Electrolytic and ibotenic acid lesions of the nucleus basalis magnocellularis interrupt long-term retention, but not acquisition of two-way active avoidance, in rats

Vale-Martínez, Anna; Guillazo-Blanch, Gemma; Martí-Nicolovius, Margarita; Nadal, Roser; Arévalo-García, Rosa; Morgado-Bernal, Ignacio

doi:10.1007/s00221-001-0917-4

Cited by 25 publications

(9 citation statements)

References 59 publications

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“…The reported deficits support the hypothesis of a role of this neural site in general learning and memory mechanisms (Dunnett et al 1985;Casamenti et al 1988;Aaltonen et al 1991;Schauz and Koch 1999;Gonzalez et al 2000;Stowell et al 2000;Moron et al 2002;Power and McGaugh 2002;Vale-Martinez et al 2002;Conner et al 2003;Frick et al 2004;Knox and Berntson 2006). Nevertheless, it must be underlined that these were permanent lesions.…”

supporting

confidence: 70%

“…It is located in the ventromedial region of the globus pallidus. This nucleus is a complex and heterogeneous structure of mainly cholinergic neurons, and at least 20%-30% of them are noncholinergic (GABA-ergic, glutamatergic, and peptidergic) (Detari et al 1999;Vale-Martinez et al 2002). The main cholinergic innervation of the cortex, a prevalently ipsilateral and topographic projection, emanates from the NBM.…”

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confidence: 99%

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The role of the nucleus basalis magnocellularis in fear conditioning consolidation in the rat

Baldi¹,

Mariottini²,

Bucherelli³

2007

Learn. Mem.

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The nucleus basalis magnocellularis (NBM) is known to be involved in the memorization of several conditioned responses. To investigate the role of the NBM in fear conditioning memorization, this neural site was subjected to fully reversible tetrodotoxin (TTX) inactivation during consolidation in adult male Wistar rats that had undergone fear training to acoustic conditioned stimulus (CS) and context. TTX was stereotaxically administered to different groups of rats at increasing intervals after the acquisition session. Memory was assessed as the conditioned freezing duration measured during retention testing, always performed 72 and 96 h after TTX administration. In this way, there was no interference with normal NBM function during either acquisition or retrieval phases, allowing any amnesic effect to be due only to consolidation disruption. The results show that for contextual fear response memory consolidation, NBM functional integrity is necessary up to 24 h post-acquisition. On the other hand, NBM functional integrity was shown to be necessary for memory consolidation of the acoustic CS fear response only immediately after acquisition and not 24-h post-acquisition. The present findings help to elucidate the role of the NBM in memory consolidation and better define the neural circuits involved in fear memories.

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supporting

confidence: 70%

mentioning

confidence: 99%

The role of the nucleus basalis magnocellularis in fear conditioning consolidation in the rat

Baldi¹,

Mariottini²,

Bucherelli³

2007

Learn. Mem.

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“…Focal neurotoxic, electrolytic or mechanical lesions of the cholinergic centres of the basal forebrain, as well as more general lesions of all the cholinergic neurons of the basal forebrain, are most frequently used to obtain such models. Focal lesions are especially directed at the nucleus basalis magnocellularis (Lescaudron and Stein, 1999; Vale‐Martínez et al ., 2002), the rodent analogue of the human nucleus basalis of Meynert, the septal area (Mulder et al ., 2005), or consist of fimbria/fornix transection leading to septo‐hippocampal cholinergic denervation (He et al ., 1992; Alonso et al ., 1996). Lesioning can be achieved by surgical or electrolytical procedures, and intraparenchymal or intracerebroventricular microinjections of neurotoxic substances, such as quinolic, kainic, N‐methyl‐D‐aspartic, ibotenic and quisqualic acids, the cholinotoxin AF64, and the immunotoxin 192 IgG‐saporin (for review, see Toledana and Álvarez, 2010).…”

Section: Pharmacological Chemical and Lesion‐induced Rodent Modelsmentioning

confidence: 99%

Animal models in the drug discovery pipeline for Alzheimer's disease

Dam

Deyn

2011

British J Pharmacology

200

137

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With increasing feasibility of predicting conversion of mild cognitive impairment to dementia based on biomarker profiling, the urgent need for efficacious disease-modifying compounds has become even more critical. Despite intensive research, underlying pathophysiological mechanisms remain insufficiently documented for purposeful target discovery. Translational research based on valid animal models may aid in alleviating some of the unmet needs in the current Alzheimer's disease pharmaceutical market, which includes disease-modification, increased efficacy and safety, reduction of the number of treatment unresponsive patients and patient compliance. The development and phenotyping of animal models is indeed essential in Alzheimer's disease-related research as valid models enable the appraisal of early pathological processes -which are often not accessible in patients, and subsequent target discovery and evaluation. This review paper summarizes and critically evaluates currently available animal models, and discusses their value to the Alzheimer drug discovery pipeline. Models dealt with include spontaneous models in various species, including senescence-accelerated mice, chemical and lesion-induced rodent models, and genetically modified models developed in Drosophila melanogaster, Caenorhabditis elegans, Danio rerio and rodents. Although highly valid animal models exist, none of the currently available models recapitulates all aspects of human Alzheimer's disease, and one should always be aware of the potential dangers of uncritical extrapolating from model organisms to a human condition that takes decades to develop and mainly involves higher cognitive functions. LINKED ARTICLESThis article is part of a themed issue on Translational Neuropharmacology. To view the other articles in this issue visit http://dx.doi.org/10. 1111/bph.2011.164.issue-4 Abbreviations Ab, amyloid-b; AD, Alzheimer's disease; APP, amyloid precursor protein; BACE1, b-site APP-cleaving enzyme 1; BPSD, behavioural and psychological signs and symptoms of dementia; EGFP, enhanced green fluorescent protein; GSK-3b, glycogen synthase kinase 3b; NFT, neurofibrillary tangle; PSEN, presenilin; SAM, senescence-accelerated mouse; SAMP, SAM-prone; TILLING, targeted induced local lesions in genomes; ZFN, zinc finger nuclease IntroductionAs the prototype of cortical dementias, Alzheimer's disease (AD) presents with prominent cognitive deficits. Initially, patients display limited forgetfulness with disruption of memory imprinting, which evolves to short-term memory disruption and, eventually, to long-term memory deficits. At more advanced stages, patients show executive dysfunctioning leading to advanced helplessness. Besides cognitive deterioration, patients display behavioural and psychological signs and symptoms of dementia (BPSD). BPSD is an umbrella term that embraces a heterogeneous group of noncognitive symptoms and behaviours, including paranoid and delusional ideation, hallucinations, activity disturbances, BJPBritish Journal of Pharmacology...

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“…Another method to induce brain lesions is to infuse agents capable of selective or non-selective destruction of cell populations or even entire structures. Electric current and chronic alcohol ingestion provide alternatives for lesioning procedures [38][39][40][41][42]. However, the lesions produced by these methods are usually non-specific and difficult to use for studies of the pathways involved in neuropathology models.…”

Section: Animal Models Of Senile Dementia and Alzheimer's Diseasementioning

confidence: 99%

Alzheimers Disease and Neural Transplantation as Prospective Cell Therapy

Oliveira¹,

Hodges

2005

CAR

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It has long been recognised that Alzheimer's disease (AD) patients present an irreversible decline of cognitive functions as consequence of cell deterioration in the forebrain cholinergic projection system (FCPS), particularly, in a structure called nucleus basalis of Meynert (nbM). The reduction of the number of cholinergic cells in the FCPS disrupts not just its functions and direct connexions but also the modulation of other systems causing interference in several aspects of behavioural performance including arousal, attention, learning and emotion. It is also common knowledge that AD is an untreatable degenerative disease with very few temporary and palliative drug therapies. Neural stem cell (NSC) grafts present a potential and innovative strategy for the treatment of many disorders of the central nervous system including AD, with the possibility of providing a more permanent remedy than present drug treatments. After grafting, these cells have the capacity to migrate to lesioned regions of the brain and differentiate into the necessary type of cells that are lacking in the diseased brain, supplying it with the cell population needed to promote recovery. The present article aims to review the main aspects of Alzheimer's disease and to explore the use of neural stem cells grafts as alternative treatment for the consequent functional deterioration.

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Electrolytic and ibotenic acid lesions of the nucleus basalis magnocellularis interrupt long-term retention, but not acquisition of two-way active avoidance, in rats

Cited by 25 publications

References 59 publications

The role of the nucleus basalis magnocellularis in fear conditioning consolidation in the rat

The role of the nucleus basalis magnocellularis in fear conditioning consolidation in the rat

Animal models in the drug discovery pipeline for Alzheimer's disease

Alzheimers Disease and Neural Transplantation as Prospective Cell Therapy

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