192-IgG-SAP [IT-01, KIT-01]

a tool for eliminating cells that express p75NTR in rat; targeted via the antibody to NGFR (192-IgG), eliminated via saporin

SKU: IT-01 Category: Antibody Type: Monoclonal | Host: mouse | Reactivity: rat | Conjugate: saporin | Usage: eliminates cells |

Intraventricular injection of 192-IgG-SAP (192-Saporin) results in almost complete elimination of LNGFR (p75NTR)-positive cells in rat. 192-IgG-SAP is directed to a cell-surface antigen that is only expressed at high levels on neurons in the cholinergic basal forebrain (CBF). The antigen, p75NTR, is not expressed on the neighboring, non-cholinergic neurons. 192-IgG-SAP specifically eliminates cholinergic neurons of the basal forebrain, medial septum, diagonal band of Broca, nucleus basalis of Meynert, and Purkinje neurons of the cerebellum. It provides researchers with a powerful lesioning tool – more specific and effective than chemical, surgical or electrolytic lesioning. Permanent and selective removal of cholinergic forebrain neurons makes an important animal model for the study of behavior, neuronal loss (e.g. Alzheimer’s disease), plasticity of other systems in response to loss, replacement therapy, and drug effects and dependence.

192-IgG-SAP is a chemical conjugate of the mouse monoclonal antibody to rat p75NTR and the ribosome-inactivating protein, saporin. It specifically eliminates cells expressing p75NTR, also known as the low affinity nerve growth factor receptor.

To eliminate p75NTR-expressing cells in mouse, use mu p75-SAP (Cat. #IT-16). To eliminate p75NTR-expressing cells in other mammals, use ME20.4-SAP (Cat. #IT-15).

192-IgG-SAP is available individually (Cat. #IT-01) or as a kit (Cat. #KIT-01) which includes 192-IgG-SAP and Mouse IgG-SAP (Cat. #IT-18).

Neurotoxic effects, mechanisms, and outcome of 192 IgG-Saporin lesions.

Petrosini L, De Bartolo P, Cutuli D (2021) Neurotoxic effects, mechanisms, and outcome of 192 IgG-Saporin lesions. RM Kostrzewa (Ed.): Handbook of Neurotoxicity . Springer, Cham doi: 10.1007/978-3-030-71519-9_79-1

Summary: 192-IgG-saporin selectively destroys basal forebrain cholinergic neurons that provide cholinergic input to the hippocampus, entire cortical mantle, amygdala, and olfactory bulb. Immunotoxic lesions by 192-IgG-saporin represent a valid animal model of Alzheimer’s disease, given the degeneration of basal cholinergic system present in this pathology. The selective lesioning of cholinergic innervation by means of 192-IgG-saporin (injected i.p. or i.c.v.) is able to interfere with experience-dependent plasticity.

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

Pain sensitivity following loss of cholinergic basal forebrain (CBF) neurons in the rat.

Vierck C, Yezierski R, Wiley R (2016) Pain sensitivity following loss of cholinergic basal forebrain (CBF) neurons in the rat. Neuroscience 319:23-34. doi: 10.1016/j.neuroscience.2016.01.038

Objective: There is a large amount of research on the involvement of cholinergic mechanisms on spinal transmission of pain signals, indicating that cholinergic agonists can attenuate this kind of pain. In contrast, some studies have shown affective reactions to pain are suppressed by cholinergic antagonists. The authors investigated the disagreement between reflexive and affective reactions.

Summary: Lesioned rats displayed decreased escape from thermal stimulation, as well as loss of the normal hyperalgesic effect of sound stress. Results indicate that the basal forebrain cholinergic system plays a role in central processing of pain.

Usage: Administration of 192-IgG-SAP with a 4-μg injection into the left lateral ventricle of rats. Animals were tested in temperature escape and sound stress models.

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

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