targeted-toxins

Luo T, Leung LS (2010) Endogenous histamine facilitates long-term potentiation in the hippocampus during walking. J Neurosci 30(23):7845-7852. doi: 10.1523/JNEUROSCI.1127-10.2010

Summary: The neurotransmitter histamine is involved in several physiological functions, such as sleep-wake activites, circadian rhythms, learning, and memory. This work examines the role of histamine in modulating synaptic plasticity. Rats received 62.5 ng injections of orexin-SAP (Cat. #IT-20) into the tuberomammillary nucleus (TMN), followed by assessment of long term potentiation (LTP) during different behavioral states. The data indicate that histaminergic neurons in the TMN facilitate basal-dendritic LTP during walking.

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

Gil-Bea FJ, Solas M, Mateos L, Winblad B, Ramirez MJ, Cedazo-Minguez A (2011) Cholinergic hypofunction impairs memory acquisition possibly through hippocampal Arc and BDNF downregulation. Hippocampus 21(9):999-1009. doi: 10.1002/hipo.20812

Summary: The authors investigated the role of activity-regulated cytoskeleton associated protein (Arc) and brain-derived neurotrophic factor (BDNF) in cholinergic-induced memory formation. Rats received 67-ng bilateral injections of 192-IgG-SAP (Cat. #IT-01) into the third ventricle after behavioral training. Lesioned animals had decreased protein and mRNA for both Arc and BDNF. Memory acquisition and recovery of acquisition were both affected. The data indicate that cholinergic denervation of the hippocampus affects the muscarinic facets of spatial memory acquisition.

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

Worlicek M, Knebel K, Linde HJ, Moleda L, Scholmerich J, Straub RH, Wiest R (2010) Splanchnic sympathectomy prevents translocation and spreading of E coli but not S aureus in liver cirrhosis. Gut 59(8):1127-1134. doi: 10.1136/gut.2009.185413

Summary: Advanced cirrhosis activates the sympathetic nervous system. This work investigates the role of the sympathetic nervous system (SNS) in spontaneous bacterial peritonitis – which is mainly caused by translocation of enteric Gram-negative bacteria. Rats received 15 µg intraperitoneal injections of anti-DBH-SAP (Cat. #IT-03). Lesioned animals displayed increased susceptibility to bacterial translocation and infection with E. coli but not S. aureus. This suggests the SNS plays an important role in the immune response to Gram-negative bacteria.

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

Easton A, Fitchett AE, Eacott MJ, Baxter MG (2011) Medial septal cholinergic neurons are necessary for context-place memory but not episodic-like memory. Hippocampus 21(9):1021-1027. doi: 10.1002/hipo.20814

Summary: Although it is clear that neurodegenerative diseases cause memory impairment, it is uncertain to what extent cholinergic deficits cause this loss of function. The authors administered a total of 150 ng of 192-IgG-SAP (Cat. #IT-01) into the medial septum and vertical limb of the diagonal band of Broca in rats. The lesioned animals were then tested in a rodent model for human episodic memory. The rats performed well on these tests, but struggled with tests that tested the association of places with context. The results suggest that hippocampal spatial representations might not be essential for episodic memory function.

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

Paban V, Farioli F, Romier B, Chambon C, Alescio-Lautier B (2010) Gene expression profile in rat hippocampus with and without memory deficit. Neurobiol Learn Mem 94(1):42-56. doi: 10.1016/j.nlm.2010.03.005

Summary: This work examined a wide range of gene expression in the rat hippocampus after bilateral injections of 192-IgG-SAP (Cat. #IT-01) – 37.5 ng per side in the medial septum, and 75 ng per side in the nucleus basalis magnocellularis. Memory loss following 192-IgG-SAP treatment was marked by gene expression that did not show the same cluster organization as learning processes. Genes showing differential expression were down-regulated, and one cluster associated with tissue remodeling could be identified.

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

Pang KCH, Jiao X, Sinha S, Beck KD, Servatius RJ (2011) Damage of GABAergic neurons in the medial septum impairs spatial working memory and extinction of active avoidance: Effects on proactive interference. Hippocampus 21(8):835-846. doi: 10.1002/hipo.20799

Summary: Recent work implicates the medial septum (MS) and diagonal band (DB) in the control of proactive interference — forgetting older information when learning new information. Rats received GAT1-SAP (Cat. #IT-32) injections into the MS and the DB (162.5 ng and 130 ng respectively, the DB injections were bilateral). The results parallel other studies using different toxins, reinforcing the indications that GABAergic MSDB neurons are an integral part of proactive interference control.

Related Products: 192-IgG-SAP (Cat. #IT-01), GAT1-SAP (Cat. #IT-32)

Hummel M, Cummons T, Lu P, Mark L, Harrison JE, Kennedy JD, Whiteside GT (2010) Pain is a salient “stressor” that is mediated by corticotropin-releasing factor-1 receptors. Neuropharmacology 59(3):160-166. doi: 10.1016/j.neuropharm.2010.05.001

Summary: Given that corticotrophin-releasing factor (CRF) plays a major role in the response to stress, the authors investigated the role CRF-1 receptors may play in the perception of pain. Both rats and mice received 10µl intrathecal injections of 10 µM CRF-SAP (Cat. #IT-13) following a spinal nerve ligation. Administration of CRF-SAP attenuated tactile hypersensitivity, indicating that CRF-1 receptors are involved in pain perception.

Related Products: CRF-SAP (Cat. #IT-13)

Emanuel AJ, Ritter S (2010) Hindbrain catecholamine neurons modulate the growth hormone but not the feeding response to ghrelin. Endocrinology 151(7):3237-3246. doi: 10.1210/en.2010-0219

Summary: In this work the authors investigated the role of hindbrain catecholamine neurons in the response to a gastrointestinal peptide, ghrelin. Rats received 42 ng injections of anti-DBH-SAP (Cat. #IT-03) into the paraventricular nucleus of the hypothalamus. Saporin (Cat. #PR-01) was used as a control. Lesioned animals had a prolonged growth hormone (GH) response to ghrelin administration as compared to controls, but the feeding response was unchanged. The results indicate that ghrelin or GH may be involved with a negative feedback response controlling GH levels.

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

Coradazzi M, Gulino R, Garozzo S, Leanza G (2010) Selective lesion of the developing central noradrenergic system: Short- and long-term effects and reinnervation by noradrenergic-rich tissue grafts. J Neurochem 114(3):761-771. doi: 10.1111/j.1471-4159.2010.06800.x

Summary: The authors removed noradrenergic neurons in the locus coeruleus/subcoeruleus complex of neonatal rats with 0.25-1.0 µg bilateral injections of anti-DBH-SAP (Cat. #IT-03). No damage was seen in dopaminergic, adrenergic, serotonergic, or cholinergic neurons after this treatment. Rats receiving fetal locus coeruleus tissue implants showed significant post-lesion recovery suggesting that this model can be used to investigate compensatory reinnervation and functional recovery in the central nervous system.

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

Klinkenberg I, Blokland A (2010) The validity of scopolamine as a pharmacological model for cognitive impairment: A review of animal behavioral studies. Neurosci Biobehav Rev 34(8):1307-1350. doi: 10.1016/j.neubiorev.2010.04.001 PMID: 20398692

Objective: To provide an overview is given of the effects of scopolamine on animal behavior.

Summary: The most important and influential articles over the past 40 years are included in the present review. The cholinergic hypothesis of memory function as originally put forward by Bartus et al. (1982) has undergone a revision after several lesion studies were performed which used the highly specific cholinergic toxin 192 IgG-SAP (Wiley et al., 1995).

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

See Also:

• Chudasama Y et al. Cholinergic modulation of visual attention and working memory: Dissociable effects of basal forebrain 192-IgG-saporin lesions and intraprefrontal infusions of scopolamine. Learn Mem 11(1):78-86, 2004.
• Wiley RG et al. Destruction of the cholinergic basal forebrain using immunotoxin to rat NGF receptor: modeling the cholinergic degeneration of Alzheimer’s disease. J Neurol Sci 128:157-166, 1995.
• Wiley RG et al. Immunolesioning: Selective destruction of neurons using immunotoxin to rat NGF receptor. Brain Res 562:149-153, 1991.
• Wrenn CC et al. The behavioral functions of the cholinergic basal forebrain: lessons from 192 IgG-saporin. Int J Dev Neurosci 16(7-8):595-602, 1998.
• Wenk GL The nucleus basalis magnocellularis cholinergic system: one hundred years of progress. Neurobiol Learn Mem 67(2):85-95, 1997.
• Baxter MG et al. Intact spatial learning in both young and aged rats following selective removal of hippocampal cholinergic input. Behav Neurosci 110:460-467, 1996.
• Baxter MG et al. Intact spatial learning in both young and aged rats following selective removal of hippocampal cholinergic input. Behav Neurosci 110:460-467, 1996.
• Baxter MG et al. Disruption of decrements in conditioned stimulus processing by selective removal of hippocampal cholinergic input. J Neurosci 17:5230-5236, 1997.
• Chiba AA et al. Selective removal of cholinergic neurons in the basal forebrain alters cued target detection. Neuroreport 10(14):3119-3123, 1999.
• McGaughy J et al. Effects of chlordiazepoxide and scopolamine, but not aging, on the detection and identification of conditional visual stimuli. J Gerontol A Biol Sci Med Sci 50(2):B90-B96, 1995.
• McGaughy J et al. Crossmodal divided attention in rats: effects of chlordiazepoxide and scopolamine. Psychopharmacology (Berl) 115(1-2):213-220, 1994.
• Torres EM et al. Behavioral, histochemical and biochemical consequences of selective immunolesions in discrete regions of the basal forebrain cholinergic system. Neuroscience 63:95-122, 1994.
• Voytko ML Cognitive functions of the basal forebrain cholinergic system in monkeys: memory or attention?. Behav Brain Res 75(1-2):13-25, 1996.