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Selective acetylcholine and dopamine lesions in neonatal rats produce distinct patterns of cortical dendritic atrophy in adulthood.
Sherren N, Pappas BA (2005) Selective acetylcholine and dopamine lesions in neonatal rats produce distinct patterns of cortical dendritic atrophy in adulthood. Neuroscience 136(2):445-456. doi: 10.1016/j.neuroscience.2005.08.053
Summary: In this work the authors examined lesions of acetylcholine afferents in 7-day-old rat pups, and the effect on dendritic development. 600 ng of 192-IgG-SAP (Cat. #IT-01) were administered to the ventricles of test animals. Various morphological changes in the retrosplenial cortex were observed, including smaller apical tufts and fewer basilar dendritic branches in layer V medial prefrontal cells. The data demonstrate that ascending acetylcholine afferents are very important in the development of cortical cytoarchitecture.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Lecozotan (SRA-333): a selective serotonin 1A receptor antagonist that enhances the stimulated release of glutamate and acetylcholine in the hippocampus and possesses cognitive-enhancing properties.
Schechter LE, Smith DL, Rosenzweig-Lipson S, Sukoff SJ, Dawson LA, Marquis K, Jones D, Piesla M, Andree T, Nawoschik S, Harder JA, Womack MD, Buccafusco J, Terry AV, Hoebel B, Rada P, Kelly M, Abou-Gharbia M, Barrett JE, Childers W (2005) Lecozotan (SRA-333): a selective serotonin 1A receptor antagonist that enhances the stimulated release of glutamate and acetylcholine in the hippocampus and possesses cognitive-enhancing properties. J Pharmacol Exp Ther 314(3):1274-1289. doi: 10.1124/jpet.105.086363
Related Products: ME20.4-SAP (Cat. #IT-15)
Cholinergic septo-hippocampal innervation is required for trace eyeblink classical conditioning.
Fontan-Lozano A, Troncoso J, Munera A, Carrion AM, Delgado-Garcia JM (2005) Cholinergic septo-hippocampal innervation is required for trace eyeblink classical conditioning. Learn Mem 12(6):557-563. doi: 10.1101/lm.28105
Summary: Classical conditioning of eyeblink responses can be used to evaluate cognitive deficits. The authors lesioned the medial septum/diagonal band of rats with 200 ng of 192-IgG-SAP (Cat. #IT-01), then examined classical and instrumental conditioning paradigms. Lesioned animals displayed a deficit in the acquisition, but not retrieval of eyeblink classical conditioning. The deficit was reversed by carbachol, a cholinergic muscarinic agonist, suggesting a role for the muscarinic system in the acquisition of new motor abilities.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Selective loss of basal forebrain cholinergic neurons by 192 IgG-saporin is associated with decreased phosphorylation of Ser glycogen synthase kinase-3beta.
Hawkes C, Jhamandas JH, Kar S (2005) Selective loss of basal forebrain cholinergic neurons by 192 IgG-saporin is associated with decreased phosphorylation of Ser glycogen synthase kinase-3beta. J Neurochem 95(1):263-272. doi: 10.1111/j.1471-4159.2005.03363.x
Summary: Glycogen synthase kinase-3ß (GSK-3ß) is an enzyme involved in a variety of biological events. In this study the authors examined the potential role of GSK-3ß in degeneration of basal forebrain cholinergic neurons. Rats were treated with 2.0 µg per ventricle injections of 192-IgG-SAP (Cat. #IT-01), then GSK-3ß and other cholinergic marker levels were assayed. The results indicate that increased GSK-3ß activity can provide some protection from 192-IgG-SAP-induced degeneration of forebrain cholinergic neurons.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Nicotine-induced switch in the nicotinic cholinergic mechanisms of facilitation of long-term potentiation induction.
Yamazaki Y, Jia Y, Hamaue N, Sumikawa K (2005) Nicotine-induced switch in the nicotinic cholinergic mechanisms of facilitation of long-term potentiation induction. Eur J Neurosci 22(4):845-860. doi: 10.1111/j.1460-9568.2005.04259.x
Summary: The authors investigated cellular mechanisms underlying improved cognitive function in Alzheimer’s disease patients upon the administration of nicotine. To model Alzheimer’s disease in rats, 2 µg of 192-IgG-SAP (Cat. #IT-01) was injected into the lateral cerebral ventricle. Examination of the lesioned animals suggests that nicotine promotes the induction of long-term potentiation by enhancing N-methyl-D-aspartate responses, and suppressing acetylcholine-mediated mechanisms in pyramidal cells.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia.
Wu M, Kc P, Mack SO, Haxhiu MA (2006) Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia. Respir Physiol Neurobiol 152(1):36-50. doi: 10.1016/j.resp.2005.07.002
Summary: Hypercapnia, an excess of CO2 in the blood, is thought to stimulate the release of acetylcholine by airway-related vagal preganglionic neurons (AVPNs). AVPNs in the nucleus ambiguus (NA) were lesioned with ten 1-µl injections of CTB-SAP (Cat. #IT-14) into the trachealis muscle of rats. Treated animals maintained rhythmic breathing patterns, but episodes of increased respiratory rate in response to hypercapnia were significantly reduced.
Related Products: CTB-SAP (Cat. #IT-14)
Sleep-disordered breathing after targeted ablation of preBotzinger complex neurons.
McKay LC, Janczewski WA, Feldman JL (2005) Sleep-disordered breathing after targeted ablation of preBotzinger complex neurons. Nat Neurosci 8(9):1142-1144. doi: 10.1038/nn1517
Summary: Sleep-disordered breathing is common in elderly humans as well as patients with neurodegenerative disease. The authors investigated the role of preBötzinger complex neurons of rats in respiratory rhythm generation. Using the fact that preBötzinger complex neurons in the ventrolateral medulla express the neurokinin-1 receptor, animals were given bilateral injections of SP-SAP (Cat. #IT-07). Beginning 7 days post-injection, lesioned animals displayed marked respiratory disturbances during both sleep and wakeful periods.
Related Products: SP-SAP (Cat. #IT-07)
Origin and immunolesioning of cholinergic basal forebrain innervation of cat primary auditory cortex.
Kamke MR, Brown M, Irvine DR (2005) Origin and immunolesioning of cholinergic basal forebrain innervation of cat primary auditory cortex. Hear Res 206(1-2):89-106. doi: 10.1016/j.heares.2004.12.014
Summary: In this study the authors assessed the use of a cholinergic immunotoxin while examining cholinergic basal forebrain input to the primary auditory cortex in cat. Six 0.5 µg injections of ME20.4-SAP (Cat. #IT-15) were made into the putamen/globus pallidus, and cholinergic cell survival was examined by immunohistochemistry. The injected area showed a large reduction in number of AChE-positive fibers in the primary auditory cortex. This provides the evidence of the efficacy of ME20.4-SAP for investigating plasticity in cat auditory cortex.
Related Products: ME20.4-SAP (Cat. #IT-15)
Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain.
Koh S, Santos TC, Cole AJ (2005) Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain. Exp Neurol 194(2):457-466. doi: 10.1016/j.expneurol.2005.03.002
Summary: It is thought that one mechanism for resistance to seizure-induced injury in immature animals is an abundance of neurotrophic growth factors. Rat pups were treated with 2 µg of 192-Saporin (Cat. #IT-01) injected into the left lateral ventricle to examine how cholinergic basal forebrain projections might affect this type of injury. The results indicate that these neurons may be critical for normal brain growth, and that they play a protective role in preventing excitotoxic neuronal injury.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Autonomic brainstem nuclei are linked to the hippocampus.
Castle M, Comoli E, Loewy AD (2005) Autonomic brainstem nuclei are linked to the hippocampus. Neuroscience 134(2):657-669. doi: 10.1016/j.neuroscience.2005.04.031
Summary: Stimulation of the vagal nerve has been reported to enhance memory, as well as be an effective treatment for epilepsy. The authors examined the underlying synaptic pathway. The right ventral CA1 hippocampal field of rats was lesioned with 42 ng of either anti-DBH-SAP (Cat. #IT-03), or 192-Saporin (Cat. #IT-01). The results indicate that both noradrenergic and cholinergic neurons are relay sites for this pathway.
Related Products: 192-IgG-SAP (Cat. #IT-01), Anti-DBH-SAP (Cat. #IT-03)
