targeted-toxins

Dias MB, Nucci TB, Margatho LO, Antunes-Rodrigues J, Gargaglioni LH, Branco LG (2007) Raphe Magnus Nucleus is involved in ventilatory but not hypothermic response to CO2. J Appl Physiol 103(5):1780-1788. doi: 10.1152/japplphysiol.00424.2007

Summary: In this work the authors investigated the role that serotonergic neurons in the Raphe Magnus Nucleus (RMg) play in ventilatory and thermal responses to hypercapnia. 0.1 µl of 1 µM anti-SERT-SAP (Cat. #IT-23) was injected into the RMg of rats. Mouse IgG-SAP (Cat. #IT-18) was used as a control. Lesioned animals had a decreased ventilatory response to CO2, but hypercapnia-induced hypothermia was not affected. The data indicate that RMg serotonergic neurons contribute to CO2 ventilatory response but not to maintenance of ventilation.

Related Products: Anti-SERT-SAP (Cat. #IT-23), Mouse IgG-SAP (Cat. #IT-18)

Rinaman L, Dzmura V (2007) Experimental dissociation of neural circuits underlying conditioned avoidance and hypophagic responses to lithium chloride. Am J Physiol Regul Integr Comp Physiol 293(4):R1495-1503. doi: 10.1152/ajpregu.00393.2007

Summary: Lithium chloride (LiCl) is frequently used to study neural attributes of “sickness behavior.” Previous work by these authors showed that noradrenergic neurons (NA) in the nucleus of the solitary tract (NST) are involved in the inhibition of food uptake by cholecystokinin. Here, 20 ng total of anti-DBH-SAP (Cat. #IT-03) was injected into the NST of rats. Lesioned animals demonstrated significantly reduced inhibition of food intake in response to LiCl, but conditioned flavor avoidance was left intact.

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

Chambon C, Paban V, Manrique C, Alescio-Lautier B (2007) Behavioral and immunohistological effects of cholinergic damage in immunolesioned rats: Alteration of c-Fos and polysialylated neural cell adhesion molecule expression. Neuroscience 147:893-905. doi: 10.1016/j.neuroscience.2007.05.022

Summary: In this work the authors looked to expand the knowledge of molecular events and brain structure changes following cholinergic immunolesion. Rats were treated with bilateral injections of 192-IgG-SAP (Cat. #IT-01); 37.5 ng per side into the medial septum, and 75 ng per side into the nucleus basalis magnocellularis. 1 month after treatment behavioral deficits were drastic and cholinergic neurons had completely disappeared. Elevated levels of polysialylated neural cell adhesion molecule were temporarily able to compensate for the loss of cholinergic neurons. NOTE: material from Chemicon, Paris.

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

Garcia-Alloza M, Ferrara BJ, Dodwell SA, Hickey GA, Hyman BT, Bacskai BJ (2007) A limited role for microglia in antibody mediated plaque clearance in APP mice. Neurobiol Dis 28(3):286-292. doi: 10.1016/j.nbd.2007.07.019

Summary: Microglia are thought to play a key role in the clearance of amyloid-b (Ab) in Alzheimer’s disease. To examine this role the authors applied 30 µl of 0.5 mg/ml Mac-1-SAP (Cat. #IT-06) to the brain surface of mice for 20 minutes. The number of microglia and plaques was determined by counting of immunohistochemical samples. Results indicate that microglia play a minor role in clearing Ab plaques, although the interaction of microglia-mediated inflammation and anti-Ab antibodies appears to be vital in this process.

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

Mattsson A, Olson L, Svensson TH, Schilstrom B (2007) Cortical cholinergic deficiency enhances amphetamine-induced dopamine release in the accumbens but not in the striatum. Exp Neurol 208(1):73-79. doi: 10.1016/j.expneurol.2007.07.012

Summary: Previous data has implicated cholinergic dysfunction in the pathogenesis of schizophrenia. Here the authors investigated whether increased amphetamine-induced release of dopamine was a response to cortical cholinergic denervation. Rats received bilateral 0.067 µg injections of 192-IgG-SAP (Cat. #IT-01) into the nucleus basalis magnocellularis, and dopamine release was monitored in the nucleus accumbens and striatum. Surprisingly, the increased dopamine release was not linked to loss of cholinergic neurons, but to blocking of muscarinic receptors.

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

Bavis RW, Powell FL, Bradford A, Hsia CCW, Peltonen JE, Soliz J, Zeis B, Fergusson ED, Fu Z, Gassmann M, Kim CB, Maurer J, McGuire M, Miller BM, O’Halloran KD, Paul RJ, Reid SG, Rusko HK, Tikkanen HO, Wilkinson KA (2007) Respiratory plasticity in response to changes in oxygen supply and demand. Integ and Comp Biol 47(4):532-551. doi: 10.1093/icb/icm070

Summary: This paper covers data presented at the First Annual Congress of Respiratory Biology. One of the subjects discussed is the use of SP-SAP (Cat. #IT-07) to elucidate the role of central chemoreceptors in the nucleus tractus solitarius during ventilatory acclimatization to hypoxia.

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

Q: Your targeted toxin data sheet gives the following instruction for disposal: “Care in disposal is mandatory; autoclaving or exposure to 1 M sodium hydroxide will inactivate the material. All labware that comes into contact with this material should be likewise treated.” I am wondering if I can deactivate saporin by using 10% bleach or if everything has to be autoclaved?

A: Yes, you can use bleach to deactivate saporin prior to disposal or reuse of labware. If you are using nanogram quantities, these are too low to be toxic, so you can discard as you do your other non-hazardous laboratory materials without fear.

Related: Targeted Toxins

Shen FM, Wang J, Ni CR, Yu JG, Wang WZ, Su DF (2007) Ketanserin-induced baroreflex enhancement in spontaneously hypertensive rats depends on central 5-HT(2A) receptors. Clin Exp Pharmacol Physiol 34:702-707. doi: 10.1111/j.1440-1681.2007.04626.x

Summary: Ketanserin is an anytihypertensive drug that effectively lowers blood pressure, decreases blood pressure variability, and enhances blood pressure response in spontaneously hypertensive rats. Using the fact that ketanserin is a selective 5-HT2A antagonist the authors investigated which of these effects utilized the 5-HT2A receptor. Following a 5 nmol ventricular injection of anti-SERT-SAP (Cat. #IT-23) the blood pressure parameters modified by ketanserin were monitored. The data suggest that the baroreflex sensitivity-enhancing effects of ketanserin use the 5-HT2A pathway, but antihypertensive effects follow a different route.

Related Products: Anti-SERT-SAP (Cat. #IT-23)

Rahman W, Sikander S, Suzuki R, Hunt SP, Dickenson AH (2007) Superficial NK1 expressing spinal dorsal horn neurones modulate inhibitory neurotransmission mediated by spinal GABA(A) receptors. Neurosci Lett 419:278-283. doi: 10.1016/j.neulet.2007.04.039

Summary: It has been shown that elimination of lamina 1 NK1 receptor-expressing neurons affects pain behaviors. The authors investigated whether eliminating these neurons would alter GABAergic spinal inhibitory systems. Rats received 10-µl injections of 10-µM SP-SAP (Cat. #IT-07) into the L4-5 regions. Data generated by electrical and mechanical stimuli suggest that although GABAergic transmission is dependent on NK1 receptor-expressing neurons, loss of these cells results in a decrease in spinal cord excitability.

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

Gibbs RB (2007) Estradiol enhances DMP acquisition via a mechanism not mediated by turning strategy but which requires intact basal forebrain cholinergic projections. Horm Behav 52:352-359. doi: 10.1016/j.yhbeh.2007.05.011

Summary: Estradiol appears to enhance cholinergic projections to the hippocampus and frontal cortex as shown by tests of response patterns and strategy in rats. The author tested whether this affect was involved with turning strategy, defined as which arm was chosen first in a T-maze. 0.22 µg injections of 192-IgG-SAP (Cat. #IT-01) were made into the medial septum of rats. Lesioned animals utilized a persistent turning strategy; they always chose the same arm of the maze first, even after the administration of estradiol. These data suggest that although the effects of estradiol are not linked to turning strategy, estradiol does interact with the cholinergic system.

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