Relevant bibliographies by topics / 192 IgG-Saporin

Academic literature on the topic '192 IgG-Saporin'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "192 IgG-Saporin"

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Book, Adam A., Ronald G. Wiley, and John B. Schweitzer. "192 IgG-saporin." Acta Neuropathologica 89, no. 6 (1995): 519–26. http://dx.doi.org/10.1007/bf00571506.

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Book, Adam A., Ronald G. Wiley, and John B. Schweitzer. "192 IgG-saporin." Acta Neuropathologica 89, no. 6 (May 1, 1995): 519–26. http://dx.doi.org/10.1007/s004010050283.

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Grindstaff, Ryan J., Regina R. Grindstaff, and J. Thomas Cunningham. "Baroreceptor sensitivity of rat supraoptic vasopressin neurons involves noncholinergic neurons in the DBB." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 5 (November 1, 2000): R1934—R1943. http://dx.doi.org/10.1152/ajpregu.2000.279.5.r1934.

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Previous studies suggest that cholinergic neurons in the diagonal band of Broca (DBB) participate in the baroreceptor-mediated inhibition of phasic vasopressin neurons in the supraoptic nucleus (SON). To test this hypothesis, extracellular recordings were obtained from putative vasopressin SON neurons of anesthetized rats injected with the cholinergic immunotoxin 192 IgG-saporin (0.8 μg/μl) in the DBB. Baroreceptor sensitivity of neurons was tested with brief phenylephrine-induced (10 μg/10 μl iv) increases in blood pressure of at least 40 mmHg. In rats injected with vehicle or unconjugated saporin, 19 of 21 and 18 of 20 phasic neurons, respectively, were inhibited by increased blood pressure. In rats injected with 192 IgG-saporin, which significantly reduced the number of choline acetyltransferase (ChAT)-positive DBB neurons, 33 of 36 phasic neurons were inhibited. Normal rats and rats with DBB saporin injections received rhodamine bead injections into the perinuclear zone (PNZ) to retrogradely label DBB neurons, and their brains were stained for ChAT. ChAT-positive DBB neurons were not retrogradely labeled from the PNZ. Together, these results indicate that the pathway relaying baroreceptor information to the SON involves noncholinergic DBB neurons.
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Harrell, Lindy E., Dee Parsons, and Krystyna Kolasa. "Hippocampal sympathetic ingrowth occurs following 192-IgG–Saporin administration." Brain Research 911, no. 2 (August 2001): 158–62. http://dx.doi.org/10.1016/s0006-8993(01)02626-9.

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Blanco-Centurion, Carlos A., Anjelica Shiromani, Elizabeth Winston, and Priyattam J. Shiromani. "Effects of hypocretin-1 in 192-IgG-saporin-lesioned rats." European Journal of Neuroscience 24, no. 7 (October 2006): 2084–88. http://dx.doi.org/10.1111/j.1460-9568.2006.05074.x.

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Moga, Margaret M. "192 IgG-saporin abolishes p75 neurotrophin receptor immunoreactivity in rat SCN." NeuroReport 9, no. 14 (October 1998): 3197–200. http://dx.doi.org/10.1097/00001756-199810050-00012.

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Wrenn, Craige C., and Ronald G. Wiley. "The behavioral functions of the cholinergic basalforebrain : lessons from 192 IgG‐SAPORIN." International Journal of Developmental Neuroscience 16, no. 7-8 (November 1998): 595–602. http://dx.doi.org/10.1016/s0736-5748(98)00071-9.

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Burk, Joshua A., Matthew W. Lowder, and Kathleen E. Altemose. "Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin." Behavioural Brain Research 195, no. 2 (December 2008): 231–38. http://dx.doi.org/10.1016/j.bbr.2008.09.006.

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Pappas, B. A., C. M. Davidson, T. Fortin, S. Nallathamby, G. A. S. Park, E. Mohr, and R. G. Wiley. "192 IgG-saporin lesion of basal forebrain cholinergic neurons in neonatal rats." Developmental Brain Research 96, no. 1-2 (October 1996): 52–61. http://dx.doi.org/10.1016/0165-3806(96)00095-8.

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Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. "Role of the Basal Forebrain Cholinergic Projection in Somatosensory Cortical Plasticity." Journal of Neurophysiology 79, no. 6 (June 1, 1998): 3216–28. http://dx.doi.org/10.1152/jn.1998.79.6.3216.

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Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. Role of the basal forebrain cholinergic projection in somatosensory cortical plasticity. J. Neurophysiol. 79: 3216–3228, 1998. Trimming all but two whiskers in adult rats produces a predictable change in cortical cell-evoked responses characterized by increased responsiveness to the two intact whiskers and decreased responsiveness to the trimmed whiskers. This type of synaptic plasticity in rat somatic sensory cortex, called “whisker pairing plasticity,” first appears in cells above and below the layer IV barrels. These are also the cortical layers that receive the densest cholinergic inputs from the nucleus basalis. The present study assesses whether the cholinergic inputs to cortex have a role in regulating whisker pairing plasticity. To do this, cholinergic basal forebrain fibers were eliminated using an immunotoxin specific for these fibers. A monoclonal antibody to the low-affinity nerve growth factor receptor 192 IgG, conjugated to the cytotoxin saporin, was injected into cortex to eliminate cholinergic fibers in the barrel field. The immunotoxin reduces acetylcholine esterase (AChE)-positive fibers in S1 cortex by >90% by 3 wk after injection. Sham-depleted animals in which either saporin alone or saporin unconjugated to 192 IgG is injected into the cortex produces no decrease in AChE-positive fibers in cortex. Sham-depleted animals show the expected plasticity in barrel column neurons. In contrast, no plasticity develops in the ACh-depleted, 7-day whisker-paired animals. These results support the conclusion that the basal forebrain cholinergic projection to cortex is an important facilitator of synaptic plasticity in mature cortex.
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Dissertations / Theses on the topic "192 IgG-Saporin"

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Peterson, William E. "Immunolesioning of identified motoneuron pools by the intramuscular injection of the immunotoxins, 192-IgG-saporin and OX7-saporin, in rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62820.pdf.

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Perry, Tracyann. "Behavioural, histological and immunocytochemical consequences following 192 IgG saporin immunolesions of the basal forebrain." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314079.

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Sherren, Nicole. "Neural and behavioral effects of intracranial 192 IgG-saporin in neonatal rats, sexually dimorphic effects?" Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape15/PQDD_0015/MQ36938.pdf.

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Cabrera, Sara Michelle. "192 IgG-Saporin lesions of the nucleus basalis magnocellularis impair serial reversal learning in rats." CSUSB ScholarWorks, 2005. https://scholarworks.lib.csusb.edu/etd-project/2778.

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In order to assess flexibility in acquiring and using conflicting response rules, rats with selective lesions of the NBM or sham-lesion controls were subjected to serial reversal training in a simple operant discrimination paradigm. The NBM lesion group did not differ from the control group in acquisition of the original rules; the NBM lesion group required more time to master the changes in rules in the first reversal, but not in subsequent reversals.
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Kitto, Michael Ryan. "Biconditional discrimination learning in rats with 192 IgG-saporin lesions of the nucleus basalis magnocellularis." CSUSB ScholarWorks, 2006. https://scholarworks.lib.csusb.edu/etd-project/3002.

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The experiment tested the hypothesis that 192 IgG-saporin lesions of the nucleus basalis magnocellularis (NBM) in rats would impair performance in a biconditional visual discrimination task, which requires configural association learning. Experiment used 22 male Long-Evan rats (Harlan Sprague-Dawley). Behavioral testing was conducted in two identical T-mazes. Rats were randomly assigned to either a bilateral 192 IgG-saporin lesion group (n = 10) or to a control group (n = 12). Results support the hypothesis that NBM is critically involved in configural but not simple association learning and suggest that NBM may be involved more generally in cognitive flexibility.
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Quinlivan, Mitchell Owen Jeffrey. "Functions of the Cholinergic System in the Morbidities Associated with Alzheimer’s Disease and the Further Evaluation of Tools for the Molecular Imaging of this System." University of Sydney, 2007. http://hdl.handle.net/2123/1933.

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Doctor of Philosophy(PhD)
The aims of this project were to contribute to the elucidation of the role of the cholinergic system in attention and memory, two cognitive processes severely compromised in Alzheimer’s disease (AD), and to evaluate and develop tools for the functional molecular imaging of this system with a view to improving knowledge of AD and other neurological disorders. Towards the first aim, the specific anti-cholinergic toxin 192 IgG-saporin (SAP) was administered to female Sprague-Dawley rats via either an intracerebroventricular (icv) or an intracortical route and animals were tested with a vibrissal-stimulation reaction-time task and an object recognition task to evaluate their attentional and mnemonic function, respectively. The second aim was approached in two ways. Firstly, relative neuronal densities from animals with icv lesions were assessed with both ex vivo and in vitro autoradiography with the specific cholinergic radiopharmaceuticals [123I]iodobenzovesamicol (123IBVM) and 125I-A-85380, ligands for the vesicular acetylcholine transporter and the nicotinic acetylcholine receptor, respectively. Secondly, a number of in vivo and in vitro studies were performed on a novel and unique molecular imaging system (TOHR), with which it had been hoped initially to image eventually SAP-lesioned animals, with a view to measuring and ameliorating its performance characteristics and assessing its in-principle suitability for small-animal molecular imaging. The behavioural studies support a critical role for the cholinergic system in normal attentional function. Additionally, in accord with literature evidence, no significant impairment was observed in mnemonic function. It is postulated however that the results observed in the intracortically-lesioned animals support the published hypothesis that cholinergic projections to the perirhinal cortex are critical for object-recognition memory. In autoradiographic studies, SAP-lesioned animals demonstrated reduced uptake of 123IBVM in multiple regions. A reduction of nicotinic receptors was also seen in SAP-lesioned animals, a novel finding supportive of the excellent characteristics of radioiodinated I-A-85380. Examination of the performance characteristics of the TOHR support in principle its utility for targeted small-animal molecular imaging studies.
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Quinlivan, Mitchell. "Rôles du système cholinergique dans le disfonctionnement cognitif associé à la maladie Alzheimer et évaluation d'outils pour l'imagerie moléculaire." Tours, 2007. http://www.theses.fr/2007TOUR3324.

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La dégénérescence des neurones cholinergiques (NC) est une caractéristique importante de la maladie Alzheimer (MA). Afin d’imiter cet aspect de la MA, nous avons utilisé une toxine permettant la destruction, dans le prosencéphale basal chez le rat, des NC. Cette technique a été validée par immunohistochimie (IHC). Les études comportementales démontrent que le système cholinergique est nécessaire pour l’attention mais que celui-ci joue également un rôle relativement mineur dans le processus mnémonique, domaines cognitifs très touchés par la MA. Dans ce cadre, nos études, utilisant des radioligands spécifiques pour les récepteurs nicotiniques (nAChR) ou le transporteur acétylcholine vésiculaire, pouvaient démontrer, et pour la première fois sur les nAChR, la lésion validée par IHC. Nous avons donc développé et décrit un système d’imagerie moléculaire pour l’étude in vivo du petit animal. Toutefois ce système n’a pas pu être encore utilisé pour l’étude de radioligand
Cholinergic neuron degeneration is a prominent hallmark of Alzheimer’s disease (AD). Using a specific immunotoxin (SAP), basal forebrain cholinergic neurons in the rat were lesioned, as assessed by immunohistochemistry (IHC), to model this facet of AD. Behavioural testing, utilising models with two different routes of SAP administration, further demonstrated the necessity of this system for normal attentional function and its relatively minor role in mnemonic function, cognitive domains greatly affected by AD. Studies with radioligands specific for the nicotinic receptor (nAChR) or the Vesicular Acetylcholine Transporter were both able to demonstrate the lesion validated by IHC, the first time a nAChR radioligand has done this in a SAP model. Although eventually it was unable to be used for the in vivo continuation of this work, studies for the development of a small-animal molecular imaging system initially intended for such a continuation are also reported
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Book chapters on the topic "192 IgG-Saporin"

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Petrosini, Laura, Paola De Bartolo, Debora Cutuli, and Francesca Gelfo. "Perinatal 192 IgG-Saporin as Neuroteratogen." In Neurotoxin Modeling of Brain Disorders—Life-long Outcomes in Behavioral Teratology, 111–23. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/7854_2015_418.

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Walsh, Thomas J. "Models of Cholinergic Degeneration: AF64A and 192-IgG-Saporin." In Advances in Behavioral Biology, 667–74. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_94.

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Schliebs, Reinhard, Steffen Roßner, Mechthild Heider, and Volker Bigl. "Targeted Immunolesion of Cholinergic Neurons by 192 IgG-Saporin." In Neurochemistry, 829–35. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_136.

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Petrosini, Laura, P. De Bartolo, and D. Cutuli. "Neurotoxic Effects, Mechanisms, and Outcome of 192-IgG Saporin." In Handbook of Neurotoxicity, 591–609. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-5836-4_79.

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Petrosini, L., P. De Bartolo, and D. Cutuli. "Neurotoxic Effects, Mechanisms, and Outcome of 192 IgG-Saporin Lesions." In Handbook of Neurotoxicity, 1–23. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71519-9_79-1.

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Petrosini, L., P. De Bartolo, and D. Cutuli. "Neurotoxic Effects, Mechanisms, and Outcome of 192 IgG-Saporin Lesions." In Handbook of Neurotoxicity, 1251–72. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_79.

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Chang, J. W., and Y. S. Park. "Use of 192 IgG-saporin as a model of dementia and its application." In Genetics, Neurology, Behavior, and Diet in Dementia, 849–63. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-815868-5.00053-0.

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