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Gene expression profile in rat hippocampus with and without memory deficit.
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)
Damage of GABAergic neurons in the medial septum impairs spatial working memory and extinction of active avoidance: Effects on proactive interference.
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)
The validity of scopolamine as a pharmacological model for cognitive impairment: A review of animal behavioral studies
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.
Does age matter? Behavioral and neuro-anatomical effects of neonatal and adult basal forebrain cholinergic lesions.
De Bartolo P, Cutuli D, Ricceri L, Gelfo F, Foti F, Laricchiuta D, Scattoni ML, Calamandrei G, Petrosini L (2010) Does age matter? Behavioral and neuro-anatomical effects of neonatal and adult basal forebrain cholinergic lesions. J Alzheimers Dis 20:207-227. doi: 10.3233/JAD-2010-1355 PMID: 20164586
Summary: The authors characterized the differences caused by age on the effect of cholinergic lesions of the basal forebrain. Seven-day-old rats received 210 ng bilateral intracerebroventricular injections of 192-IgG-SAP (Cat. #IT-01). Eighty-day-old rats received 4 µg bilateral intracerebroventricular injections of 192-IgG-SP. Both experimental groups displayed similar behavior, indicating that development of a depleted cholinergic system yields similar results to cholinergic dysfunction in adulthood.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Unique contributions of distinct cholinergic projections to motor cortical plasticity and learning.
Conner JM, Kulczycki M, Tuszynski MH (2010) Unique contributions of distinct cholinergic projections to motor cortical plasticity and learning. Cereb Cortex 20(11):2739-2748. doi: 10.1093/cercor/bhq022
Summary: This work mapped the basal cholinergic forebrain system associations with skilled motor learning and motor function recovery after cortical injury. Rats were lesioned with 192-IgG-SAP (Cat. #IT-01). The animals received either two rostrocaudal injections of 75-112 ng; two 19 ng injections into the “prefrontal depletion site”; or two 19 ng injections into the “motor cortex depletion site.” Loss of motor cortex cholinergic systems disrupts map plasticity and skilled motor behavior, indicating that control of these systems rests within the motor cortex.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Recent progress in research on ribosome inactivating proteins.
Ng TB, Wong JH, Wang H (2010) Recent progress in research on ribosome inactivating proteins. Curr Protein Pept Sci 11(1):37-53. doi: 10.2174/138920310790274662
Summary: This review discusses recent literature on ribosome inactivating proteins including the use of saporin-based conjugates in neuroscience and cancer research. Brief descriptions of research done using 192-IgG-SAP (Cat. #IT-01), OX7-SAP (Cat. #IT-02), dermorphin-SAP (Cat. #IT-12), anti-SERT-SAP (Cat. #IT-23), SSP-SAP (Cat. #IT-11), anti-DBH-SAP (Cat. #IT-03), CTB-SAP (Cat. #IT-14), and other conjugates are provided along with basic information about ribosome inactivating proteins.
Related Products: 192-IgG-SAP (Cat. #IT-01), OX7-SAP (Cat. #IT-02), Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Anti-SERT-SAP (Cat. #IT-23), SSP-SAP (Cat. #IT-11), Anti-DBH-SAP (Cat. #IT-03), CTB-SAP (Cat. #IT-14)
Distinct neural pathways mediate alpha7 nicotinic acetylcholine receptor-dependent activation of the forebrain.
Thomsen MS, Hay-Schmidt A, Hansen HH, Mikkelsen JD (2010) Distinct neural pathways mediate alpha7 nicotinic acetylcholine receptor-dependent activation of the forebrain. Cereb Cortex 20(9):2092-2102. doi: 10.1093/cercor/bhp283
Summary: a7 nicotinic acetylcholine receptor (nAChR) agonists are potential treatments for some aspect of schizophrenia. The authors examine whether cholinergic neurons in the horizontal limb of the diagonal band of Broca (HDB) are a target for this treatment. Rats received 300 ng injections of 192-IgG-SAP (Cat. #IT-01) into the HDB. The results demonstrate that cholinergic neurons in the HDB are essential for a7 nAChR agonist activation of the medial prefrontal cortex.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Estrogen therapy and cognition: a review of the cholinergic hypothesis.
Gibbs RB (2010) Estrogen therapy and cognition: a review of the cholinergic hypothesis. Endocr Rev 31(2):224-253. doi: 10.1210/er.2009-0036
Summary: This review discusses estrogen therapy for use in postmenopausal women. In this context the issues revolve around benefits vs. harm of such therapy on the brain and cognitive impairment associated with aging and Alzheimer’s disease. Use of 192-IgG-SAP (Cat. #IT-01) to investigate this paradigm is described.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Amyloid-beta expression in retrosplenial cortex of triple transgenic mice: relationship to cholinergic axonal afferents from medial septum.
Robertson RT, Baratta J, Yu J, LaFerla FM (2009) Amyloid-beta expression in retrosplenial cortex of triple transgenic mice: relationship to cholinergic axonal afferents from medial septum. Neuroscience 164:1334-1346. doi: 10.1016/j.neuroscience.2009.09.024
Summary: In this work the authors developed a model to examine the relationship between afferent projections and the formation of amyloid-beta (Aβ) deposits. Mice received 1.86 µg unilateral injections of 192-IgG-SAP (Cat. #IT-01) into the lateral ventricle. Lesioned animals had persistent Aβ immunoreactivity in layer III of the granular division of retrosplenial cortex (RSg). This data indicates that septal cholinergic axonal projections transport Aβ or amyloid precursor protein to layer III of the RSg.
Related Products: 192-IgG-SAP (Cat. #IT-01), mu p75-SAP (Cat. #IT-16)
Effects of combined neonatal cholinergic lesion and chronic cerebral hypoperfusion on CA1 cytoarchitecture.
Rennie KE, Ward C, Fréchette M, Pappas BA (2009) Effects of combined neonatal cholinergic lesion and chronic cerebral hypoperfusion on CA1 cytoarchitecture. Neuroscience 2009 Abstracts 736.23/M38. Society for Neuroscience, Chicago, IL.
Summary: Neonatal lesioning of the basal forebrain cholinergic (BFC) system alters cytoarchitecture of pyramidal cells in both the hippocampus and neocortex of the adult rat, indicating a role for the BFC in forebrain development. In addition to altering forebrain development, neonatal cholinergic lesion may also exacerbate the brain’s response to pathological factors that emerge as the brain ages. One factor that might interact with BFC lesion is reduced cerebral blood flow (hypoperfusion). Examining this interaction is especially interesting because both BFC degeneration and reduced cerebral blood flow are characteristics of Alzheimer’s disease. In the rat, chronic cerebrovascular insufficiency by itself reportedly causes the degeneration of hippocampal CA1 pyramidal cells, alters amyloid processing and produces spatial memory impairments. We hypothesized that neonatal cholinergic lesion using the cholinotoxin 192-IgG-saporin would render the hippocampus more vulnerable to the neuropathological effects of chronic forebrain hypoperfusion induced by permanent bilateral occlusion of the carotid arteries (2VO). We previously reported that combined BFC lesion and 2VO impaired working memory in the Morris water maze and increased anxiety-like behaviours on the elevated plus apparatus, whereas neither of these treatments alone caused any of these effects. Here we report the effects of neonatal BFC lesion, 2VO, or their combined application on hippocampal CA1 cytoarchitecture using quantitative Golgi analysis. Rats subjected to 2VO showed increased apical branch length and spines, and increased basal spines. Neonatal BFC lesion on its own had only restricted effects on apical branch length at certain branch orders and no effect on spines. However, at a number of branch orders the stimulating effect of 2VO on apical spines occurred only in animals subjected to neonatal BFC lesion, indicating that this lesion modulated the response to 2VO. To our knowledge, this is the first examination of the effects of 2VO on CA1 neuron cytoarchitecture. Surprisingly, it increased rather than decreased dendritic length and spines. Furthermore, while the BFC lesion had minimal effects on its own, it was permissive to some of the effects of 2VO on dendritic spines. Taken together with our previous data, this study suggests that pre-existing cholinergic dysfunction alters aspects of both the behavioural and neural consequences of chronic hypoperfusion. These results may have implications for Alzheimer’s disease where cholinergic dysfunction and hypoperfusion are co-expressed
Related Products: 192-IgG-SAP (Cat. #IT-01)