Wrenn CC, Lappi DA, Wiley RG (1999) Lack of effect of intraventricular OX7-saporin on working memory in the rat. Neuroscience 1999 Abstracts 559.5. Society for Neuroscience, Miami, FL.
Summary: The immunotoxin 192 IgG-saporin (192-sap) has been shown by our laboratory and others to be a highly selective agent for the production of lesions of the rat cholinergic basal forebrain(CBF). Such lesions can be produced by either intraventricular (i.c.v.) or intraparenchymal injection of the immunotoxin and can result in cognitive deficits. One potential shortcoming of i.c.v. injection of 192-sap is that it kills cerebellar Purkinje cells in addition to killing the neurons of the CBF. Thus, it is unclear whether or not cognitive deficits that arise after i.c.v. 192-sap are due to loss of the CBF or loss of Purkinje cells. We addressed this problem by injecting rats i.c.v. with saline, 2 µg 192-sap, 4 µg 192-sap, or 1 µg OX7-saporin(OX7-sap). OX7-sap is an immunotoxin shown by our laboratory to selectively lesion Purkinje cells after i.c.v. injection. The 1 µg dose was chosen based on pilot anatomical work which showed this dose to produce Purkinje cell loss of similar pattern and extent to that produced by 4 µg of 192-sap. These rats were tested in a radial maze working memory paradigm, and it was found that the 4 µg 192-sap group made significantly more working memory errors than either the saline or OX7-sap injected groups. These data suggest that Purkinje cell loss alone is not sufficient to disrupt cognitive processes. (Supported by Departmento f Veterans Affairs and the Vanderbilt Center for Molecular Neuroscience).
Related Products: 192-IgG-SAP (Cat. #IT-01), OX7-SAP (Cat. #IT-02)