2004 Targeting Trends Review

Madden CJ, Sved AF (2003) Rostral ventrolateral medulla C1 neurons and cardiovascular regulation. Cell Mol Neurobiol 23(4-5):739-749. doi: 10.1023/a:1025000919468

Summary: The authors review the use of anti-DBH-SAP (Cat. #IT-03) to study the role of C1 neurons within the rostral ventromedial medulla in cardiovascular regulation. This immunotoxin specifically removes C1 neurons containing dopamine beta-hydroxylase.

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

Wiley RG, Harrison MB, Levey A, Lappi DA (2003) Destruction of midbrain dopaminergic neurons by using an immunotoxin to the dopamine transporter. Cell Mol Neurobiol 23:839-850. doi: 10.1023/a:1025065306264

Summary: The authors demonstrate the effective and specific removal of neurons expressing the dopamine transporter in the substantia nigra pars compacta and the ventral tegmental area with anti-DAT-SAP (Cat. #IT-25). A 21-µg icv injection produced a highly significant loss of midbrain dopaminergic neurons, creating a useful model for Parkinson’s disease.

Related Products: Anti-DAT-SAP (Cat. #IT-25)

Dudkin KN, Chueva IV, Makarov FN (2003) [Interaction between sensory and cognitive processes in visual recognition: the role of the associative areas of the cerebral cortex] Russian. Ross Fiziol Zh Im I M Sechenova 89(10):1226-1239.

Summary: The authors used ME20.4-SAP(Cat. #IT-15).

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

I’Anson H, Sundling LA, Roland SM, Ritter S (2003) Immunotoxic destruction of distinct catecholaminergic neuron populations disrupts the reproductive response to glucoprivation in female rats. Endocrinology 144(10):4325-4331. doi: 10.1210/en.2003-0258

Summary: The authors hypothesized that hindbrain catcholamine neurons suppressed estrous cycles during chronic glucoprivation as an extension of their role in glucoprivic feeding. 42-ng bilateral injections of anti-DBH-SAP (Cat. #IT-03) were made into the paraventricular nucleus of female rats. Lesioned rats demonstrated inhibition of reproductive function during chronic glucose deficit, but not when a normal amount of glucose was available.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Saporin (Cat. #PR-01)

Tomaszewicz M, Rossner S, Schliebs R, Cwikowska J, Szutowicz A (2003) Changes in cortical acetyl-CoA metabolism after selective basal forebrain cholinergic degeneration by 192IgG-saporin. J Neurochem 87(2):318-324. doi: 10.1046/j.1471-4159.2003.01983.x

Objective: To investigate whether cortical cholinergic input affects acetyl-CoA metabolism in cholinoceptive cortical target regions.

Summary: Alzheimer’s disease subjects often show deficits in cerebral glucose metabolism. The data show evidence of differential distribution of acetyl-CoA in subcellular compartments of cholinergic and non-cholinergic nerve terminals.

Usage: Rats received 4 µg 192-IgG-SAP (Cat. #IT-01) into the left lateral ventricle.

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

Gadd CA, Murtra P, De Felipe C, Hunt SP (2003) Neurokinin-1 receptor-expressing neurons in the amygdala modulate morphine reward and anxiety behaviors in the mouse. J Neurosci 23(23):8271-8280. doi: 10.1523/JNEUROSCI.23-23-08271.2003

Summary: Mice lacking the neurokinin-1 (NK-1) receptor are insensitive to opiates in models of drug abuse. To assess what areas of the brain may be involved in this process, the authors used 1.0-µl injections of 1.0 µM SP-SAP (Cat. #IT-07) to eliminate NK-1 receptor-positive neurons in the nucleus accumbens, dorsomedial caudate putamen or amygdala of mice. Only mice with amygdala lesions displayed behavior comparable to NK-1 receptor knockout mice—increase in anxiety-like behavior, reduction in stimulant effect of morphine. These data suggest that the amygdala plays an important role in anxiety behaviors and the response to opiates.

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

Gardell LR, Vanderah TW, Gardell SE, Wang R, Ossipov MH, Lai J, Porreca F (2003) Enhanced evoked excitatory transmitter release in experimental neuropathy requires descending facilitation. J Neurosci 23(23):8370-8379. doi: 10.1523/JNEUROSCI.23-23-08370.2003

Summary: The authors examine whether afferent discharge produced by nerve injury and central changes in experimental neuropathic pain might interact at the spinal level. Rats were treated with 48 ng of dermorphin-SAP (Cat. #IT-12) and various markers for neuropathic pain were evaluated. The results link several consequences of the post-injury state, including support for increased afferent input as a driving force for neuropathic pain.

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

Birthelmer A, Lazaris A, Riegert C, Marques Pereira P, Koenig J, Jeltsch H, Jackisch R, Cassel JC (2003) Does the release of acetylcholine in septal slices originate from intrinsic cholinergic neurons bearing p75NTR receptors? A study using 192 IgG-saporin lesions in rats. Neuroscience 122(4):1059-1071. doi: 10.1016/j.neuroscience.2003.09.001

Summary: The authors used 0.8 µg injections of 192-Saporin (Cat. #IT-01) into the medial septum and diagonal band of Broca to investigate whether release of acetylcholine was due to neurons expressing the p75 NTR.

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

Scattoni ML, Calamandrei G, Ricceri L (2003) Neonatal cholinergic lesions and development of exploration upon administration of the GABAa receptor agonist muscimol in preweaning rats. Pharmacol Biochem Behav 76(2):213-221. doi: 10.1016/s0091-3057(03)00191-6

Summary: The authors investigated GABAergic development in young rats lesioned with two 0.42-ng injections of 192-Saporin (Cat. #IT-01) into the third ventricle. The rats were then treated with the GABA agonist muscimol chloride and observed during locomotor and exploration tests. No change was noted in GABAergic agonist reactivity in lesioned animals.

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

Kanai T, Uraushihara K, Okazawa A, Hibi T, Watanabe M (2003) Macrophage-derived IL-18 targeting for the treatment of Crohn’s disease. Curr Drug Targets Inflamm Allergy 2(2):131-136. doi: 10.2174/1568010033484250

Summary: A single intravenous injection of Mac-1-SAP (Cat. #IT-06) significantly reduced the amount of intestinal inflammation in a 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis model.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)