sfn2001

Janni G, Jasmin L, Ohara PT (2001) Schwann cells can enter the demyelinated spinal cord from dorsal roots via scar tissue. Neuroscience 2001 Abstracts 157.4. Society for Neuroscience, San Diego, CA.

Summary: We have studied the routes of entry of Schwann cells into the demyelinated spinal cord. Following application of the toxin CTB-Sap (B fragment of Cholera toxin conjugated to Saporin) into the intrathecal space of adult rats there occurs massive loss of oligodendrocytes with secondary demyelination of the lumbar spinal cord with sparing of axons. Concurrent with the demyelination, an arachnoiditis develops that results in dorsal roots becoming adherent to the lateral spinal cord. Light and electron microscopy showed that Schwann cells in the dorsal roots were always separated from the demyelinated axons by a mesenchymal interface part of which was formed by the dorsal root perineurium. Within 15 days of the demyelination, Schwann cell precursors (p75 immunopositive) migrated from the dorsal roots into the spinal cord via the adhesions and were found to divide within the cord. Schwann cell myelination of demyelinated central axons was consistently observed by day 30. Therefore the Schwann precursors were able to migrate into demyelinated spinal cord through non-neuronal cellular barriers without being in direct contact with demyelinated axons. These findings suggest that, under appropriate conditions, Schwann cells might be introduced therapeutically into the demyelinated spinal cord via intrathecal application and avoid direct spinal injection.

Related Products: CTB-SAP (Cat. #IT-14)

Burk JA, Herzog CD, Porter MC, Mahoney J, Bruno JP, Sarter M (2001) Interactions between partial cortical cholinergic deafferentation and aging on sustained attention performance in rats. Neuroscience 2001 Abstracts 202.5. Society for Neuroscience, San Diego, CA.

Summary: Previous studies have provided only limited support for the idea that aging alone impairs the functions of basal forebrain corticopetal cholinergic neurons. Conversely, aging has been hypothesized to exacerbate the functional consequences of prior insult to, or degenerative processes in, the basal forebrain cholinergic system. The present study assessed the effects of aging on the sustained attention performance of rats with moderate lesion-induced loss of cortical cholinergic inputs. Previous studies on the effects of extensive (> 70 %) cortical cholinergic deafferentation indicated that the integrity of this system is necessary for the animals’ ability to detect rare and unpredictable visual signals. In the present longitudinal experiment, moderate (< 50 %) 192 IgG-saporin-induced loss of cortical cholinergic inputs, produced in well-trained, 16 month-old rats, did not – as was intended - immediately affect their attentional performance. Animals continued to undergo attentional performance training for the remainder of their lives. At the age of 31 months, impairments in performance began to emerge in lesioned animals. Compared to their sham-lesioned counterparts, lesioned animals exhibited a steeper decrement in their ability to detect hits in the course of a test session. At this age, the performance of sham-lesioned animals did not differ from their earlier performance prior to and immediately after the lesion. These results support the general hypothesis that aging serves to exacerbate the effects of pre-existing degeneration of the basal forebrain cholinergic system.

Related Products: 192-IgG-SAP (Cat. #IT-01)