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Anti-amnesic properties of (+/-)-PPCC, a novel sigma receptor ligand, on cognitive dysfunction induced by selective cholinergic lesion in rats.
Antonini V, Prezzavento O, Coradazzi M, Marrazzo A, Ronsisvalle S, Arena E, Leanza G (2009) Anti-amnesic properties of (+/-)-PPCC, a novel sigma receptor ligand, on cognitive dysfunction induced by selective cholinergic lesion in rats. J Neurochem 109:744-754. doi: 10.1111/j.1471-4159.2009.06000.x
Summary: Sigma-1 receptors are found throughout the central nervous system, and are thought to be a target for regenerative therapy in Alzheimer’s disease. Rats received 3.0 µg or 5.0 µg of 192-IgG-SAP (Cat. #IT-01) injected intracerebroventricularly. The lesioned animals displayed dose-dependent deficits in water maze performance. Treatment with the sigma-1 receptor agonist (±)-PPCC significantly improved both reference and working memory performance in treated animals, indicating that (±)-PPCC-mediated positive effects are probably a function of the sigma-1 receptor.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Cognitive performances of cholinergically depleted rats following chronic donepezil administration.
Cutuli D, Foti F, Mandolesi L, De Bartolo P, Gelfo F, Federico F, Petrosini L (2009) Cognitive performances of cholinergically depleted rats following chronic donepezil administration. J Alzheimers Dis 17(1):161-176. doi: 10.3233/JAD-2009-1040 PMID: 19221411
Summary: The authors examined whether donepezil could improve cognitive functions in rats with lesions of the cholinergic cells in the forebrain. Treated animals received 4 µg bilateral intracerebroventricular injections of 192-IgG-SAP (Cat. #IT-01), followed by treatment with donepezil or a control. Donepezil-treated animals performed significantly better than control animals.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Developmental forebrain cholinergic lesion and environmental enrichment: behaviour, CA1 cytoarchitecture and neurogenesis.
Frechette M, Rennie K, Pappas BA (2009) Developmental forebrain cholinergic lesion and environmental enrichment: behaviour, CA1 cytoarchitecture and neurogenesis. Brain Res 1252:172-182. doi: 10.1016/j.brainres.2008.11.082
Summary: The authors investigated the effect of neonatal cholinergic lesions on plasticity in the presence or absence of enrichment. Each lateral ventricle of 7 day-old rats received 300 ng of 192-IgG-SAP (Cat. #IT-01). Although the lesions did not attenuate neurobehavioral plasticity, there were several physiological changes that occurred despite the environmental enrichment.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Effects of the selective lesions of cholinergic septohippocampal neurons on different forms of memory and learning process.
Dashniani MG, Beseliia GV, Maglakelidze GA, Burdzhanadze MA, Chkhikvishvili N (2009) Effects of the selective lesions of cholinergic septohippocampal neurons on different forms of memory and learning process. Georgian Med News 166:81-85.
Summary: The hippocampus is crucial for the ability to recollect everyday events and factual knowledge. Here the authors looked at the role of the septo-hippocampal cholinergic system of the medial septum in learning and memory. Rats received 200 ng injections of 192-IgG-SAP (Cat. #IT-01) into the medial septum. Mouse IgG-SAP (Cat. #IT-18) was used as a control. The data suggest that although the septo-hippocampal region is essential for spatial learning, hippocampal acetyl cholinesterase may not be essential for all types of hippocampal-dependent memory.
Related Products: 192-IgG-SAP (Cat. #IT-01), Mouse IgG-SAP (Cat. #IT-18)
Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin.
Burk JA, Lowder MW, Altemose KE (2008) Attentional demands for demonstrating deficits following intrabasalis infusions of 192 IgG-saporin. Behav Brain Res 195:231-238. doi: 10.1016/j.bbr.2008.09.006
Summary: Attentional processing has been shown to be dependent on basal forebrain cholinergic inputs to the cerebral cortex. In this work the authors wished to specify which components should be used to demonstrate deficits following the loss of these neurons. Rats received 200 ng intrabasalis infusions of 192-IgG-SAP (Cat. #IT-01). Testing of lesioned animals indicated that attentional deficits are due to increase of overall attentional task demands as opposed to any single task parameter.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Selective lesion of septal cholinergic neurons in rats impairs acquisition of a delayed matching to position T-maze task by delaying the shift from a response to a place strategy.
Fitz NF, Gibbs RB, Johnson DA (2008) Selective lesion of septal cholinergic neurons in rats impairs acquisition of a delayed matching to position T-maze task by delaying the shift from a response to a place strategy. Brain Res Bull 77:356-360. doi: 10.1016/j.brainresbull.2008.08.016
Summary: It has been theorized that the effect of cholinergic lesions of the medial septum on learning depend on the stressful nature of the task being learned. The authors injected 0.2 µg of 192-IgG-SAP (Cat. #IT-01) into the medial septum of rats then examined the strategies used by these animals to learn a delayed matching to position T-maze task. Lesioned animals were less able to switch from one strategy to another, indicating that this mechanism is the primary one affected by septal cholinergic lesions.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Organization of food protection behavior is differentially influenced by 192 IgG-saporin lesions of either the medial septum or the nucleus basalis magnocellularis.
Martin MM, Winter SS, Cheatwood JL, Carter LA, Jones JL, Weathered SL, Wagner SJ, Wallace DG (2008) Organization of food protection behavior is differentially influenced by 192 IgG-saporin lesions of either the medial septum or the nucleus basalis magnocellularis. Brain Res 1241:122-135. doi: 10.1016/j.brainres.2008.09.018
Summary: In this work the authors used a food-protection model to investigate the role of cholinergic neurons in the processing of information from internal and external sources. Rats received the following amounts of 192-IgG-SAP (Cat. #IT-01): 15 ng or 20 ng into the medial septum (MS), or 20 ng into the nucleus basalis magnocellularis (NB). While the NB lesions reduced the number of successful food protection behaviors, lesions in the MS disrupted the temporal organization of this behavior.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Involvement of the habenula in cognition through its regulatory role upon monoamine and acetylcholine transmissions
Lecourtier L (2008) Involvement of the habenula in cognition through its regulatory role upon monoamine and acetylcholine transmissions. Neuroscience 2008 Abstracts 698.4. Society for Neuroscience, Washington, DC.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Enhanced sensitivity to phencyclidine following cortical cholinergic denervation
Savage ST, Oberg J, Pernold K, Mattsson A (2008) Enhanced sensitivity to phencyclidine following cortical cholinergic denervation. Neuroscience 2008 Abstracts 842.7/X2. Society for Neuroscience, Washington, DC.
Summary: Alterations in cholinergic signaling in the brain have been implicated as a contributing factor in the pathogenesis of schizophrenia. We have recently shown that cholinergic denervation of cortex cerebri by stereotaxic infusion of the immunotoxin 192 IgG-saporin in the nucleus basalis magnocellularis in adult rats, leads to an enhanced sensitivity to amphetamine. Thus, saporin lesioned rats show a marked increase in locomotor activity, as well as a potentiated dopamine release in nucleus accumbens when challenged with amphetamine. We hypothesize that the loss of cortical cholinergic input alters the activity of cortical glutamatergic neurons and in turn, their regulation of subcortical dopamine neurons. We have previously shown that this cortical cholinergic denervation leads to an increased locomotor response to the NMDA receptor antagonist phencyclidine (PCP), suggesting that disruption of cortical cholinergic activity can lead to disturbances of glutamatergic transmission. In current studies we are investigating attention and memory functions of rats with cholinergic denervation of neocortex using the novel object recognition task. Preliminary data from these investigations shows impairment in performance under PCP-challenge in saporin lesioned rats as compared to sham lesioned controls. These results indicate that cortical cholinergic deficits, in addition to leading to a dramatic potentiation of the locomotor response to PCP, can also lead to an enhanced sensitivity to PCP-induced cognitive impairments. Using pharmacological magnetic resonance imaging (MRI) we are investigating possible spatiotemporal differences in brain activation in rats with cortical cholinergic deficits following administration of PCP. Preliminary data have provided indications of a greater activation in cortical areas in saporin lesioned rats as compared to sham lesioned controls following PCP-challenge. Evaluations of possible alterations in social behavior following cortical cholinergic denervation are ongoing. Social interaction will be investigated under normal conditions, as well as after PCP-challenge. Preliminary results from these studies together with our previous results indicate that loss of cortical acetylcholine can lead to alterations in glutamatergic signaling. These observations are compatible with a possible role of cholinergic deficits in schizophrenia, and provide a possible link between different hypotheses of the disorder.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Effects of cholinergic deafferentation of medial, prefrontal cortex on a cross-modal divided attention task
Carter ES, Newman LA, Galler JR, Mcgaughy J (2008) Effects of cholinergic deafferentation of medial, prefrontal cortex on a cross-modal divided attention task. Neuroscience 2008 Abstracts 590.6/TT58. Society for Neuroscience, Washington, DC.
Summary: Previous research has shown that cholinergic lesions of the nucleus basalis magnocellularis impair cross-modal divided attention (Turchi and Sarter 1997). Cholinergically lesioned rats showed increased response latencies relative to sham-lesioned rats if required to divide attention but did not differ from sham-lesioned rats when tested in a focused attention condition. In the present study, the effects of selective cholinergic depletion of the medial, prefrontal cortex were assessed in the same cross-modal divided attention task (CMDAT). Male, Long-Evans rats were trained on one set of conditional response rules for visual stimuli and another for auditory stimuli. In the CMDAT, rats received 20 trials of either auditory or visual stimuli followed by twenty trials of the alternate modality (focused attention). Within the same session rats received 60 trials of a randomized sequence of all possible stimuli (divided attention). These trials were followed by two additional blocks of focused attention (20 trials/block) so the trial block sequence was Focused Attention 1 (FA1): Divided Attention (DA) : Focused attention 2 (FA2). Subjects received infusions of 192 IgG saporin (pACh-LX) or its vehicle (SHAM-LX) to the prelimbic cortex. Response latencies for all subjects were longer under conditions of divided attention when performance was compared to the first block of focused attention trials. However in pACh-LX rats response latencies in the second block of focused attention trials were longer than in the divided attention trials. The slowed performance in the FA2 block may suggest cognitive fatigue after performing the divided attention trials or may be due to the effects of prolonged time on task. To address this question, a novel sequence of trials DA : FA1 : FA2 was tested. This session showed no difference in response latencies across blocks in either group. The lack of increased response latencies in FA2 suggests the effect in the standard task is related to cognitive fatigue after completion of the DA block and prolonged time on task. The accuracy of pACh-LX rats was decreased in the divided attention block relative to SHAM-LX rats in this block and relative to pACh-LX rats’ own performance in the DA block of the standard task. This loss of accuracy with decreased latency suggests that lesioned rats show a cost of divided attention if no focused attention blocks precede divided attention testing. These data support the hypothesis that cholinergic afferents to the prefrontal cortex mediate divided attention and a loss of these afferents exacerbates cognitive fatigue.
Related Products: 192-IgG-SAP (Cat. #IT-01)