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2339 entries

Attenuation of the bidirectional effects of chlordiazepoxide and FG 7142 on conditioned response suppression and associated cardiovascular reactivity by loss of cortical cholinergic inputs.

Stowell JR, Berntson GG, Sarter M (2000) Attenuation of the bidirectional effects of chlordiazepoxide and FG 7142 on conditioned response suppression and associated cardiovascular reactivity by loss of cortical cholinergic inputs. Psychopharmacol 150(2):141-149. doi: 10.1007/s002130000443

Summary: The benzodiazepine receptor (BR) is involved in anxiety. It has been hypothesized that cholinergic projections from the CBF are necessary for modulation of the BR by agonists and inverse agonists. Stowell et al. directly injected 0.18 µg 192-Saporin (Cat #IT-01) into each hemisphere of the CBF in adult rats. The treated rats had altered responses to external stimuli during an operant conditioned task. These results indicate that the CBF plays an important role in response to fear and anxiety-related stimuli. This system may also mediate the actions of BR ligands.

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

Repeated immunolesions display diminished stress response signal.

Gu Z, Yu J, Werrbach-Perez K, Perez-Polo JR (2000) Repeated immunolesions display diminished stress response signal. Int J Dev Neurosci 18:177-183. doi: 10.1016/s0736-5748(99)00086-6

Summary: Cholinergic neurons in the basal forebrain are involved in neurotrophin release in general injury response although this response is impaired in the aged individual. Addition of pharmacological doses of NGF can repair this mechanism. Gu et al. used 192-Saporin (Cat. #IT-01) to model the endogenous stimulation of NGF in response to injury. They found that a one-time administration of 192-Saporin was more effective than chronic repeated administrations for inducing an increase in NGF levels. These results indicate that chronic lesions may cause a desensitization that differs from the acute toxic model.

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

Intracerebroventricular infusion of CHO5, a rat monoclonal antibody directed against mouse low-affinity nerve growth factor receptor (p75NTR), specifically labels basal forebrain cholinergic neurons in mouse brain.

Rossner S, Schliebs R, Bigl V (2000) Intracerebroventricular infusion of CHO5, a rat monoclonal antibody directed against mouse low-affinity nerve growth factor receptor (p75NTR), specifically labels basal forebrain cholinergic neurons in mouse brain. Metab Brain Dis 15(1):17-27. doi: 10.1007/BF02680011 PMID: 10885538

Summary: 192-Saporin (Cat. #IT-01) has long been a useful tool for neurobiological research in the rat. For various reasons, many researchers want to perform the same studies in the mouse but have been prevented from doing so by the lack of a suitable antibody against the mouse p75NTR. Rossner et al. describe a rat monoclonal antibody against the mouse p75NTR (Cat. #AB-N02) that demonstrates co-localization of p75NTR and ChAT, and also co-localization of p75NTR and TrkA in the mouse basal forebrain. Internalization and retrograde transport of this antibody in cholinergic basal forebrain neurons is also shown. This evidence indicates that the anti-mouse p75NTR will be effective for use as an immunotoxin.

Related Products: 192-IgG-SAP (Cat. #IT-01), mu p75-SAP (Cat. #IT-16), Antibody to NGFR (Cat. #AB-N02)

Preserved olfactory short-term memory after combined cholinergic and serotonergic lesions using 192 IgG-Saporin and 5,7-dihydroxytryptamine in rats [published erratum appears in Neuroreport 2000 Mar 20;11(4):inside back cover].

Wirth S, Lehmann O, Bertrans F, Lazarus C, Jeltsch H, Cassel JC (2000) Preserved olfactory short-term memory after combined cholinergic and serotonergic lesions using 192 IgG-Saporin and 5,7-dihydroxytryptamine in rats [published erratum appears in Neuroreport 2000 Mar 20;11(4):inside back cover]. Neuroreport 11:347-350. doi: 10.1097/00001756-200002070-00025

Usage: 192-SAP (Cat. #IT-01) 2 µg, intracerebroventricular

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

Selective impairment of corticotropin-releasing factor1 (CRF1) receptor-mediated function using CRF coupled to saporin.

Maciejewski-Lenoir D, Heinrichs SC, Liu X-J, Ling N, Tucker A, Xie Q, Lappi DA, Grigoriadis DE (2000) Selective impairment of corticotropin-releasing factor1 (CRF1) receptor-mediated function using CRF coupled to saporin. Endocrinol 141:498-504. doi: 10.1210/endo.141.2.7336

Summary: Corticotropin-releasing factor 1 (CRF1) is a 41-amino acid peptide which mediates many of the body’s behavioral, autonomic, immune, and endocrine responses to stress. Reduced activation of the CRF systems plays a role in a variety of psychiatric and metabolic disease states. Maciejewski-Lenoir et al. have developed a CRF-SAP targeted toxin that can eliminate cells expressing the CRF1 but not CRF2a receptors. These data indicate that CRF-SAP (Cat. #IT-13) may be useful as a tool to examine receptor-selective impairment of CRF system function.

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

Nerve growth factor (NGF) augments cortical and hippocampal cholinergic functioning after p75NGF receptor-mediated deafferentation but impairs inhibitory avoidance and induces fear-related behaviors.

Winkler J, Ramirez GA, Thal LJ, Waite JJ (2000) Nerve growth factor (NGF) augments cortical and hippocampal cholinergic functioning after p75NGF receptor-mediated deafferentation but impairs inhibitory avoidance and induces fear-related behaviors. J Neurosci 20:834-844. doi: 10.1523/JNEUROSCI.20-02-00834.2000

Usage: 192-SAP (Cat. #IT-01) 1.0 or 2.7 µg in 10 µl, intracerebroventricular

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

Loss of nerve: a molecular approach to better treatment of chronic pain.

Friedrich MJ (2000) Loss of nerve: a molecular approach to better treatment of chronic pain. JAMA 283(2):187-188. doi: 10.1001/jama.283.2.187

Summary: The use of SP-SAP (Cat. #IT-07) as a promising new method for chronic pain relief is discussed in this review article. Chronic pain has classically been treated in ways that frequently have adverse effects on the patient’s quality of life. Friedrich touches on recently developed toxins that are useful in techniques of molecular neurosurgery. These techniques allow the dissection of pain pathways in the brain and spinal cord which will provide not only a greater understanding of these pathways but also potential therapies for chronic pain and other pain conditions.

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

Sustained effect of metrifonate on cerebral glucose metabolism after immunolesion of basal forebrain cholinergic neurons in rats.

Bassant MH, Poindessous-Jazat F, Schmidt BH (2000) Sustained effect of metrifonate on cerebral glucose metabolism after immunolesion of basal forebrain cholinergic neurons in rats. Eur J Pharmacol 387:151-162. doi: 10.1016/s0014-2999(99)00742-6

Usage: 192-SAP (Cat. #IT-01) 134 ng in 0.2 μl, basal forebrain

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

In vivo [125I]-iodobenzovesamicol binding reflects cortical cholinergic deficiency induced by specific immunolesion of rat basal forebrain cholinergic system.

Sorger D, Schliebs R, Kampfer I, Rossner S, Heinicke J, Dannenberg C, Georgi P (2000) In vivo [125I]-iodobenzovesamicol binding reflects cortical cholinergic deficiency induced by specific immunolesion of rat basal forebrain cholinergic system. Nucl Med Biol 27:23-31. doi: 10.1016/s0969-8051(99)00087-6

Usage: 192-SAP (Cat. #IT-01), 2 µg into each lateral ventricle

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

Combined lesions of cholinergic and serotonergic neurons in the rat brain using 192 IgG-Saporin and 5,7-dihydroxytryptamine: neurochemical and behavioural characterization.

Lehmann O, Jeltsch H, Lehnardt O, Pain L, Lazarus C, Cassel JC (2000) Combined lesions of cholinergic and serotonergic neurons in the rat brain using 192 IgG-Saporin and 5,7-dihydroxytryptamine: neurochemical and behavioural characterization. Eur J Neurosci 12:67-79. doi: 10.1046/j.1460-9568.2000.00881.x

Summary: Lesioning of septohippocampal pathways has often been used as a model for Alzheimer’s disease because these lesions alter cognitive capabilities such as spatial memory. Recent work in the behavioral neurosciences has shown that other neurotransmitter systems such as GABAergic, noradrenergic, and serotonergic systems also play a role in learning and memory. Lehmann et al. combined the effects of the cholinergic immunotoxin 192-SAP (Cat. #IT-01) and the serotonergic toxin 5,7-dihydroxytryptamine to examine interactions between these two pathways. The effects of lesioning these two pathways in concert indicate that they both play roles in cognitive functions related to working memory. [192-SAP 2 µg/lateral ventricle]

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

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