targeted-toxins

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)

Schreihofer AM, Guyenet PG (2000) Sympathetic reflexes after depletion of bulbospinal catecholaminergic neurons with anti-DBH-saporin. Am J Physiol Regul Integr Comp Physiol 279:R729-R742. doi: 10.1152/ajpregu.2000.279.2.R729

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

Read the featured article in Targeting Trends.

Herron P, Schweitzer JB (2000) Effects of cholinergic depletion on neural activity in different laminae of the rat barrel cortex. Brain Res 872:71-76. doi: 10.1016/s0006-8993(00)02454-9

Summary: 192-SAP (Cat. #IT-01) 8.0 µg/300 g body weight, nucleus basalis of Meynert

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

Tremere LA, Pinaud R, Grosche J, Hartig W, Rasmusson DD (2000) Antibody for human p75 LNTR identifies cholinergic basal forebrain of non-primate species. NeuroReport 11(10):2177-2183. doi: 10.1097/00001756-200007140-00023 PMID: 10923666

Summary: 192-SAP (Cat. #IT-01) is a highly successful reagent for eliminating cholinergic neurons in rats. Because the targeting antibody only recognizes rat p75, it is unable to be used in other species. Tremere et al. have stained basal forebrain sections with ME20.4, a monoclonal antibody to human p75 (Cat. #AB-N07) and found excellent cross-reactivity in dog, raccoon, cat, pig and rabbit. The authors state that an ME20.4-saporin conjugate could be used to produce cholinergic basal forebrain lesions in several species.

Related Products: NGFr (ME20.4, p75) Mouse Monoclonal (Cat. #AB-N07), 192-IgG-SAP (Cat. #IT-01)

Gill TM, Sarter M, Givens B (2000) Sustained visual attention performance-associated prefrontal neuronal activity: evidence for cholinergic modulation. J Neurosci 20:4745-4757. doi: 10.1523/JNEUROSCI.20-12-04745.2000

Summary: Preliminary evidence suggests that demands on attention levels are associated with changes in levels of cortical acetylcholine. Gill et al. used .05 µg 192-Saporin (Cat. #IT-01) by intracortical infusion to demonstrate the role cholinergic neurons play in the ability of rats to pay attention. The researchers monitored medial prefrontal cortex (MPC) activity in the rat brain before and after elimination of cholinergic neurons with 192-Saporin. The results suggest that the cholinergic inputs to the MPC influence the increases of neuronal activity associated with paying attention.

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

Pappas BA, Nguyen T, Brownlee B, Tanasoiu D, Fortin T, Sherren N (2000) Ectopic noradrenergic hyperinnervation does not functionally compensate for neonatal forebrain acetylcholine lesion. Brain Res 867:90-99. doi: 10.1016/s0006-8993(00)02263-0

Summary: Removal of cholinergic forebrain neurons in the neonatal rat causes an ingrowth of hippocampal material to the affected area. The behavioral effect of this treatment increases working, but not reference memory errors on the radial arm maze. Pappas et al. used 300 ng 192-Saporin (Cat. #IT-01) by i.c.v. injection to lesion the forebrain of 1- to 3-day old rats coupled with a 6-OHDA lesion to remove hippocampal ingrowths in order to investigate whether these neurons can compensate for cholinergic function in memory. Their results indicate noradrenergic neurons from the hippocampus do not functionally compensate for loss of CBF neurons even though losses of these neurons did not drastically affect the behavior of these animals.

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

Ferencz I, Leanza G, Nanobashvili A, Kokaia M, Lindvall O (2000) Basal forebrain neurons suppress amygdala kindling via cortical but not hippocampal cholinergic projections in rats. Eur J Neurosci 12:2107-2116. doi: 10.1046/j.1460-9568.2000.00077.x

Summary: Cholinergic mechanisms have been implicated in human epilepsy, possibly in the role of seizure suppression. Ferencz et al. used 2.5 µg 192-Saporin (Cat. #IT-01) by i.c.v. injection to investigate the effect of eliminating cholinergic projections to the hippocampal formation and cerebral cortex on the induction of epilepsy through electrical stimulation of the rat brain. The researchers used the specificity of 192-Saporin to determine that the loss of specific projections to the amygdala accelerates development of seizures. The hippocampus does not influence this process.

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

Angner RT, Kelly RM, Wiley RG, Walsh TJ, Reuhl KR (2000) Preferential destruction of cerebellar Purkinje cells by OX7-saporin. Neurotoxicol 21:395-403.

Summary: Purkinje cells function as inhibitors and are the sole output of the cerebellar cortex. Angner et al. eliminate these cells in rats with 1-2 µg OX7-SAP (Cat. #IT-02), an immunotoxin that binds the Thy 1.1 antigen. The treated rats show effects of loss of inhibitory control, including a time-dependent increase in motor activity and decreased motor coordination.

Related Products: OX7-SAP (Cat. #IT-02)

Murakami K, Yokofujita J, Kuroda M (2000) [Non-cholinergic projections from basal forebrain to medial limbic cortex of rat]. Kaibogaku Zasshi 75:285-297.

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

Barefoot HC, Baker HF, Ridley RM (2000) Synergistic effects of unilateral immunolesions of the cholinergic projections from the basal forebrain and contralateral ablations of the inferotemporal cortex and hippocampus in monkeys. Neuroscience 98(2):243-251. doi: 10.1016/s0306-4522(00)00131-7

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