levels, and a dilute urine was not found in the 30 Gy implanted rats. Morphological changes support these behavioral results since only two 30 Gy implanted rats showed necrosis in the fimbria, internal capsule, and other areas of the brain. These results suggest that grafts of fetal neural tissue exert a beneficial influence on the host brain, although the mechanism by which the implant exerts its effect is still unknown. Evidence supporting the role of trophic factors is reviewed. These preliminary results suggest a potential for tissue grafts in the treatment of CNS irradiated patients.

Animals↗
PubMed1986

Localized herpes simplex lymphadenitis.

Despite the marked immunocompromised status of most affected patients, visceral herpes simplex virus (HSV) infections in adults remain localized to the esophagus, with only rare examples of dissemination. Lymph node involvement with herpes simplex has been noted in three reported cases, but only in the context of a widespread fatal infection. This report describes two patients who presented with localized herpetic lymphadenitis documented by light microscopy, immunohistochemistry, and DNA hybridization technics.

Aged↗