| 1. |
- Blomqvist, Anders, 1949-, et al.
(författare)
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Neural Mechanisms of Inflammation-Induced Fever
- 2018
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Ingår i: The Neuroscientist. - : Sage Publications. - 1073-8584 .- 1089-4098. ; 24:4, s. 381-399
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Forskningsöversikt (refereegranskat)abstract
- Fever is a common symptom of infectious and inflammatory disease. It is well-established that prostaglandin E-2 is the final mediator of fever, which by binding to its EP3 receptor subtype in the preoptic hypothalamus initiates thermogenesis. Here, we review the different hypotheses on how the presence of peripherally released pyrogenic substances can be signaled to the brain to elicit fever. We conclude that there is unequivocal evidence for a humoral signaling pathway by which proinflammatory cytokines, through their binding to receptors on brain endothelial cells, evoke fever by eliciting prostaglandin E-2 synthesis in these cells. The evidence for a role for other signaling routes for fever, such as signaling via circumventricular organs and peripheral nerves, as well as transfer into the brain of peripherally synthesized prostaglandin E-2 are yet far from conclusive. We also review the efferent limb of the pyrogenic pathways. We conclude that it is well established that prostaglandin E-2 binding in the preoptic hypothalamus produces fever by disinhibition of presympathetic neurons in the brain stem, but there is yet little understanding of the mechanisms by which factors such as nutritional status and ambient temperature shape the response to the peripheral immune challenge.
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| 2. |
- Brozzoli, C, et al.
(författare)
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Multisensory representation of the space near the hand: from perception to action and interindividual interactions
- 2014
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 20:2, s. 122-135
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Tidskriftsartikel (refereegranskat)abstract
- When interacting with objects and other people, the brain needs to locate our limbs and the relevant visual information surrounding them. Studies on monkeys showed that information from different sensory modalities converge at the single cell level within a set of interconnected multisensory frontoparietal areas. It is largely accepted that this network allows for multisensory processing of the space surrounding the body (peripersonal space), whose function has been linked to the sensory guidance of appetitive and defensive movements, and localization of the limbs in space. In the current review, we consider multidisciplinary findings about the processing of the space near the hands in humans and offer a convergent view of its functions and underlying neural mechanisms. We will suggest that evolution has provided the brain with a clever tool for representing visual information around the hand, which takes the hand itself as a reference for the coding of surrounding visual space. We will contend that the hand-centered representation of space, known as perihand space, is a multisensory-motor interface that allows interaction with the objects and other persons around us.
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| 3. |
- Casile, A, et al.
(författare)
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The mirror neuron system: a fresh view
- 2011
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 17:5, s. 524-538
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Tidskriftsartikel (refereegranskat)abstract
- Mirror neurons are a class of visuomotor neurons in the monkey premotor and parietal cortices that discharge during the execution and observation of goal-directed motor acts. They are deemed to be at the basis of primates’ social abilities. In this review, the authors provide a fresh view about two still open questions about mirror neurons. The first question is their possible functional role. By reviewing recent neurophysiological data, the authors suggest that mirror neurons might represent a flexible system that encodes observed actions in terms of several behaviorally relevant features. The second question concerns the possible developmental mechanisms responsible for their initial emergence. To provide a possible answer to question, the authors review two different aspects of sensorimotor development: facial and hand movements, respectively. The authors suggest that possibly two different “mirror” systems might underlie the development of action understanding and imitative abilities in the two cases. More specifically, a possibly prewired system already present at birth but shaped by the social environment might underlie the early development of facial imitative abilities. On the contrary, an experience-dependent system might subserve perception-action couplings in the case of hand movements. The development of this latter system might be critically dependent on the observation of own movements.
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| 4. |
- Cavaliere, Carlo, et al.
(författare)
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Neuroimaging of Narcolepsy and Primary Hypersomnias
- 2020
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Ingår i: The Neuroscientist. - : SAGE PUBLICATIONS INC. - 1073-8584 .- 1089-4098. ; 26:4, s. 310-327
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Forskningsöversikt (refereegranskat)abstract
- Advances in neuroimaging open up the possibility for new powerful tools to be developed that potentially can be applied to clinical populations to improve the diagnosis of neurological disorders, including sleep disorders. At present, the diagnosis of narcolepsy and primary hypersomnias is largely limited to subjective assessments and objective measurements of behavior and sleep physiology. In this review, we focus on recent neuroimaging findings that provide insight into the neural basis of narcolepsy and the primary hypersomnias Kleine-Levin syndrome and idiopathic hypersomnia. We describe the role of neuroimaging in confirming previous genetic, neurochemical, and neurophysiological findings and highlight studies that permit a greater understanding of the symptoms of these sleep disorders. We conclude by considering some of the remaining challenges to overcome, the existing knowledge gaps, and the potential role for neuroimaging in understanding the pathogenesis and clinical features of narcolepsy and primary hypersomnias.
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| 5. |
- Covacu, R, et al.
(författare)
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Effects of Neuroinflammation on Neural Stem Cells
- 2017
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 23:1, s. 27-39
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Tidskriftsartikel (refereegranskat)abstract
- Neural stem/progenitor cells (NSCs/NPCs) are present in different locations in the central nervous system. In the subgranular zone (SGZ) there is a constant generation of new neurons under normal conditions. New neurons are also formed from the subventricular zone (SVZ) NSCs, and they migrate anteriorly as neuroblast to the olfactory bulb in rodents, whereas in humans migration is directed toward striatum. Most CNS injuries elicit proliferation and migration of the NSCs toward the injury site, indicating the activation of a regenerative response. However, regeneration from NSC is incomplete, and this could be due to detrimental cues encountered during inflammation. Different CNS diseases and trauma cause activation of the innate and adaptive immune responses that influence the NSCs. Furthermore, NSCs in the brain react differently to inflammatory cues than their counterparts in the spinal cord. In this review, we have summarized the effects of inflammation on NSCs in relation to their origin and briefly described the NSC activity during different neurological diseases or experimental models.
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| 6. |
- Cullheim, S, et al.
(författare)
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Classic major histocompatibility complex class I molecules: new actors at the neuromuscular junction
- 2010
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 16:6, s. 600-607
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Tidskriftsartikel (refereegranskat)abstract
- The presence and function of immune molecules in the central nervous system (CNS) have been under debate for a long time. There is mounting evidence that molecules fundamental for immune function are indeed expressed by both neurons and glia and that such molecules may have important nonimmunological function for the organization and stability of synaptic connections. Here, we present data showing that the classic form of major histocompatibility complex (MHC) class I molecules is expressed in spinal motoneurons, in particular in their axons and presynaptically at their synapses with skeletal muscles, the neuromuscular junctions (NMJs). The expression is strongly increased after axon lesion in the peripheral nerve. In the absence of classic MHC I, the organization of NMJs is disturbed with NMJs in higher numbers than normal, thereby equipping single muscle fibers with multiple NMJs. It is suggested that these effects are mediated by the classic MHC class I in the motor axons, possibly through effects mediated by the peripherally myelinating Schwann cells, which express receptors for classic MHC class I. The presence of immune molecules normally used by other cells for antigen presentation in peripheral motor axons may have implications for the onset of specific motoneuron disease.
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| 7. |
- Endo, T, et al.
(författare)
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Cortical changes following spinal cord injury with emphasis on the Nogo signaling system
- 2009
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1073-8584. ; 15:3, s. 291-299
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Tidskriftsartikel (refereegranskat)abstract
- After spinal cord injury, structural as well as functional modifications occur in the adult CNS. Sites of plastic changes include the injured spinal cord itself as well as cortical and subcortical structures. Previously, cortical reorganization in response to sensory deprivation has mainly been studied using peripheral nerve injury models, and has led to a degree of understanding of mechanisms underlying reorganization and plastic changes. Deprivation or damage-induced CNS plasticity is not always beneficial for patients, and may underlie the development of conditions such as neuropathic pain and phantom sensations. Therefore, efforts not only to enhance, but also to control the capacity of plastic changes in the CNS, are of clinical relevance. Novel methods to stimulate plasticity as well as to monitor it, such as transcranial magnetic stimulation and functional magnetic resonance imaging, respectively, may be useful in diverse clinical situations such as spinal cord injury and stroke. Here, human and animal studies of spinal cord injury are reviewed, with special emphasis on the contribution of the Nogo signaling system to cortical plasticity.
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| 8. |
- Fried, K, et al.
(författare)
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Nerve injury-induced pain in the trigeminal system
- 2001
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1073-8584. ; 7:2, s. 155-165
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Tidskriftsartikel (refereegranskat)abstract
- This article reviews some recent findings on peripheral mechanisms related to the development of oro-facial pain after trigeminal nerve injury. Chronic injury-induced oro-facial pain is not in itself a life-threatening condition, but patients suffering from this disorder undoubtedly have a reduced quality of life. The vast majority of the work on pain mechanisms has been carried out in spinal nerve systems. Those studies have provided great insight into mechanisms of neuropathic spinal pain, and much of the data from them is obviously relevant to studies of trigeminal pain. However, it is now clear that the pathophysiology of the trigeminal nerve (a cranial nerve) is in many ways different to that found in spinal nerves. Whereas some of the changes seen in animal models of trigeminal nerve injury mimic those occurring after spinal nerve injury (e.g., the development of spontaneous activity from the damaged axons), others are different, such as the time-course of the spontaneous activity, some of the neuropeptide changes in the trigeminal ganglion, and the lack of sprouting of sympathetic terminals in the ganglion. Recent findings provide new insights that help our understanding of the etiology of chronic injury-induced oro-facial pain. Future investigations will hopefully explain how data gained from these studies relate to clinical pain experience in man and should enable the rapid development of new therapeutic regimes.
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| 9. |
- Gustafsson, Lennart
(författare)
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Comment on "disruption in the inhibitory architecture of the cell minicolumn : implications for autism"
- 2004
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Ingår i: The Neuroscientist. - : SAGE Publications. - 1073-8584 .- 1089-4098. ; 10:3, s. 189-191
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Narrow neural columns have been suggested to be a neuroanatomical abnormality in autism. A previous hypothetical explanation, an unbalance between excitatory and inhibitory lateral feedback in the neocortex, has been found to be difficult to reconcile with the relatively high comorbidity of autism with epilepsy. Two alternative explanations are discussed, an early low capacity for producing serotonin, documented in autism, and insufficient production of nitric oxide. An early low level of serotonin has in animal experiments caused narrow neural columns. Insufficient nitric oxide is known from neural network theory to cause narrow neural columns.
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| 10. |
- Hallbeck, Martin, et al.
(författare)
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Neuron-to-Neuron Transmission of Neurodegenerative Pathology
- 2013
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Ingår i: The Neuroscientist. - : Sage Publications. - 1073-8584 .- 1089-4098. ; 19:6, s. 560-566
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Forskningsöversikt (refereegranskat)abstract
- One of the hallmarks of neurodegenerative dementia diseases is the progressive loss of mental functions and the ability to manage activities of daily life. This progression is caused by the spread of the disease to more and more brain areas via anatomical connections. The pathophysiological process responsible for this spread of disease has long been sought after. There has been an increased understanding that the driving force of these neurodegenerative diseases could be the small, soluble intraneuronal accumulations of neurodegenerative proteins rather than the large, extracellular accumulations. Recently we have shown that the mechanism of spread of Alzheimer's disease most likely depends on the neuron-to-neuron spread of such soluble intraneuronal accumulations of -amyloid through neuritic connections. Similar transmissions have been shown for several other neurodegenerative proteins but little is known about the cellular mechanisms and about any potential strategies that might stop this spread. Resolving these questions requires good cellular models. We have established a unique model of synaptic transmission between human neuronal-like cells, something that has previously been difficult to target. This opens the possibility of developing potential inhibitors of progression of these devastating diseases.
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| 11. |
- Igelström, Kajsa, 1980-
(författare)
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Is Slack an intrinsic seizure terminator?
- 2013
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Ingår i: The Neuroscientist. - : Sage Publications. - 1073-8584 .- 1089-4098. ; 19, s. 248-254
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Tidskriftsartikel (refereegranskat)abstract
- Understanding how epileptic seizures are initiated and propagated across large brain networks is difficult, but an even greater mystery is what makes them stop. Failure of spontaneous seizure termination leads to status epilepticus—a state of uninterrupted seizure activity that can cause death or permanent brain damage. Global factors, like changes in neuromodulators and ion concentrations, are likely to play major roles in spontaneous seizure cessation, but individual neurons also have intrinsic active ion currents that may contribute. The recently discovered gene Slack encodes a sodium-activated potassium channel that mediates a major proportion of the outward current in many neurons. Although given little attention, the current flowing through this channel may have properties consistent with a role in seizure termination.
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| 12. |
- Jankowska, Elzbieta, et al.
(författare)
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How can corticospinal tract neurons contribute to ipsilateral movements? A question with implications for recovery of motor functions.
- 2006
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1073-8584. ; 12:1, s. 67-79
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Tidskriftsartikel (refereegranskat)abstract
- In this review, the authors discuss some recent findings that bear on the issue of recovery of function after corticospinal tract lesions. Conventionally the corticospinal tract is considered to be a crossed pathway, in keeping with the clinical findings that damage to one hemisphere, for example, in stroke, leads to a contralateral paresis and, if the lesion is large, a paralysis. However, there has been great interest in the possibility of compensatory recovery of function using the undamaged hemisphere. There are several substrates for this including ipsilaterally descending corticospinal fibers and bilaterally operating neuronal networks. Recent studies provide important evidence bearing on both of these issues. In particular, they reveal networks of neurons interconnecting two sides of the gray matter at both brainstem and spinal levels, as well as intrahemispheric transcallosal connections. These may form "detour circuits" for recovery of function, and here the authors will consider some possibilities for exploiting these networks for motor control, even though their analysis is still at an early stage.
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| 13. |
- Larsson, Max, et al.
(författare)
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Synaptic Plasticity and Pain : Role of Ionotropic Glutamate Receptors
- 2011
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Ingår i: The Neuroscientist. - : Sage Publications. - 1073-8584 .- 1089-4098. ; 17:3
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Tidskriftsartikel (refereegranskat)abstract
- Pain hypersensitivity that develops after tissue or nerve injury is dependent both on peripheral processes in the affected tissue and on enhanced neuronal responses in the central nervous system, including the dorsal horn of the spinal cord. It has become increasingly clear that strengthening of glutamatergic sensory synapses, such as those established in the dorsal horn by nociceptive thin-caliber primary afferent fibers, is a major contributor to sensitization of neuronal responses that leads to pain hypersensitivity. Here, the authors review recent findings on the roles of ionotropic glutamate receptors in synaptic plasticity in the dorsal horn in relation to acute and persistent pain.
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| 14. |
- Naito, E
(författare)
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Sensing limb movements in the motor cortex: how humans sense limb movement
- 2004
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1073-8584. ; 10:1, s. 73-82
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Tidskriftsartikel (refereegranskat)abstract
- We can precisely control only what we can sense. Sensing limb position or limb movement is essential when we precisely control our limb movements. It has been generally believed that somatic perception takes place in the neuronal network of somatosensory areas. Recent neuroimaging techniques (PET, fMRI, transcranial magnetic stimulation) have revealed in human brains that motor areas participate in somatic perception of limb movements during kinesthetic illusion in the absence of actual limb movement. In particular, the primary motor cortex, which is an executive locus of voluntary limb movements, is primarily responsible for kinesthetic perception of limb movements. This probably forms the most efficient circuits for voluntary limb movements between the controlled muscles and the motor areas.
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| 15. |
- Savic, I
(författare)
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Brain imaging studies of the functional organization of human olfaction
- 2002
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1073-8584. ; 8:3, s. 204-211
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Tidskriftsartikel (refereegranskat)abstract
- It is believed that sensory functions are organized in a hierarchical and parallel manner. The sense of smell differs in several aspects from other senses: odors can immediately elicit emotional evocations, they are remembered after a long time, and they are difficult to label. This raises the question of whether odorous stimuli may be processed differently from the other sensory stimuli. New data from brain imaging studies suggest that this is not the case and that the specific characteristics of the sense of smell can be attributed to the engagement of limbic structures at an early stage in the signal processing.
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| 16. |
- Shi, MC, et al.
(författare)
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Role of Adaptive Immune and Impacts of Risk Factors on Adaptive Immune in Alzheimer's Disease: Are Immunotherapies Effective or Off-Target?
- 2022
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 28:3, s. 254-270
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Tidskriftsartikel (refereegranskat)abstract
- The pathogenesis of Alzheimer’s disease (AD) is complex. Still it remains unclear, which resulted in all efforts for AD treatments with targeting the pathogenic factors unsuccessful over past decades. It has been evidenced that the innate immune is strongly implicated in the pathogenesis of AD. However, the role of adaptive immune in AD remains mostly unknown and the results obtained were controversial. In the review, we summarized recent studies and showed that the molecular and cellular alterations in AD patients and its animal models involving T cells and B cells as well as immune mediators of adaptive immune occur not only in the peripheral blood but also in the brain and the cerebrospinal fluid. The risk factors that cause AD contribute to AD progress by affecting the adaptive immune, indicating that adaptive immunity proposes a pivotal role in this disease. It may provide a possible basis for applying immunotherapy in AD and further investigates whether the immunotherapies are effective or off-target?
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| 17. |
- Verharen, J. P. H., et al.
(författare)
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How Reward and Aversion Shape Motivation and Decision Making: A Computational Account
- 2020
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Ingår i: Neuroscientist. - : SAGE Publications. - 1073-8584. ; 26:1, s. 87-99
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Tidskriftsartikel (refereegranskat)abstract
- Processing rewarding and aversive signals lies at the core of many adaptive behaviors, including value-based decision making. The brain circuits processing these signals are widespread and include the prefrontal cortex, amygdala and striatum, and their dopaminergic innervation. In this review, we integrate historic findings on the behavioral and neural mechanisms of value-based decision making with recent, groundbreaking work in this area. On the basis of this integrated view, we discuss a neuroeconomic framework of value-based decision making, use this to explain the motivation to pursue rewards and how motivation relates to the costs and benefits associated with different courses of action. As such, we consider substance addiction and overeating as states of altered value-based decision making, in which the expectation of reward chronically outweighs the costs associated with substance use and food consumption, respectively. Together, this review aims to provide a concise and accessible overview of important literature on the neural mechanisms of behavioral adaptation to reward and aversion and how these mediate motivated behaviors.
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| 18. |
- Verkhratsky, A, et al.
(författare)
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Glial Asthenia and Functional Paralysis: A New Perspective on Neurodegeneration and Alzheimer's Disease
- 2015
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 21:5, s. 552-568
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Tidskriftsartikel (refereegranskat)abstract
- Neuroglia are represented by several population of cells heterogeneous in structure and function that provide for the homeostasis of the brain and the spinal cord. Neuroglial cells are also central for neuroprotection and defence of the central nervous system against exo- and endogenous insults. At the early stages of neurodegenerative diseases including Alzheimer’s disease neuroglial cells become asthenic and lose some of their homeostatic, neuroprotective, and defensive capabilities. Astroglial reactivity, for example, correlates with preservation of cognitive function in patients with mild cognitive impairment and prodromal Alzheimer’s disease. Here, we overview the experimental data indicating glial paralysis in neurodegeneration and argue that loss of glial function is fundamental for defining the progression of neurodegenerative diseases.
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| 19. |
- Zechel, S, et al.
(författare)
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Expression and functions of fibroblast growth factor 2 (FGF-2) in hippocampal formation
- 2010
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1089-4098. ; 16:4, s. 357-373
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Tidskriftsartikel (refereegranskat)abstract
- Among the 23 members of the fibroblast growth factor (FGF) family, FGF-2 is the most abundant one in the central nervous system. Its impact on neural cells has been profoundly investigated by in vitro and in vivo studies as well as by gene knockout analyses during the past 2 decades. Key functions of FGF-2 in the nervous system include roles in neurogenesis, promotion of axonal growth, differentiation in development, and maintenance and plasticity in adulthood. From a clinical perspective, its prominent role for the maintenance of lesioned neurons (e.g., ischemia and following transection of fiber tracts) is of particular relevance. In the unlesioned brain, FGF-2 is involved in synaptic plasticity and processes attributed to learning and memory. The focus of this review is on the expression of FGF-2 and its receptors in the hippocampal formation and the physiological and pathophysiological roles of FGF-2 in this region during development and adulthood.
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| 20. |
- Zilberter, Y, et al.
(författare)
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Dendritic release of retrograde messengers controls synaptic transmission in local neocortical networks
- 2005
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Ingår i: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry. - : SAGE Publications. - 1073-8584. ; 11:4, s. 334-344
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Tidskriftsartikel (refereegranskat)abstract
- The contribution of retrograde signaling to information processing in the brain has been contemplated for a long time, especially with respect to central nervous system development and long-term synaptic plasticity. During the past few years, however, the concept of retrograde signaling has been expanding to include short-term modifications of synaptic efficacy. The classic point of view on synaptic transmission represents it as a unidirectional transfer of information from presynaptic to postsynaptic sites. This paradigm has, however, been questioned in several experimental studies of neurons in different brain regions. These results suggest that a fast retrograde signal, which provides feedback, exists in active synaptic contacts. In particular, it was found that the dendritic release of retrograde messengers controls the efficacy of synaptic transmission in both excitatory and inhibitory connections between neocortical pyramidal cells and interneurons. The present review discusses these findings and the mechanisms underlying synaptic retrograde signaling.
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| 21. |
- Åkerblom, Malin, et al.
(författare)
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MicroRNAs as Neuronal Fate Determinants.
- 2014
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Ingår i: Neuroscientist. - : SAGE Publications. - 1089-4098. ; 20:3, s. 235-242
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Forskningsöversikt (refereegranskat)abstract
- Since the discovery of short, regulatory microRNAs (miRNA) 20 years ago, the understanding of their impact on gene regulation has dramatically increased. Differentiation of cells requires comprehensive changes in regulatory networks at all levels of gene expression. Posttranscriptional regulation by miRNA leads to rapid modifications in the protein level of large gene networks, and it is therefore not surprising that miRNAs have been found to influence the fate of differentiating cells. Several recent studies have shown that overexpression of a single miRNA in different cellular contexts results in forced differentiation of nerve cells. Loss of this miRNA constrains neurogenesis and promotes gliogenesis. This miRNA, miR-124, is probably the most well-documented example of a miRNA that controls nerve cell fate determination. In this review we summarize the recent findings on miR-124, potential molecular mechanisms used by miR-124 to drive neuronal differentiation, and outline future directions.
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