References

Schreihofer AM, Stornetta RL, Guyenet PG (2000) Regulation of sympathetic tone and arterial pressure by rostral ventrolateral medulla after depletion of C1 cells in rat. J Physiol 529(1):221-236. doi: 10.1111/j.1469-7793.2000.00221.x

Summary: The rostral ventrolateral medulla (RVLM) controls and maintains basal sympathetic vasomotor tone, and is also vital to many sympathetic reflexes. Sympathetic nerve activity and arterial pressure correlate with the C1 adrenergic neurons in the RVLM, but there are also non-catecholaminergic neurons present. Schreihofer et al. used anti-DBH-SAP (Cat. #IT-03) to eliminate the C1 cells of the RVLM to investigate the non-catecholaminergic neuron contribution to vasomotor tone. Their data indicate C1 cells are necessary for full expression of sympathoexitatory responses generated by the RVLM.

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

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Tierney ML, Unwin N (2000) Electron microscopic evidence for the assembly of soluble pentameric extracellular domains of the nicotinic acetylcholine receptor. J Mol Biol 303(2):185-196. doi: 10.1006/jmbi.2000.4137 PMID: 11023785

Related Products: Nicotinic Acetylcholine Receptor alpha 1 (mAb 35) Rat Monoclonal (Cat. #AB-N36)

Gu Z, Wortwein G, Yu J, Perez-Polo JR (2000) Model for aging in the basal forebrain cholinergic system. Antiox Redox Signal 2(3):437-447. doi: 10.1089/15230860050192215

Summary: A wide range of evidence indicates that cholinergic neurons play a role in memory and learning. Loss of these neurons is seen both in aged subjects and Alzheimer’s Disease patients. The authors discuss the use of 192-Saporin (Cat. #IT-01) to model this phenomenon. Many lesioning methods have been developed, including fimbria-fornix transections, mechanical lesions with radiofrequency or electrolysis, and intracerebral injections of excitotoxins. Information obtained through these methods suffers because non-cholinergic neurons are depleted as well as the desired cholinergic neurons. 192-Saporin provides a solution by specifically targeting and eliminating cholinergic neurons expressing p75 in the basal forebrain, closely mimicking a key component of aging.

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

Beach T (2000) Featured Article: CBF lesioning in rabbits. Targeting Trends 1(1)

Related Products: ME20.4-SAP (Cat. #IT-15)

Read the featured article in Targeting Trends.

See Also:

• Beach TG et al. Cholinergic deafferentation of the rabbit cortex: a new animal model of Abeta deposition. Neurosci Lett 283:9-12, 2000.

Lappi DA, Wiley RG (2000) Entering through the doors of perception: characterization of a highly selective Substance P receptor-targeted toxin. Neuropeptides 34(5):323-328. doi: 10.1054/npep.2000.0827

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12)

Silveira DC, Holmes GL, Schachter SC, Geula C, Schomer DL (2000) Increased susceptibility to generalized seizures after immunolesions of the basal forebrain cholinergic neurons in rats. Brain Res 878:223-227. doi: 10.1016/s0006-8993(00)02703-7

Usage: 192-SAP (Cat. #IT-01), 4 µg intracerebroventricular injection

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

Taylor BK, Roderick RE, Basbaum AI (2000) Brainstem noradrenergic control of nociception is abnormal in the spontaneously hypertensive rat. Neurosci Lett 291:139-142. doi: 10.1016/s0304-3940(00)01389-6

Usage: anti-DBH-SAP (Cat. #IT-03), 5 µg

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

McNerney ME, Pardi D, Pugh PC, Nai Q, Margiotta JF (2000) Expression and channel properties of alpha-bungarotoxin-sensitive acetylcholine receptors on chick ciliary and choroid neurons. J Neurophysiol 84(3):1314-1329. doi: 10.1152/jn.2000.84.3.1314 PMID: 10980005

Related Products: Nicotinic Acetylcholine Receptor alpha 1 (mAb 35) Rat Monoclonal (Cat. #AB-N36)

Wiley RG (2000) Neuropeptide-toxin conjugates in pain research and treatment. (Review). Reg Anesth Pain Med 25(5):546-548. doi: 10.1053/rapm.2000.8457

Summary: Several lines of evidence indicate dorsal horn neurons that respond to substance P (SP) play a role in nociception. Wiley discusses the attributes of SP-SAP (Cat. #IT-07), a targeted toxin that eliminates cells expressing the neurokinin-1 receptor. Animals treated with this material using a lumbar intrathecal injection show a decrease in both hyperalgesia and allodynia in several pain models. The success of SP-SAP indicates that other neuropeptides, hormones, and growth factors would be useful as targeted toxins.

Related Products: SP-SAP (Cat. #IT-07)

Bannerman P, Nichols W, Puhalla S, Oliver T, Berman M, Pleasure D (2000) Early migratory rat neural crest cells express functional gap junctions: Evidence that neural crest cell survival requires gap junction function. J Neurosci Res 61:605-615. doi: 10.1002/1097-4547(20000915)61:6<605::AID-JNR4>3.0.CO;2-U PMID: 10972957

Summary: Gap junctions are vital for intercellular communication, especially during development. Neural crest cells develop into several types of neural cells, often migrating as a mass of cells to their final destinations. Bannerman et al. use the anti-p75 antibody (Cat. #AB-N01) to confirm the presence of p75 in neural crest cells. The authors examine how crucial survival signals are communicated during migration and demonstrate that interfering with gap junction formation causes death of neural crest cells.

Related Products: NGFr (mu p75) Rabbit Polyclonal (Cat. #AB-N01)