saporin

Tronson NC, Schrick C, Guzman YF, Huh KH, Srivastava DP, Penzes P, Guedea AL, Gao C, Radulovic J (2009) Segregated populations of hippocampal principal CA1 neurons mediating conditioning and extinction of contextual fear. J Neurosci 29:3387-3394. doi: 10.1523/JNEUROSCI.5619-08.2009

Summary: This work examines what cell groups are responsible for controlling contextual fear. 180 ng of mu p75-SAP (Cat. #IT-16) was injected into the medial septum of mice. Saporin (Cat. #PR-01) was used as a control. In lesioned animals, fear extinction was lost along with the cholinergic input from the medial septum, while fear conditioning was left intact.

Related Products: mu p75-SAP (Cat. #IT-16), Saporin (Cat. #PR-01)

Rivat C, Vera-Portocarrero LP, Ibrahim MM, Mata HP, Stagg NJ, De Felice M, Porreca F, Malan TP (2009) Spinal NK-1 receptor-expressing neurons and descending pathways support fentanyl-induced pain hypersensitivity in a rat model of postoperative pain. Eur J Neurosci 29:727-737. doi: 10.1111/j.1460-9568.2009.06616.x

Summary: Opioids activate hyperalgesia and allodynia. The authors test the hypothesis that NK-1 receptor-containing ascending pathways play a role in sensitivity to fentanyl. Rats received an intrathecal injection of SP-SAP (Cat. #IT-07), and controls received saporin (Cat. #PR-01). The data indicate that these ascending pathways have a role in fentanyl-induced hyperalgesia.

Related Products: SP-SAP (Cat. #IT-07), Saporin (Cat. #PR-01)

Hess PR, Buntzman AS, Murray SL, Young EF, Frelinger JA (2009) Featured Article: Selective deletion of CD8+ T cells by saporin-coupled MHC class I tetramers. Targeting Trends 10(1)

Related Products: Streptavidin-ZAP (Cat. #IT-27), Saporin Goat Polyclonal, affinity-purified FITC-labeled (Cat. #AB-15APFL)

Read the featured article in Targeting Trends.

See Also:

• Hess PR et al. Selective deletion of antigen-specific CD8+ T cells by MHC class I tetramers coupled to the type I ribosome-inactivating protein saporin. Blood 109:3300-3307, 2007.

Zhang W, Gardell S, Zhang D, Xie JY, Agnes RS, Badghisi H, Hruby VJ, Rance N, Ossipov MH, Vanderah TW, Porreca F, Lai J (2009) Neuropathic pain is maintained by brainstem neurons co-expressing opioid and cholecystokinin receptors. Brain 132:778-787. doi: 10.1093/brain/awn330

Summary: It has been hypothesized that a subset of rostral ventromedial medulla (RVM) neurons co-expressing the cholecystokinin type 2 receptor and the mu-opioid receptor are responsible for the maintenance of neuropathic pain. Rats were treated with 50-ng bilateral RVM injections of Dermorphin-SAP (Cat. #IT-12), CCK-SAP (Cat. #IT-31), or saporin (Cat. #PR-01) as a control. Lesion of the RVM neurons prevented hyperalgesia in response to CCK treatment, and shortened abnormal pain states caused by sciatic nerve injury.

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), CCK-SAP (Cat. #IT-31), Saporin (Cat. #PR-01)

Bee LA, Dickenson AH (2008) Descending facilitation from the brainstem determines behavioural and neuronal hypersensitivity following nerve injury and efficacy of pregabalin. Pain 140:209-223. doi: 10.1016/j.pain.2008.08.008

Summary: Rostral ventromedial medulla (RVM) facilitatory On cells are thought to be involved in the mechanisms that control chronic pain. Dermorphin-SAP (Cat. #IT-12, 3 pmol injected into the RVM of rats) was used to examine how mu-opioid receptor expressing facilitatory cells fit into this circuit. Saporin (Cat. #PR-01) was used as a control. The results show that activity in the RVM may influence the outcome of nerve injury.

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Saporin (Cat. #PR-01)

Pedrino GR, Rosa DA, Korim WS, Cravo SL (2008) Renal sympathoinhibition induced by hypernatremia: Involvement of A1 noradrenergic neurons. Auton Neurosci 142(1-2):55-63. doi: 10.1016/j.autneu.2008.06.006

Summary: A1 noradrenergic neurons in the caudal ventrolateral medulla (CVLM) are thought to contribute to body fluid homeostasis and cardiovascular regulation. In order to examine the role these neurons play on inhibition of renal sympathetic nerve activity (RSNA) induced by hypertonic saline infusion, rats received 6.3 ng of anti-DBH-SAP (Cat. #IT-03) into the CVLM. Saporin (Cat. #PR-01) was used as a control. Animals treated with anti-DBH-SAP displayed lengthened duration of the pressor response and sustained RSNA.

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

Colombari DS, Pedrino GR, Freiria-Oliveira AH, Korim WS, Maurino IC, Cravo SL (2008) Lesions of medullary catecholaminergic neurons increase salt intake in rats. Brain Res Bull 76:572-578. doi: 10.1016/j.brainresbull.2008.04.001

Summary: Catecholaminergic neurons in the caudal ventrolateral medulla (CVLM) are thought to contribute to cardiovascular regulation and body fluid homeostasis. Bilateral 6.3-ng injections of anti-DBH-SAP (Cat. #IT-03) were administered to the CVLM of rats. Saporin (Cat. #PR-01) was used as a control. After lesioning and challenge with either furosemide/captopril or water deprivation, intake of 0.3 M NaCl and water were observed. The data indicate medullary catecholaminergic neurons play an inhibitory role in sodium appetite.

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

McKay LC, Feldman JL (2008) Unilateral ablation of preBotzinger Complex disrupts breathing during sleep but not wakefulness. Am J Respir Crit Care Med 178(1):89-95. doi: 10.1164/rccm.200712-1901OC

Summary: Previous data has shown that ablation of preBötzinger complex (preBötC) neurokinin 1 expressing (NK1R) neurons disrupts breathing patterns in both sleep and wakefulness. The initial disruption is during sleep, with the eventual onset of ataxic breathing while the animals are awake. Here rats received a unilateral injection of SP-SAP (Cat. #IT-07, 6.7 ng) into the left preBötC. SP plus unconjugated saporin (Cat. #PR-01) was used as a control. Unilaterally treated rats did not develop disrupted breathing patterns during wakefulness.

Related Products: SP-SAP (Cat. #IT-07), Saporin (Cat. #PR-01)

Zinck ND, Downie JW (2008) IB4 afferent sprouting contributes to bladder dysfunction in spinal rats. Exp Neurol 213:293-302. doi: 10.1016/j.expneurol.2008.06.006

Summary: Spinal cord injury can cause inefficient bladder function, but the direct cause is not well understood. Most work has focused on afferent neurons that contain CGRP and respond to NGF. Here the authors investigate the role of isolectin B4 (IB4)-expressing neurons that are supported by GDNF. Rats received intrathecal injections of either 2.4 µg IB4-SAP (Cat. #IT-10) or 3 µg control saporin (Cat. #PR-01). The data suggest that IB4-afferent sprouting is involved in bladder dysfunction following spinal cord transection.

Related Products: IB4-SAP (Cat. #IT-10), Saporin (Cat. #PR-01)

Darmani NA, Wang Y, Abad J, Ray AP, Thrush GR, Ramirez J (2008) Utilization of the least shrew as a rapid and selective screening model for the antiemetic potential and brain penetration of substance P and NK1 receptor antagonists. Brain Res 1214:58-72. doi: 10.1016/j.brainres.2008.03.077

Summary: This work investigated the role of central tachykinin NK1 receptors in delayed phase vomiting caused by chemotherapeutics. Least shrews received 1.2 mg/kg intraperitoneal injections of SSP-SAP (Cat. #IT-11). Saporin (Cat. #PR-01) and blank-SAP (Cat. #IT-21) were used as controls. In response to administration of a NK1 receptor agonist lesioned animals vomited less than the control group, indicating an important role for NK1 receptors in emesis.

Related Products: SSP-SAP (Cat. #IT-11), Saporin (Cat. #PR-01), Blank-SAP (Cat. #IT-21)