targeted-toxins

Heldmann U, Mine Y, Kokaia Z, Ekdahl CT, Lindvall O (2011) Selective depletion of Mac-1-expressing microglia in rat subventricular zone does not alter neurogenic response early after stroke. Exp Neurol 229(2):391-398. doi: 10.1016/j.expneurol.2011.03.005

Summary: One result of ischemic stroke is migration of newly formed neuroblasts into the injured area from the subventricular zone (SVZ). The authors investigated the role of microglia, which also accumulate in the SVZ after stroke, in this process. Rats received 5-µg or 10-µg intracerebroventricular injections of Mac-1-SAP (Cat. #IT-33) with varying schedules as to injection and sacrifice. The data indicate that the presence of microglia after stroke does not affect the number or migration of neuroblasts from the SVZ.

Related Products: Mac-1-SAP rat (Cat. #IT-33)

Ocampo-Garces A, Ibanez F, Perdomo G, Torrealba F (2011) Orexin-B-saporin lesions in the lateral hypothalamus enhance photic masking of rapid eye movement sleep in the albino rat. J Sleep Res 20:3-11. doi: 10.1111/j.1365-2869.2010.00864.x

Summary: Photic masking occurs when photic input to the retina interferes with REM sleep. Rats that received 200 ng of orexin-SAP (Cat. #IT-20) into the lateral hypothalamus experienced dramatically less REM sleep during normal light cycles. Placing them in a skeleton photoperiod (brief pulses of light, one in the morning and one in the evening), however, caused REM sleep during the rest phase to return to normal. This data suggests that photic masking may explain some effects of narcolepsy and cataplexy.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Paban V, Chambon C, Farioli F, Alescio-Lautier B (2011) Gene regulation in the rat prefrontal cortex after learning with or without cholinergic insult. Neurobiol Learn Mem 95(4):441-452. doi: 10.1016/j.nlm.2011.02.005

Summary: Microarray technology was used to screen gene expression in a model of attention and memory deficit. Rats received bilateral injections of 192-IgG-SAP (Cat. #IT-01) into the medial septum and nucleus basalis magnocellularis (37.5 ng per side and 75 ng per side respectively). Gene expression in memory loss following the lesion was defined by one cluster related to cytoskeleton organization and proliferation, and glial and vascular remodeling. These are processes associated with brain repair after injury.

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

Rennie K, Frechette M, Pappas BA (2011) The effects of neonatal forebrain cholinergic lesion on adult hippocampal neurogenesis. Brain Res 1373(10):79-90. doi: 10.1016/j.brainres.2010.11.091

Summary: Intraventricular injections of 192-IgG-SAP (Cat. #IT-01) have been shown to reduce the number of cells expressing a marker for immature neuroblasts in the dentate gyrus, as well as possibly impairing the response to environmental enrichment. This study looked to expand on those observations. 300 ng of 192-IgG-SAP was infused into each ventricle of post-natal day 7 rats. The data suggest that the lesion accelerates the death of newborn cells, but does not affect survival rate or phenotypic differentiation.

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

Li AJ, Wang Q, Ritter S (2011) Participation of hindbrain AMP-activated protein kinase in glucoprivic feeding. Diabetes 60(2):436-442. doi: 10.2337/db10-0352

Summary: Catecholamine neurons innervating the medial hypothalamus are involved in the control of glucoprivic feeding as well as other responses to glucose deficit. Rats received bilateral 82-ng injections of anti-DBH-SAP (Cat. #IT-03) into the paraventricular hypothalamic nucleus. Saporin (Cat. #PR-01) was used as a control. Lesioned animals did not respond to the administration of a competitive glucose inhibitor, nor did they display phosphorylation of pAMPKα, suggesting that AMPK may be part of a glucose- sensing mechanism.

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

Gibbs RB, Chipman AM, Nelson D (2011) Donepezil plus estradiol treatment enhances learning and delay-dependent memory performance by young ovariectomized rats with partial loss of septal cholinergic neurons. Horm Behav 59(4):503-511. doi: 10.1016/j.yhbeh.2011.01.011

Summary: Among the beneficial effects of estrogen on the brain are improved cognitive performance and prevention of age-related cognitive decline. These positive effects diminish over time following loss of ovarian function. To investigate the role of cholinergic neurons in this process, rats received 96-250 ng of 192-IgG-SAP (Cat. #IT-01) into the medial septal nucleus followed by a cholinergic enhancer and estradiol therapy. The dual therapy had a positive effect on partially lesioned animals, but did not improve the performance of animals with severe lesions.

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

Leung LS, Petropoulos S, Shen B, Luo T, Herrick I, Rajakumar N, Ma J (2011) Lesion of cholinergic neurons in nucleus basalis enhances response to general anesthetics. Exp Neurol 228(2):259-269. doi: 10.1016/j.expneurol.2011.01.019

Summary: Consciousness and response to general anesthesia have been linked to acetylcholine in the brain. The authors treated rats with 150-ng bilateral injections of 192-IgG-SAP (Cat. #IT-01) into the nucleus basalis magnocellularis to examine this connection. Lesioned animals were more affected by propofol and phenobarbitol than control animals. Some effects of halothane were also increased. The data indicate a role for acetylcholine in the brain in the response to general anesthesia.

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

Q: Is there a saporin derivative available that selectively destroys all or some hippocampal neurons?

A: Assuming that you mean to eliminate cell bodies from the hippocampus, rather than just projections, a neat paper by Martin et al. describes the use of SSP-SAP (Cat #IT-11) to do this. NPY-SAP (Cat. #IT-28) could also be interesting.

Related: SSP-SAP (Cat. #IT-11), NPY-SAP (Cat. #IT-28)

References

1. Martin JL et al. Focal inhibitory interneuron loss and principal cell hyperexcitability in the rat hippocampus after microinjection of a neurotoxic conjugate of saporin and a peptidase-resistant analog of substance P. J Comp Neurol 436:127-152, 2001.

Q: I am interested in your product GAT1-SAP (Cat. #IT-32). Before ordering, I would like to know how long it takes until the toxin produces a lesion; Is seven days enough?

A: The usual time-course for saporin toxins is that behavioral effects start appearing at four days and usually plateau at seven days. However, keep in mind that it takes some time for dead cells to be cleared out, so histology on the animal should wait until at least two weeks after administration.

Related: Targeted Toxins

Goehler LE, Gaykema RPA (2011) Featured Article: Targeted lesion of caudal brainstem catecholamine neurons reveals their role in symptoms of fatigue. Targeting Trends 12(1)

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

Read the featured article in Targeting Trends.