References

Ferreira G, Meurisse M, Tillet Y, Lévy F (2001) Distribution and co-localization of choline acetyltransferase and p75 neurotrophin receptors in the sheep basal forebrain: implications for the use of a specific cholinergic immunotoxin. Neuroscience 104(2):419-439. doi: 10.1016/s0306-4522(01)00075-6 PMID: 11377845

Summary: ME20.4 is a monoclonal antibody (Cat. #AB-N07) that has been shown to bind the p75 receptor in rabbit, sheep, dog, cat, raccoon, pig, and several primate species. Ferreira et al. investigate ME20.4-SAP (bilateral, 150 µl per ventricle, 50-150 µg total; Cat. #IT-15) use in sheep to assess distribution and localization of p75. The authors demonstrate 80-95% loss of basal forebrain cholinergic neurons and acetylcholinesterase-positive fibers in the hippocampus, olfactory bulb, and entorhinal cortex.

Related Products: ME20.4-SAP (Cat. #IT-15), NGFr (ME20.4, p75) Mouse Monoclonal (Cat. #AB-N07)

Sidebotham EL, Woodward MN, Kenny SE, Lloyd DA, Vaillant CR, Edgar DH (2001) Assessment of protein gene product 9.5 as a marker of neural crest-derived precursor cells in the developing enteric nervous system. Pediatr Surg Int 17:304-307. doi: 10.1007/s003830100599 PMID: 11409167

Related Products: Antibody to NGFR (Cat. #AB-N02)

Hartlage-Rübsamen M, Schliebs R (2001) Sequential upregulation of cell adhesion molecules in degenerating rat basal forebrain cholinergic neurons and in phagocytotic microglial cells. Brain Res 897(1-2):20-26. doi: 10.1016/s0006-8993(01)02093-5

Summary: Neurodegeneration, found in brain disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, is marked by a significant microglial response. This microglial activation is characterized by increased migratory activity and potential cytotoxic action on injured neurons. The interaction of microglial cells with degenerating axons and neural somata is known to be mediated by expression of cell adhesion molecules. The authors use a single intracerebroventricular injection of 192-Saporin (4 µg; Cat. #IT-01) to initiate neurodegeneration of choline acetyltransferase-immunoreactive neurons and follow the expression of two cell adhesion molecules, ICAM-1 and LFA-1, using immunohisto-chemistry. The results indicate that these adhesion molecules may function as intercellular recognition signals through which degenerating cholinergic neurons actively participate in their own targeting and removal by microglia.

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

de Rosa E, Hasselmo ME, Baxter MG (2001) Contribution of the cholinergic basal forebrain to proactive interference from stored odor memories during associative learning in rats. Behav Neurosci 115(2):314-327.

Summary: Proactive interference (PI) is the damaging effect of previously learned information on the acquisition of new, related information. Human patients with basal forebrain (BF) damage due to aneurysms are sensitive to PI. The authors administered 192-Saporin (Cat. #IT-01) to the horizontal limb of the diagonal band of Broca (two 0.2-µl injections of 0.175 µg/µl in each hemisphere) in rats and evaluated performance in an olfactory discrimination task. The treated rats had more difficulty acquiring an overlapping odor pair when muscarinic receptors were blocked by scopalomine. These results indicate that cholinergic neurons have a role in the modulation of PI in associative learning.

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

Sarter M, Givens B, Bruno JP (2001) The cognitive neuroscience of sustained attention: where top-down meets bottom-up. Brain Res Brain Res Rev 35(2):146-160. doi: 10.1016/s0165-0173(01)00044-3

Summary: The findings from human and animal studies provide the basis for a relatively precise description of the neuronal circuits mediating sustained attention, and the dissociation between these circuits and those mediating the ‘arousal’ components of attention.

Usage: The absence of attentional effects of infusions of 192-IgG-SAP into the primary and secondary visual cortex supports the notion that performance in such a task cannot be attributed solely to the ACh-mediated enhancement of the primary processing of sensory stimuli serving as targets in this task.

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

See Also:

• Gill TM et al. Sustained visual attention performance-associated prefrontal neuronal activity: evidence for cholinergic modulation. J Neurosci 20:4745-4757, 2000.

Zheng F, Khanna S (2001) Selective destruction of medial septal cholinergic neurons attenuates pyramidal cell suppression, but not excitation in dorsal hippocampus field CA1 induced by subcutaneous injection of formalin. Neuroscience 103(4):985-998. doi: 10.1016/s0306-4522(01)00006-9

Summary: Previously, the authors have shown that an injection of formalin in the hindpaw of rats will excite a select population of CA1 pyramidal cells within a larger suppressed population. This response is accompanied by increased theta activation. The authors selectively eliminated medial septal cholinergic neurons using 192-Saporin (0.4 µl; Cat. #IT-01) to investigate the role of these neurons in response to a persistent noxious stimulus such as a formalin injection. The data indicate a CA1 network modulated by cholinergic neurons in the medial septal region may influence pyramidal cell theta and pyramidal cell suppression.

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

Deuchars J, Deuchars S (2001) It’s enough to raise your blood pressure!. Trends Neurosci 24(4):200. doi: 10.1016/s0166-2236(00)01800-2

Summary: The authors review studies completed by Schreihofer and Guyenet using anti-DBH-SAP (Cat. #IT-03) to eliminate C1 adrenergic neurons. The results show that, although C1 neurons play a role in some sympathoexcitatory responses, they are probably not responsible for maintaining sympathetic tone.

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

Sarter M, Bruno JP, Miner LA, McGaughy J (2000) Development of a method for intraparenchymal infusions of 192 IgG-Saporin: a comment on Pizzo et al. (1999) [letter; comment]. J Neurosci Methods 96:169-170. doi: 10.1016/s0165-0270(99)00196-x PMID: 10720682

Summary: Letter pertaining to use of 192-SAP

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

See Also:

• Pizzo DP et al. Intraparenchymal infusions of 192 IgG-saporin: development of a method for selective and discrete lesioning of cholinergic basal forebrain nuclei. J Neurosci Methods 91:9-19, 1999.

Salhany JM, Cordes KS, Sloan RL (2001) Characterization of immunoglobulin binding to isolated human erythrocyte membranes: evidence for selective, temperature-induced binding of naturally occurring autoantibodies to the cytoskeleton. Biochim Biophys Acta 1511(1):168-180. doi: 10.1016/s0005-2736(01)00280-2 PMID: 11248215

Related Products: 192-IgG Mouse Monoclonal, Alexa488-labeled (Cat. #AB-N43FLA)

Ritter S, Bugarith K, Dinh TT (2001) Immunotoxic destruction of distinct catecholamine subgroups produces selective impairment of glucoregulatory responses and neuronal activation. J Comp Neurol 432(2):197-216. doi: 10.1002/cne.1097

Summary: Control of regulatory responses to low glucose levels in the brain have been linked to catecholaminergic neurons. Studies of these neurons have been hindered by the lack of a selective and precise lesioning agent. Ritter et al. use anti-DBH-SAP (Cat. #IT-03) to create very precise lesions of catecholamine neurons in the paraventricular nucleus of the hypothalamus and spinal cord. Injection of anti-DBH-SAP into the spinal cord eliminates cells with caudal projections while injection into the paraventricular nucleus of the hypothalamus eliminated cells with rostral projections. This ability to selectively eliminate very specific subpopulations of cells is a valuable characteristic in dissecting neuronal function.

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