targeted-toxins

Pallera AM, Schweitzer JB, Book AA, Wiley RG (1994) 192 IgG-saporin causes a major loss of synaptic content in rat olfactory bulb. Exp Neurol 127:265-277. doi: 10.1006/exnr.1994.1102

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

Heckers S, Mesulam M-M (1994) Two types of cholinergic projections to the rat amygdala. Neuroscience 60:383-397. doi: 10.1016/0306-4522(94)90252-6

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

Lappi DA, Ying W, Barthelemy I, Martineau D, Prieto I, Benatti L, Soria M, Baird A (1994) Expression and activities of a recombinant basic fibroblast growth factor-saporin fusion protein. J Biol Chem 269(17):12552-12558. PMID: 8175664

Related Products: FGF-SAP (Cat. #IT-38)

Waite JJ, Wardlow ML, Chen AC, Lappi DA, Wiley RG, Thal LJ (1994) Time course of cholinergic and monoaminergic changes in rat brain after immunolesioning with 192 IgG-saporin. Neurosci Lett 169:154-158. doi: 10.1016/0304-3940(94)90379-4

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

Heckers S, Ohtake T, Wiley R, Lappi DA, Geula C, Mesulam M-M (1994) Complete and selective cholinergic denervation of rat neocortex and hippocampus but not amygdala by an immunotoxin against the p75 NGF receptor. J Neurosci 14:1271-1289. doi: 10.1523/JNEUROSCI.14-03-01271.1994

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

Wiley RG, Lappi DA (1994) Suicide Transport and Immunolesioning. R.G. Landes, Houston.

This book is available in many university libraries and can also be purchased here

Book AA, Wiley RG, Schweitzer JB (1994) 192 IgG-saporin: I. Specific lethality for cholinergic neurons in the basal forebrain of the rat. J Neuropathol Exp Neurol 53:95-102. doi: 10.1097/00005072-199401000-00012

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

Roberts RC, Harrison MB, Francis SMN, Wiley RG (1993) Differential effects of suicide transport lesions of the striatonigral or striatopallidal pathways on subsets of striatal neurons. Exp Neurol 124:242-252. doi: 10.1006/exnr.1993.1194

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Leanza G, Nilsson O, Wiley RG, Bjorklund A (1993) Dose-related effects of 192 IgG-saporin on basal forebrain cholinergic neurons: Biochemical, immunocytochemical and behavioral studies on neonatal and adult rats. Neuroscience 1993 Abstracts 771.12.

Summary: Highly selective and efficient depletions of the NGF receptor-positive cholinergic neurons in the basal forebrain, associated with profound behavioral changes, have been reported after treatment with 192 IgG-saporin, a recently introduced immunotoxin. In the present study, the effects of different doses of the toxin conjugate were compared following bilateral injections in the lateral ventricles of infant (2-3 days post-natal, 0.2 to 0.8 µg dose-range) and adult rats (1.25 to 10 µg dose-range). Five to eight weeks post-injection, dose-related behavioral effects of the lesion were evaluated in water maze, passive avoidance and locomotor activity tests, followed by biochemical and histologic analyses performed on tissue specimens. In the adult rats, the immunotoxin produced severe dose-dependent cognitive deficits in water maze task performance and passive avoidance retention that correlated with decline in choline acetyltransferase (ChAT) activity in neocortical and hippocampal areas (up to 95% reduction) and depletion of NGF receptor-positive neurons in the septal-diagonal band area and nucleus basalis (>95%). Similar dose-related patterns of ChAT activity reduction and neuronal loss throughout the basal forebrain were seen in rats neonatałly injected with the immunotoxin. ChAT levels in other regions such as brainstem, cerebellum or the spinal cord were found largely unaffected in both adult and neonatałly lesioned rats. The present results confirm 192 IgG-saporin as a powerful tool to induce specific and robust cholinergic lesions either during development or adulthood and emphasize the crucial role of the forebrain cholinergic system in cognitive functions.

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Picklo MJ, Wiley RG, Lappi DA, Robertson D (1993) Noradrenergic lesioning using anti-DBH immunotoxin. Neuroscience 1993 Abstracts 771.10. Society for Neuroscience, Washington, DC.

Summary: Current methods of lesioning noradrenergic neurons have significant drawbacks due either to incompleteness, partial specificity, or reversibility. We sought to determine if an immunotoxin to dopamine ß-hydroxylase (DBH) would efficiently destroy noradrenergic neurons in vivo. The MAB3O8 monoclonal antibody to bovine DBH was obtained from Chemicon International (Temecula, CA). Antibody was disulfide coupled to the ribosome inactivating protein, saporin, using SPDP. The resulting immunotoxin was injected into anesthetized adult, male Sprague-Dawley rats. Injection sites in individual animals were the submandibular gland (3.1-12.5 µg), intravenous (6-31 µg), and intraventricular (1.8-4.8 µg). Three days after systemic injections, rats were reanesthetized and transcardially perfused with aldehyde fixative. Frozen sections of peripheral ganglia were processed for Nissi staining. In sections from sympathetic ganglia, most neurons showed severe chromatolysis characteristic of the cytotoxic effect of immunotoxins containing saporin. Sensory ganglia showed small numbers of similarly poisoned neurons. Eleven days after intraventricular injections, rats were sacrificed and brain sections stained either with cresyl violet (N¡ssl) or for tyrosine hydroxylase (TH) using indirect immunoperoxidase technique. Nissi staining of the locus coeruleus showed a decrease in the numbers of neurons as was confirmed by staining for TH. Dopaminergic neurons in the midbrain appeared unaffected as did catecholaminergic neurons in the caudal brainstem. We conclude that anti-DBH-saporin efficiently destroys noradrenergic neurons in the CNS and PNS. This immunotoxin may be a valuable lesioning tool with greater selectivity than has been previously available.

Related Products: Anti-DBH-SAP (Cat. #IT-03)