targeted-toxins

Wiley RG (2001) Toxin-induced death of neurotrophin-sensitive neurons. (eds. Rush RA). In: Neurotrophin Protocols. Methods in Molecular Biology. 169:217-222. Humana Press. doi: 10.1385/1-59259-060-8:217

Summary: Wiley discusses some of the specifics of using 192-Saporin (Cat. #IT-01) to eliminate cells expressing the rat p75 low-affinity nerve growth factor receptor. Wiley also describes the sequence of events following treatment with 192-Saporin from binding of the immunotoxin through ribosomal inactivation and cell death. Methods of handling the immunotoxin and injection are also addressed.

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

Schreihofer A (2001) Featured Article: Immunolesioning: From spinal cord to brain. Targeting Trends 2(1)

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

Read the featured article in Targeting Trends.

See Also:

• Schreihofer AM et al. Sympathetic reflexes after depletion of bulbospinal catecholaminergic neurons with anti-DBH-saporin. Am J Physiol Regul Integr Comp Physiol 279:R729-R742, 2000.
• Schreihofer AM et al. Role of presympathetic C1 neurons in the sympatholytic and hypotensive effects of clonidine in rats. Am J Physiol Regul Integr Comp Physiol 279:R1753-R1762, 2000.
• Schreihofer AM et al. Regulation of sympathetic tone and arterial pressure by rostral ventrolateral medulla after depletion of C1 cells in rat. J Physiol 529(1):221-236, 2000.

Perry T, Hodges H, Gray JA (2001) Behavioural, histological and immunocytochemical consequences following 192 IgG-Saporin immunolesions of the basal forebrain cholinergic system. Brain Res Bull 54(1):29-48. doi: 10.1016/s0361-9230(00)00413-5

Summary: 192-Saporin (Cat. #IT-01) has been used extensively as a model for Alzheimer’s Disease. The neuronal deficits caused by intraparenchymal forebrain injections (0.3-0.51 µg/µl) are apparent during tasks demanding attentional processing, but not standard tasks of learning and memory. Perry et al. compare the testing strategies for each deficit. They find that the water maze may not demand enough attentional processing to demonstrate deficits caused by this lesion. The authors also study long-term effects of 192-Saporin in rats. Although the authors produced very useful data at five to six months, they found evidence of an inflammatory response and non-specific cell death eleven months post treatment, indicating 192-Saporin may be problematic for very long-term experiments.

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

Sawamura S, Kingery WS, Davies MF, Agashe GS, Clark JD, Kobilka BK, Hashimoto T, Maze M (2000) Antinociceptive action of nitrous oxide is mediated by stimulation of noradrenergic neurons in the brainstem and activation of a2B adrenoceptors. J Neurosci 20(24):9242-9251. doi: 10.1523/JNEUROSCI.20-24-09242.2000

Summary: Nitrous oxide has been used extensively in surgical anesthesia for more than 150 years, but the molecular mechanism of action has not yet been defined. Sawamura et al. investigate whether noradrenergic neurons in the brainstem are involved in the analgesic action of nitrous oxide. The authors injected rats with anti-DBH-SAP (Cat. #IT-03) to destroy pontine noradrenergic neurons. The treated rats demonstrated the usual sedative effects of nitrous oxide, but the analgesic effects were reduced or blocked. Coupled with data from null mice for the alpha2B adrenoceptor, the data indicates that alpha2 adrenoceptor subtypes and ligands are involved in the analgesic but not sedative effects of nitrous oxide.

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

Jasmin L, Janni G, Moallem TM, Lappi DA, Ohara PT (2000) Schwann cells are removed from the spinal cord after effecting recovery from paraplegia. J Neurosci 20(24):9215-9223. doi: 10.1523/JNEUROSCI.20-24-09215.2000

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

Berger-Sweeney J, Stearns NA, Frick KM, Beard B, Baxter MG (2000) Cholinergic basal forebrain is critical for social transmission of food preferences. Hippocampus 10(6):729-738. doi: 10.1002/1098-1063(2000)10:6<729::AID-HIPO1010>3.0.CO;2-M PMID: 11153718

Objective: To examine whether the cholinergic basal forebrain plays a role in non-spatial associative memory, specifically, the social transmission of food preferences.

Summary: The authors lesioned rats with 192-IgG-SAP to create selective lesions of basal forebrain cholinergic neurons and examine the rats ability to recall learned social food preference. It was shown that this type of memory was strongly associated with cholinergic activity and implicates the cholinergic projection to the neocortex in the formation of social memories.

Usage: Rats were subjected to 192 IgG-SAP (IT-01) injections at 0.175 mg/ml spread across the medial septum and vertical limb of the diagonal band of Broca bilaterally for a total of 2 microliters.

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Turchi J, Sarter M (2000) Cortical cholinergic inputs mediate processing capacity: Effects of 192 IgG-saporin-induced lesions on olfactory span performance. Eur J Neurosci 12:4505-4514.

Summary: Many experiments support the theory that the basal forebrain (BF) is involved in major aspects of attention that influence learning and memory. Elimination of cholinergic neurons in the BF by 192-Saporin (Cat. #IT-01) has been shown to reduce the ability of rats to perform a task while paying attention to more than one thing. The authors tested the treated rat’s ability to identify one olfactory stimuli from an increasing amount of such stimuli. While the performance of the treated rats returned to control levels within four weeks post-lesion, their performance reflected increased time between tests. These data indicate that cholinergic neurons of the BF play a role in attentional capacities.

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

Villa AEP, Tetko IV, Dutoit P, Vantini G (2000) Non-linear cortico-cortical interactions modulated by cholinergic afferences from the rat basal forebrain. BioSystems 58:219-228. doi: 10.1016/s0303-2647(00)00126-x

Summary: Elimination of the cholinergic neurons of the basal forebrain (BF) is an excellent model for some aspects of Alzheimer’s Disease (AD). 192-Saporin (Cat. #IT-01) is a very effective tool for elimination of cholinergic neurons in the BF. Villa et al. investigate whether field potential changes in the brains of lesioned animals mimic changes observed in the brains of human AD patients. The data presented indicate depletion of cholinergic neurons from the BF of both rats and humans produces similar changes in field potential.

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Haas CA, Hollerbach E, Deller T, Naumann T, Frotscher M (2000) Up-regulation of growth-associated protein 43 mRNA in rat medial septum neurons axotomized by fimbria-fornix transection. Eur J Neurosci 12:4233-4242. doi: 10.1046/j.0953-816x.2000.01329.x

Summary: Axonal growth and regeneration is limited in adult mammals, however, if injured CNS neurons are in an environment permissive for growth, they can regenerate. Transection of septohippocampal fibers is a widely used method for studying CNS neuron response to injury. These fibers are composed of both cholinergic and GABAergic neurons. Haas et al. used a combination of cholinergic lesioning by 192-Saporin (Cat. #IT-01) and double staining to investigate whether both cell types were involved in neuron regeneration. The findings show that both transmitter phenotypes up-regulate mRNA levels of a protein associated with growth and synaptogenesis in developing neurons, and plasticity in adult neurons.

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

Pain L, Jeltsch H, Lehmann O, Lazarus C, Laalou FZ, Cassel JC (2000) Central cholinergic depletion induced by 192 IgG-saporin alleviates the sedative effects of propofol in rats. Brit J Anaesth 85(6):869-873. doi: 10.1093/bja/85.6.869

Summary: In order to examine the effect of cholinergic depletion on the sedative potency of propofol in rats the authors injected 1 µg of 192-Saporin (Cat. #IT-01) into each lateral ventricle. The findings indicate a ~50% reduction in sedative potency in lesioned rats.

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