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At least 55 records · Page 3Linked to original sources
PubMed1995

Parameter identification of a neurological control model for the pathological head movements of cerebellar patients.

The objective of this research is to explore the role of the cerebellum in the human motor control system. The present study quantitatively compares the neurological control signals effecting fast, horizontal head rotations in normal subjects to those in patients with a cerebellar lesion. The method involves the use of a computer simulation model for one degree-of-freedom movements. A method for unconstrained global optimization, first proposed by Hans Bremermann (1970), is used to identify the timing and magnitudes of the input neurological control signals to the model, which are compared to recorded electromyograms (EMGs). Experimentally recorded kinematics from cerebellar patients and from normal subjects were used to drive the parameter search. These simulations found that cerebellar patients' neurological control signals were altered with respect to those of normal subjects, and suggest that the electromyographic activity of cerebellar patients may comprise at least five bursts of activity whereas normal subjects typically exhibit only three. The results are discussed with respect to the hypothesis that the cerebellum may be involved in both the timing and magnitudes of the neurological control signals effecting voluntary movement.

Algorithms↗
PubMed2006

[Dissection of cavernous nerves in rat and model of neurological erectile dysfunction].

OBJECTIVES: To identify rat cavernous nerve and establish a rat model of erectile dysfunction caused by injury of cavernous nerve. METHODS: Ten rats were undergone dissections. 30 experimental rats were randomized into 2 groups, cavernous nerve were identified by electrical stimulation. One month after surgery, rat models were evaluated by electrical stimulation. RESULTS: The anatomic structure of cavernous nerve in rats are highly similar to human beings, the erection can be evoked by stimulating cavernous nerves, and after cavernous nerve injury it can not be evoked (P < 0.05). CONCLUSION: Because of the highly similarity of cavernous nerve between rats and human beings, so as the suitable price, rat should be used as the ideal ED experimental animal. The model of ED caused by cavernous nerve injury is reliable.

Animals↗
PubMedDate not supplied

[The use of a primary astrocyte culture for modelling HIV neurological infection].

The article deals with the results of the experiment substantiating the in vitro model of HIV neuro-infection. In this work primary glial (astrocytic) tissue cultures obtained from normal human and animal (guinea pig) brain tissue were used. As revealed in this investigation, the following phenomena could be observed in human brain tissue monolayer culture, infected with HIV and subsequently subcultured: (a) the stimulation of tissue-cell growth; (b) the formation of multinuclear glial cells; (c) the presence of virus-specific proteins in astrocyte cytoplasm, detected by immunofluorescent and electrophoretic techniques; (d) the presence of HIV-1 DNA provirus in infected astrocytes. Cyto-destruction was not observed, reverse transcriptase activity was absent.

AIDS Dementia Complex↗
PubMed2001

In vivo microdialysis in an animal model of neurological disease: thiamine deficiency (Wernicke) encephalopathy.

In vivo microdialysis allows for the constant monitoring of brain neurotransmitters in the extracellular fluid of awake and freely moving animals. Considerations including factors affecting probe recoveries, the blood-brain barrier, and tissue reactions to probe implantation are discussed in this paper. Details of the application of in vivo microdialysis to an animal model of encephalopathy are then presented. Thiamine deficiency encephalopathy is an animal model of Wernicke encephalopathy, a neurological disorder observed in alcoholics and in patients with severely compromised nutrition. Regionally selective neuronal cell death is observed in both patients and animals with thiamine deficiency (TD). Various thalamic nuclei suffer significant TD-induced cell death, and NMDA receptor-mediated glutamate excitotoxicity has been proposed as an underlying causative factor. A detailed methodology for the examination of the role of glutamate excitotoxicity using in vivo microdialysis in the neuronal cell death due to thiamine deficiency is presented.

Animals↗
PubMed1998

Fibroblast models of neurological disorders: fluorescence measurement studies.

Biochemical studies of human fibroblasts from patients with neurological disorders have revealed a wealth of information on how such disorders occur. In this review, Gerald Connolly describes how recently developed fluorescence video imaging techniques have been used to study the physiology of skin fibroblasts isolated from patients with certain neurological disorders, including those produced by Alzheimer's disease, Lesch-Nyhan syndrome, mitochondrial disorders, amyotrophic lateral sclerosis and lysosomal disorders. The results of these studies indicate disruptions in cell homeostasis, particularly specific changes in Ca2+ homeostasis and autofluorescence, which mirror changes thought to occur in the CNS of neurologically impaired patients. More extensive studies of these 'systemic changes' using new fluorescent indicators, combined with advances in imaging techniques, are predicted to increase the potential usefulness of human skin fibroblasts as experimental models and to help diagnose and treat neurological disorders.

Alzheimer Disease↗
PubMedDate not supplied

The evolution of the clinician-scientist model of neurological rehabilitation.

Over the past three or four decades two treatment technologies have been evolving in parallel, recently to some extent merging. The first of these technologies is behaviour analysis, with its emphasis on identification and manipulation of variables external to the individual as controlling agents. The second is neurological rehabilitation, with a characteristic focus of resources on recovery of function following neurological damage. The histories of both of these technologies are similar in that they emerged from basic laboratory research with non-human subjects, followed by extension of findings to research with humans, culminating in widespread formal application of results. The past 5 years have seen a convergence of behaviour analytic and neurological rehabilitation techniques resulting in major shifts in treatment service delivery systems. We briefly chronicle the emergence of these two technologies from their basic underpinnings through world-wide use. Further, discussion is provided describing our and others' experience with the combining of behaviour and neurological rehabilitation. Finally, we give an account of an innovative neurological rehabilitation service delivery system designed to deliver effective cost-efficient treatment in the patient's natural environment. Implicit in the design and implementation of this real-world model of rehabilitation is the combination of behavioural technology and neurological rehabilitation towards the achievement of functional outcomes which endure. Our purpose in the above is to provide an introduction to present use and future potential of behaviour analytic methodologies and technologies in rehabilitation.

Ambulatory Care↗
PubMed2003

Invertebrate models of neurologic disease: insights into pathogenesis and therapy.

The search for cures of human diseases can be very slow, expensive, and serendipitous. Roughly five decades of basic research in a handful of model systems has revealed that most animals are quite similar to one another especially at the cellular and molecular levels. The commonalities allow one to use animal models to investigate human disease mechanisms. Here, we review contributions demonstrating the use of invertebrate models to investigate human neurodegenerative diseases. We conclude that the integration of fly and worm models into programs seeking to identify therapeutic strategies for neurodegenerative disease can significantly speed progress toward finding cures for these devastating diseases.

Animals↗
PubMed2003

Depletion of wild-type huntingtin in mouse models of neurologic diseases.

Huntington's disease (HD) is caused by a mutation in the gene encoding for huntingtin resulting in selective neuronal degeneration. Because HD is an autosomal dominant disorder, affected individuals have one copy of the mutant and one copy of the wild-type allele. Huntingtin has antiapoptotic properties and is critical for cell survival. However, the important role of wild-type huntingtin in both HD and other neurological diseases has not been fully recognized. We demonstrate disease-associated decreased levels of full-length huntingtin in brains of transgenic mouse models of HD, ischemia, trauma, and in spinal cord after injury. In addition, overexpression of wild-type huntingtin confers in vivo protection of neurodegeneration after ischemia. We propose that in HD, in addition to a toxic gain-of-function of mutant huntingtin, a parallel depletion of wild-type huntingtin results in a detrimental loss-of-function, playing an important role in disease progression.

Animals↗
PubMed1990

Nociceptive reflexes and the somatic dysfunction: a model.

A model of somatic dysfunction is developed in which restriction in mobility and autonomic, visceral, and immunologic changes are produced by pain-related sensory neurons and their reflexes. Nociceptors are known to produce muscular guarding reactions, as well as autonomic activation, when musculoskeletal or visceral tissue is stressed or damaged. This guarding causes abnormal musculoskeletal position and range of motion. Local inflammatory responses and autonomic reflexes further reinforce nociceptor activity, maintaining restriction. Nociceptive autonomic reflexes also evoke changes in visceral and immunologic function. Finally, maintenance of muscles, joints, and related tissues in an abnormal guarding position causes changes in the connective tissues, solidifying the abnormal position. Stretching these tissues into a normal range of motion will restimulate the nociceptor, reflexly reinforcing the somatic dysfunction. This model has evolved from Korr's neurologic model but emphasizes the nociceptor and its reflexes as a source of the connective tissue, circulatory, visceral, and immunologic changes seen in the somatic dysfunction.

Bone and Bones↗
PubMed2005

Chronic implantation of deep brain stimulation leads in animal models of neurological disorders.

Deep brain stimulation (DBS) has routinely been used as a treatment option in Parkinson's disease (PD), tremor disorders and, more recently, dystonia. Here, we describe a method of implantation of DBS leads in the monkey model of PD. By adapting procedures used in human patients, we have devised implantation techniques that can be readily applied to any animal model in which stimulation of subcortical structures is desired. The procedure for implantation consists of microelectrode mapping of the target structure, DBS lead preparation and implantation, and verification of lead placement. The stimulation system described in this paper allows for simultaneous recording of neuronal activity (during stimulation) and observation of animal behavior without restriction of the subject's head or body. In addition, we detail techniques for stimulation and recording from distant structures (utilizing either a one or two chamber system) to facilitate examination of the effects of DBS on neural activity. Thus, the correlation of changes in neuronal activity with behavior during stimulation of subcortical structures can be accomplished. In addition, the use of leads in primates which are analogous in size to human devices allows for close reproduction of the effects of stimulation as observed in humans.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2004

Glutamate transporters: animal models to neurologic disease.

Glutamate is the primary excitatory amino acid neurotransmitter in the central nervous system and its activity is carefully modulated in the synaptic cleft by glutamate transporters. A number of glutamate transporters have been identified in the central nervous system and each has a unique physiologic property and distribution. Glutamate transporter dysfunction may either be an initiating event or part of a cascade leading to cellular dysfunction and ultimately cell death. Animal models of glutamate transporter dysfunction have revealed a significant role for these proteins in pathologic conditions such as neurodegenerative diseases, epilepsy, stroke, and central nervous system tumors. Recent work has focused on glutamate transporter biology in human diseases with an emphasis on how manipulation of these transporter proteins may lead to therapeutic interventions in neurologic disease.

Amino Acid Transport System X-AG↗
PubMed2002

Mouse models for neurological disease.

The mouse has many advantages over human beings for the study of genetics, including the unique property that genetic manipulation can be routinely carried out in the mouse genome. Most importantly, mice and human beings share the same mammalian genes, have many similar biochemical pathways, and have the same diseases. In the minority of cases where these features do not apply, we can still often gain new insights into mouse and human biology. In addition to existing mouse models, several major programmes have been set up to generate new mouse models of disease. Alongside these efforts are new initiatives for the clinical, behavioural, and physiological testing of mice. Molecular genetics has had a major influence on our understanding of the causes of neurological disorders in human beings, and much of this has come from work in mice.

Animals↗
PubMed2000

Neuroengineering models of brain disease.

The techniques of computational simulation have begun to be applied to modeling neurological disease and mental illness. Such neuroengineering models provide a conceptual bridge between molecular/cellular pathology and cognitive performance. We consider models of Alzheimer's disease, Parkinson's disease, and schizophrenia. Each of these diseases involves a disorder of neuromodulation coupled with underlying neuronal pathology. Parallels arising between these models suggests that a common set of computational mechanisms may account for functional loss across a spectrum of brain diseases. In particular, we focus on attractor-based network dynamics and how they arise from neural architectures, on mechanisms for linking sequences of attractor states and their role in cognition, and on the role of neuromodulation in controlling these processes. These studies suggest new approaches to understanding the forebrain circuits underlying cognition, and point toward a new tool for dissecting the pathophysiology of brain disease.

Alzheimer Disease↗
PubMed2006

Neuroprotection by ovarian hormones in animal models of neurological disease.

Ovarian hormones can protect against brain injury, neurodegeneration, and cognitive decline. Most attention has focused on estrogens and accumulating data demonstrate that estrogen seems to specifically protect cortical and hippocampal neurons from ischemic injury and from damage due to severe seizures. Although multiple studies demonstrate protection by estrogen, in only a few instances is the issue of how the steroid confers protection known. Here, we first review data evaluating the neuroprotective effects of estrogens, a selective estrogen receptor modulator (SERM), and estrogen receptor alpha- and beta-selective ligands in animal models of focal and global ischemia. Using focal ischemia in ovariectomized ERalphaKO, ERbetaKO, and wild-type mice, we clearly established that the ERalpha subtype is the critical ER mediating neuroprotection in mouse focal ischemia. In rats and mice, the middle cerebral artery occlusion (MCAO) model was used to represent cerebrovascular stroke, while in gerbils the two-vessel occlusion model, representing global ischemia, was used. The gerbil global ischemia model was used to evaluate the neuroprotective effects of estrogen, SERMs, and ERalpha- and ERbeta-selective compounds in the hippocampus. Analysis of neurogranin mRNA, a marker of viability of hippocampal neurons, with in situ hybridization, revealed that estrogen treatment protected the dorsal CA1 regions not only when administered before, but also when given 1 h after occlusion. Estrogen rarely is secreted alone and studies of neuroprotection have been less extensive for a second key ovarian hormone progesterone. In the second half of this review, we present data on neuroprotection by estrogen and progesterone in animal model of epilepsy followed by exploration into ovarian steroid effects on neuronal damage in models of multiple sclerosis and traumatic brain injury.

Animals↗
PubMed2004

Towards a mutant map of the mouse--new models of neurological, behavioural, deafness, bone, renal and blood disorders.

With the completion of the first draft of the human genome sequence, the next major challenge is assigning function to genes. One approach is genome-wide random chemical mutagenesis, followed by screening for mutant phenotypes of interest and subsequent mapping and identification of the mutated genes in question. We (a consortium made up of GlaxoSmithKline, the MRC Mammalian Genetics Unit and Mouse Genome Centre, Harwell, Imperial College, London, and the Royal London Hospital) have used ENU mutagenesis in the mouse for the rapid generation of novel mutant phenotypes for use as animal models of human disease and for gene function assignment (Nolan et al., 2000). As of 2003, 35,000 mice have been produced to date in a genome-wide screen for dominant mutations and screened using a variety of screening protocols. Nearly 200 mutants have been confirmed as heritable and added to the mouse mutant catalogue and, overall, we can extrapolate that we have recovered over 700 mutants from the screening programme. For further information on the project and details of the data, see http://www.mgu.har.mrc.ac.uk/mutabase.

Animals↗