| 1. |
- Grillner, Sten, et al.
(författare)
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Modeling a vertebrate motor system : pattern generation, steering and control of body orientation
- 2007
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Ingår i: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 165, s. 221-234
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Forskningsöversikt (refereegranskat)abstract
- The lamprey is one of the few vertebrates in which the neural control system for goal-directed locomotion including steering and control of body orientation is well described at a cellular level. In this report we review the modeling of the central pattern-generating network, which has been carried out based on detailed experimentation. In the same way the modeling of the control system for steering and control of body orientation is reviewed, including neuromechanical simulations and robotic devices.
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| 2. |
- Nyberg, Fred, et al.
(författare)
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Neuropeptides in hyperthermia
- 2007
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Ingår i: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 277-293
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Forskningsöversikt (refereegranskat)abstract
- Brain damage as a result of hyperthermia or heat-stress has been the focus of attention in many areas of neuroscience in recent years. Heat-induced alterations in structural components of the central nervous system (CNS) will obviously also influence the relevant transmitter systems, which may be involved in a variety of different behaviors. Indeed, many studies have indicated that excitatory amino acids, and monoaminergic and peptidergic systems are affected during hyperthermia. This chapter will address past and current research on various neuropeptides that have been implicated in the consequences of hyperthermia and various other heat disorders. However, considering the large and even increasing number of identified neuroactive peptides, it is necessary to limit this chapter to a few peptides or peptide systems, which have received particular attention in relation to hyperthermia. Among these are the opioid peptides, the tachykinins, calcitonin gene-related peptide (CGRP), and peptides belonging to the angiotensin system. Most of these neuropeptides are not only affected by hyperthermia and abnormal alterations in the body temperature but also are involved in the endogenous mechanisms of regulating body temperature. This review does not endeavor to fully cover the field but it does aim to give the reader an idea of how various neuropeptides may be involved in the control of body heat and how peptidergic systems are affected during various thermal changes, including both immediate and long-term consequences.
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| 3. |
- Persson, Jonas, et al.
(författare)
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Altered brain activity in healthy seniors : what does it mean?
- 2006
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Ingår i: Progress in Brain Research. - Amsterdam : Elsevier. - 0079-6123 .- 1875-7855. ; 157, s. 45-56
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Age-related performance decreases are frequently observed on various memory tasks. Recent brain imaging studies using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) suggest a link between altered patterns of brain activity in older adults and memory performance. Convergent neuroimaging evidence shows that older adults have decreased activity in multiple regions important for memory tasks. Such relative under-activation in older adults is likely related to age-related reductions in cognitive performance. Age-comparative neuroimaging studies have also provided convincing support for regional over-activation by older adults. Such findings indicate that the older brain can re-organize to better cope with cognitive and other challenges. Although over-activation may play a compensatory role when cognitive decline is limited, under-activation seems to be the typical pattern when cognitive impairment is in a more progressed state. This pattern of age-related changes suggests that compensation through over-activation is restricted to the early stages of cognitive impairment in aging.
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| 4. |
- Sharma, Hari Shanker, et al.
(författare)
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Blood-cerebrospinal fluid barrier in hyperthermia
- 2007
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Ingår i: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 459-478
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Forskningsöversikt (refereegranskat)abstract
- The blood-CSF barrier (BCSFB) in choroid plexus works with the blood-brain barrier (BBB) in cerebral capillaries to stabilize the fluid environment of neurons. Dysfunction of either transport interface, i.e., BCSFB or BBB, causes augmented fluxes of ions, water and proteins into the CNS. These barrier disruptions lead to problems with edema and other compromised homeostatic mechanisms. Hyperthermic effects on BCSFB permeability and transport are not as well known as for BBB. However, it is becoming increasingly appreciated that elevated prostaglandin synthesis from fever/heat activation of cyclooxygenases (COXs) in the BCSFB promotes water and ion transfer from plasma to the ventricles; this harmful fluid movement into the CSF-brain interior can be attenuated by agents that inhibit the COXs. Moreover, new functional data from our laboratory animal model indicate that the BCSFB (choroidal epithelium) and the CSF-bordering ependymal cells are vulnerable to whole body hyperthermia (WBH). This is evidenced from the fact that rats subjected to 4h of heat stress (38 degrees C) showed a significant increase in the translocation of Evans blue and (131)Iodine from plasma to cisternal CSF, and manifested blue staining of the dorsal surface of the hippocampus and caudate nucleus. Degeneration of choroidal epithelial cells and underlying ependyma, a dilated ventricular space and damage to the underlying neuropil were frequent. A disrupted BCSFB is associated with a marked increase in edema formation in the hippocampus, caudate nucleus, thalamus and hypothalamus. Taken together, these findings suggest that the breaching of the BCSFB in hyperthermia significantly contributes to cell and tissue injuries in the CNS.
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| 5. |
- Sharma, Hari Shanker
(författare)
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Interaction between amino acid neuro transmitters and opioid receptors in hyperthermia-induced brain pathology
- 2007
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Ingår i: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 295-317
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Forskningsöversikt (refereegranskat)abstract
- This review is focused on the possible interaction between amino acid neurotransmitters and opioid receptors in hyperthermia-induced brain dysfunction. A balance between excitatory and inhibitory amino acids appears to be necessary for normal brain function. Increased excitotoxicity and a decrease in inhibitory amino acid neurotrarismission in hyperthermia are associated with brain pathology and cognitive impairment. This is supported by recent data from our laboratory that show a marked increase in glutamate and aspartate and a decrease in GABA and glycine in several brain areas following heat stress at the time of brain pathology. Blockade of multiple opioid receptors with naloxone restored the heat stress-induced decline in GABA and glycine and thwarted the elevation of glutamate and aspartate in the CNS. In naloxone-treated stressed animals, cognitive dysfunction and brain pathology are largely absent. Taken together, these new findings suggest that an intricate balance between excitatory and inhibitory amino acids is important for brain function in heat stress. In addition, opioid receptors play neuromodulatory roles in amino acid neurotransmission in hyperthermia.
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| 6. |
- Sharma, Hari Shanker
(författare)
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Methods to produce hyperthermia-induced brain dysfunction
- 2007
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Ingår i: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 173-199
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Forskningsöversikt (refereegranskat)abstract
- The recent increase in the frequency and intensity of killer heat waves across the globe has aroused worldwide medical attention to exploring therapeutic strategies to attenuate heat-related morbidity and/or mortality. Death due to heat-related illnesses often exceeds >50% of heat victims. Those who survive are crippled with lifetime disabilities and exhibit profound cognitive, sensory, and motor dysfunction akin to premature neurodegeneration. Although more than 50% of the world populations are exposed to summer heat waves; our understanding of detailed underlying mechanisms and the suitable therapeutic strategies have still not been worked out. One of the basic reasons behind this is the lack of a reliable experimental model to simulate clinical hyperthermia. This chapter describes a suitable animal model to induce hyperthermia in rats (or mice) comparable to the clinical situation. The model appears to be useful for studying the effects of heat-related illnesses on changes in various organs and systems, including the central nervous system (CNS). Since hyperthermia is often associated with profound brain dysfunction, additional methods to examine some crucial parameters of brain injury, e.g., blood-brain barrier (BBB) breakdown and brain edema formation, are also described.
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| 7. |
- Sharma, Hari Shanker, et al.
(författare)
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Nanoparticles aggravate heat stress induced cognitive deficits, blood-brain barrier disruption, edema formation and brain pathology
- 2007
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Ingår i: Progress in Brain Research. - 0079-6123 .- 1875-7855. ; 162, s. 245-273
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Forskningsöversikt (refereegranskat)abstract
- Our knowledge regarding the influence of nanoparticles on brain function in vivo during normal or hyperthermic conditions is still lacking. Few reports indicate that when nanoparticles enter into the central nervous system (CNS) they may induce neurotoxicity. On the other hand, nanoparticle-induced drug delivery to the brain enhances neurorepair processes. Thus, it is likely that the inclusion of nanoparticles in body fluid compartments alters the normal brain function and/or its response to additional stress, e.g., hyperthermia. New data from our laboratory show that nanoparticles derived from metals (e.g., Cu, Ag or Al, approximately 50-60nm) are capable of inducing brain dysfunction in normal animals and aggravating the brain pathology caused by whole-body hyperthermia (WBH). Thus, normal animals treated with nanoparticles (for 1 week) exhibited mild cognitive impairment and cellular alterations in the brain. Subjection of these nanoparticle-treated rats to WBH resulted in profound cognitive and motor deficits, exacerbation of blood-brain barrier (BBB) disruption, edema formation and brain pathology compared with naive animals. These novel observations suggest that nanoparticles enhance brain pathology and cognitive dysfunction in hyperthermia. The possible mechanisms of nanoparticle-induced exacerbation of brain damage in WBH and its functional significance in relation to our current knowledge are discussed in this review.
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| 8. |
- Sharma, Hari Shanker, et al.
(författare)
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Nanoparticles influence pathophysiology of spinal cord injury and repair
- 2009
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Ingår i: Progress in Brain Research. - Amsterdam : Elsevier. - 0079-6123 .- 1875-7855. - 9780444534316 ; 180, s. 155-180
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Forskningsöversikt (refereegranskat)abstract
- Spinal cord injury (SCI) is a serious clinical problem for which no suitable therapeutic strategies have been worked out so far. Recent studies suggest that the SCI and its pathophysiological responses could be altered by systemic exposure to nanoparticles. Thus, SCI when made in animals intoxicated with engineered nanoparticles from metals or silica dust worsened the outcome. On the other hand, drugs tagged with titanium (TiO2) nanoparticles or encapsulated in liposomes could enhance their neuroprotective efficacy following SCI. Thus, to expand our knowledge on nanoparticle-induced alterations in the spinal cord pathophysiology further research is needed. These investigations will help to develop new strategies to achieve neuroprotection in SCI, for example, using nanodrug delivery. New results from our laboratory showed that nanoparticle-induced exacerbation of cord pathology following trauma can be reduced when the suitable drugs tagged with TiO2 nanowires were administered into the spinal cord as compared to those drugs given alone. This indicates that nanoparticles depending on the exposure and its usage could induce both neurotoxicity and neuroprotection. This review discusses the potential adverse or therapeutic utilities of nanoparticles in SCI largely based on our own investigations. In addition, possible mechanisms of nanoparticle-induced exacerbation of cord pathology or enhanced neuroprotection following nanodrug delivery is described in light of recently available data in this rapidly emerging field of nanoneurosciences.
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