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201 to 225 of 677Toll-like receptor signaling in neural plasticity and disease.
Toll-like receptors (TLRs) are a family of innate immune system receptors that respond to pathogen-derived and tissue damage-related ligands. TLR signaling in immune cells, glia and neurons can play roles in the pathogenesis of stroke, Alzheimer's disease (AD) and multiple sclerosis (MS). Recent findings suggest that TLR signaling also influences multiple dynamic processes in the developing and adult central nervous system including neurogenesis, axonal growth and structural plasticity. In addition, TLRs are implicated in the regulation of behaviors including learning, memory and anxiety. This review describes recently discovered and unexpected roles for TLRs in neuroplasticity, and the implications of these findings for future basic and translational research studies.
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Neuroplasticity subserving motor skill learning.
Recent years have seen significant progress in our understanding of the neural substrates of motor skill learning. Advances in neuroimaging provide new insight into functional reorganization associated with the acquisition, consolidation, and retention of motor skills. Plastic changes involving structural reorganization in gray and white matter architecture that occur over shorter time periods than previously thought have been documented as well. Data from experimental animals provided crucial information on plausible cellular and molecular substrates contributing to brain reorganization underlying skill acquisition in humans. Here, we review findings demonstrating functional and structural plasticity across different spatial and temporal scales that mediate motor skill learning while identifying converging areas of interest and possible avenues for future research.
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Neuroplasticity in the context of motor rehabilitation after stroke.
Approximately one-third of patients with stroke exhibit persistent disability after the initial cerebrovascular episode, with motor impairments accounting for most poststroke disability. Exercise and training have long been used to restore motor function after stroke. Better training strategies and therapies to enhance the effects of these rehabilitative protocols are currently being developed for poststroke disability. The advancement of our understanding of the neuroplastic changes associated with poststroke motor impairment and the innate mechanisms of repair is crucial to this endeavor. Pharmaceutical, biological and electrophysiological treatments that augment neuroplasticity are being explored to further extend the boundaries of poststroke rehabilitation. Potential motor rehabilitation therapies, such as stem cell therapy, exogenous tissue engineering and brain-computer interface t…
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Synaptic plasticity in sleep: learning, homeostasis and disease.
Sleep is a fundamental and evolutionarily conserved aspect of animal life. Recent studies have shed light on the role of sleep in synaptic plasticity. Demonstrations of memory replay and synapse homeostasis suggest that one essential role of sleep is in the consolidation and optimization of synaptic circuits to retain salient memory traces despite the noise of daily experience. Here, we review this recent evidence and suggest that sleep creates a heightened state of plasticity, which may be essential for this optimization. Furthermore, we discuss how sleep deficits seen in diseases such as Alzheimer's disease and autism spectrum disorders might not just reflect underlying circuit malfunction, but could also play a direct role in the progression of those disorders.
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Cerebral palsy: clinical care and neurological rehabilitation.
Cerebral palsy (CP) is defined as motor impairment that limits activity, and is attributed to non-progressive disturbances during brain development in fetuses or infants. The motor disorders of CP are frequently accompanied by impaired cognition, communication, and sensory perception, behavioural abnormalities, seizure disorders, or a combination of these features. CP is thought to affect three to four individuals per 1000 of the general population. The incidence, prevalence, and most common causes of CP have varied over time because of changes in prenatal and paediatric care. Medical management of children and adults involves care from primary-care physicians with input from specialists in neurology, orthopaedics, and rehabilitation medicine. Physicians should also work in conjunction with rehabilitation therapists, educators, nurses, social care providers, and schoolteachers. The focus…
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Acetylcholine-dopamine balance hypothesis in the striatum: an update.
The imbalance between cholinergic activity and dopaminergic activity in the striatum causes a variety of neurological disorders, such as Parkinson's disease. During sensorimotor learning, the arrival of a conditioned stimulus reporting a reward evokes a pause response in the firing of the tonically active cholinergic interneurons in targeted areas of the striatum, whereas the same stimulus triggers an increase in the firing frequency of the dopaminergic neurons in the substantia nigra pars compacta. The pause response of the cholinergic interneurons begins with an initial depolarizing phase followed by a pause in spike firing and ensuing rebound excitation. The timing of the pause phase coincides well with the surge in dopaminergic firing, indicating that a dramatic rise in dopamine (DA) release occurs while nicotinic receptors remain unbound by acetylcholine. The pause response begins w…
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Roles for pituitary adenylate cyclase-activating peptide (PACAP) expression and signaling in the bed nucleus of the stria terminalis (BNST) in mediating the behavioral consequences of chronic stress.
Anxiety disorders are frequently long-lasting and debilitating for more than 40 million American adults. Although stressor exposure plays an important role in the etiology of some anxiety disorders, the mechanisms by which exposure to stressful stimuli alters central circuits that mediate anxiety-like emotional behavior are still unknown. Substantial evidence has implicated regions of the central extended amygdala, including the bed nucleus of the stria terminalis (BNST) and the central nucleus of the amygdala as critical structures mediating fear- and anxiety-like behavior in both humans and animals. These areas organize coordinated fear- and anxiety-like behavioral responses as well as peripheral stress responding to threats via direct and indirect projections to the paraventricular nucleus of the hypothalamus and brainstem regions (Walker et al. Eur J Pharmacol 463:199-216, 2003, Prog…
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Neural reorganization following sensory loss: the opportunity of change.
There is growing evidence that sensory deprivation is associated with crossmodal neuroplastic changes in the brain. After visual or auditory deprivation, brain areas that are normally associated with the lost sense are recruited by spared sensory modalities. These changes underlie adaptive and compensatory behaviours in blind and deaf individuals. Although there are differences between these populations owing to the nature of the deprived sensory modality, there seem to be common principles regarding how the brain copes with sensory loss and the factors that influence neuroplastic changes. Here, we discuss crossmodal neuroplasticity with regards to behavioural adaptation after sensory deprivation and highlight the possibility of maladaptive consequences within the context of rehabilitation.
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The neurobiological properties of tianeptine (Stablon): from monoamine hypothesis to glutamatergic modulation.
Tianeptine is a clinically used antidepressant that has drawn much attention, because this compound challenges traditional monoaminergic hypotheses of depression. It is now acknowledged that the antidepressant actions of tianeptine, together with its remarkable clinical tolerance, can be attributed to its particular neurobiological properties. The involvement of glutamate in the mechanism of action of the antidepressant tianeptine is consistent with a well-developed preclinical literature demonstrating the key function of glutamate in the mechanism of altered neuroplasticity that underlies the symptoms of depression. This article reviews the latest evidence on tianeptine's mechanism of action with a focus on the glutamatergic system, which could provide a key pathway for its antidepressant action. Converging lines of evidences demonstrate actions of tianeptine on the glutamatergic system…
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Lab and field experiments: are they the same animal?
To advance our understanding of biological processes we often plan our experiments based on published data. This can be confusing though, as data from experiments performed in a laboratory environment are sometimes different from, or completely opposite to, findings from similar experiments performed in the "real world". In this mini-review, we discuss instances where results from laboratory experiments differ as a result of laboratory housing conditions, and where they differ from results gathered in the field environment. Experiments involving endocrinology and behavior appear to be particularly susceptible to influence from the environment in which they are performed. As such, we have attempted to promote discussion of the influence of housing environment on the reproductive axis, circadian biology and behavior, immune function, stress biology, neuroplasticity and photoperiodism. For …
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Lewis DA, González-Burgos G (2008)reviewMEDLINE-indexed journal, not yet read by usNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology300 citations Neuroplasticity of neocortical circuits in schizophrenia.
The core features of schizophrenia include deficits in cognitive processes mediated by the circuitry of the dorsolateral prefrontal cortex (DLPFC). These deficits are associated with a range of molecular and morphological alterations in the DLPFC, each of which could be a cause, consequence, or compensation in relation to other changes, and thus reflect the neuroplasticity of the brain in response to the underlying disease process. In this review, we consider disturbances in excitatory, inhibitory, and modulatory connections of DLPFC circuitry from the perspective of disease- and development-related neuroplasticity and discuss their implications for the identification of novel therapeutic targets.
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Kalivas PW, O'Brien C (2008)reviewMEDLINE-indexed journal, not yet read by usNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology491 citations Drug addiction as a pathology of staged neuroplasticity.
Using addictive drugs can evolve from controlled social use into the compulsive relapsing disorder that characterizes addiction. This transition to addiction results from genetic, developmental, and sociological vulnerabilities, combined with pharmacologically induced plasticity in brain circuitry that strengthens learned drug-associated behaviors at the expense of adaptive responding for natural rewards. Advances over the last decade have identified the brain circuits most vulnerable to drug-induced changes, as well as many associated molecular and morphological underpinnings. This growing knowledge has contributed to an expanded understanding of how drugs usurp normal learning circuitry to create the pathology of addiction, as evidenced by involuntary activation of reward circuits in response to drug-associated cues and simultaneous reports of drug craving. This new understanding provi…
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McClung CA, Nestler EJ (2008)reviewMEDLINE-indexed journal, not yet read by usNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology259 citations Neuroplasticity mediated by altered gene expression.
Plasticity in the brain is important for learning and memory, and allows us to respond to changes in the environment. Furthermore, long periods of stress can lead to structural and excitatory changes associated with anxiety and depression that can be reversed by pharmacological treatment. Drugs of abuse can also cause long-lasting changes in reward-related circuits, resulting in addiction. Each of these forms of long-term plasticity in the brain requires changes in gene expression. Upon stimulation, second messenger pathways are activated that lead to an enhancement in transcription factor activity at gene promoters. This stimulation results in the expression of new growth factors, ion channels, structural molecules, and other proteins necessary to alter the neuronal circuit. With repeated stimulation, more permanent modifications to transcription factors and chromatin structure are made…
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Transcranial direct current stimulation in stroke recovery.
Transcranial direct current stimulation (TDCS) is an emerging technique of noninvasive brain stimulation that has been found useful in examining cortical function in healthy subjects and in facilitating treatments of various neurologic disorders. A better understanding of adaptive and maladaptive poststroke neuroplasticity and its modulation through noninvasive brain stimulation has opened up experimental treatment options using TDCS for patients recovering from stroke. We review the role of TDCS as a facilitator of stroke recovery, the different modes of TDCS, and the potential mechanisms underlying the neural effects of TDCS.
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The dorsal raphe nucleus and serotonin: implications for neuroplasticity linked to major depression and Alzheimer's disease.
The dorsal raphe nucleus (DRN) is a heterogeneous brainstem nucleus located in the midbrain and pons. Via widespread projections, which target a multitude of brain areas, its neurons utilize many transmitters to control various physiological functions, including learning, memory and affect. Accordingly, the DRN has been strongly associated with brain dysfunction, especially mood disorders such as depression, but also Alzheimer's disease. The DRN's most abundant transmitter, serotonin, has received the most attention in studies on both normal brain function and disease, and lately its involvement in the regulation of neuroplasticity has been under particular scrutiny. This chapter begins with a systematic overview of what we currently know about the anatomy of the DRN and its neurons, including their ascending projections. It continues with a review of the transmitters of the DRN, followe…
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Effects of prenatal restraint stress on the hypothalamus-pituitary-adrenal axis and related behavioural and neurobiological alterations.
Chronic hyper-activation of the hypothalamus-pituitary axis is associated with the suppression of reproductive, growth, thyroid and immune functions that may lead to various pathological states. Although many individuals experiencing stressful events do not develop pathologies, stress seems to be a provoking factor in those individuals with particular vulnerability, determined by genetic factors or earlier experience. Exposure of the developing brain to severe and/or prolonged stress may result in hyper-activity of the stress system, defective glucocorticoids-negative feedback, altered cognition, novelty seeking, increased vulnerability to addictive behaviour, and mood-related disorders. Therefore, stress-related events that occur in the perinatal period can permanently change brain and behaviour of the developing individual. Prenatal restraint stress (PRS) in rats is a well-documented m…
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Cenci MA (2007)reviewMEDLINE-indexed journal, not yet read by usTrends in neurosciences204 citations Dopamine dysregulation of movement control in L-DOPA-induced dyskinesia.
The nigrostriatal dopamine (DA) system has an essential role in the selection and control of movement sequences, and its degeneration causes the characteristic motor symptoms of Parkinson's disease. Parkinsonian motor symptoms are alleviated by L-DOPA, but this treatment induces motor fluctuations and dyskinesias (abnormal involuntary movements). Clinical and experimental findings indicate that the motor complications of L-DOPA pharmacotherapy are triggered by transient and large changes in extracellular DA levels. The disruption of presynaptic DA homeostasis sets in motion a cascade of postsynaptic alterations, which prime the brain for a complicated motor response to dopaminomimetic treatment. L-DOPA-induced dyskinesia provides a paradigm to study how the dysregulation of DA release and clearance results in maladaptive neuroplasticity sustaining abnormal patterns of movement.
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Stress during development: Impact on neuroplasticity and relevance to psychopathology.
Development represents a critical moment for shaping adult behavior and may set the stage to disease vulnerability later in life. There is now compelling evidence that stressful experiences during gestation or early in life can lead to enhanced susceptibility for mental illness. In this paper we review the data from experimental studies aimed at investigating behavioral, hormonal, functional and molecular consequences of exposure to stressful events during prenatal or early postnatal life that might contribute to later psychopathology. The use of the newest methodology in the field and the intensive efforts produced by researchers have opened the possibility to reveal the complex, finely tuned and previously unappreciated sets of molecular interactions between different factors that are critical for neurodevelopment thus leading to important discoveries regarding perinatal life. The majo…
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Neural circuitry and neuroplasticity in mood disorders: insights for novel therapeutic targets.
Summary: Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotro…
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Enteric neuroplasticity evoked by inflammation.
Neuroplastic changes in the enteric nervous system (ENS) may be observed in physiological states, such as development and aging, or occur as a consequence of different pathological conditions, ranging from enteric neuropathies (e.g., Hirschsprung's disease) to intestinal (e.g., inflammatory bowel disease) or extra-intestinal diseases (e.g., Parkinson's disease). Studying ENS plasticity may help to elucidate the pathophysiology of several diseases and have a bearing on the development of new pharmacological interventions. In the present review, we would like to focus on neuronal plasticity evoked by gastrointestinal inflammation occurring in inflammatory bowel disease and in a subset of patients with severe derangement of gut motility due to an enteric neuropathy characterized by an inflammatory infiltrate of the enteric plexuses. Major features of neuroplasticity within the enteric micro…
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Memory formation by neuronal synchronization.
Cognitive functions not only depend on the localization of neural activity, but also on the precise temporal pattern of activity in neural assemblies. Synchronization of action potential discharges provides a link between large-scale EEG recordings and cellular plasticity mechanisms. Here, we focus on the role of neuronal synchronization in different frequency domains for the subsequent stages of memory formation. Recent EEG studies suggest that synchronized neural activity in the gamma frequency range (around 30-100 Hz) plays a functional role for the formation of declarative long-term memories in humans. On the cellular level, gamma synchronization between hippocampal and parahippocampal regions may induce LTP in the CA3 region of the hippocampus. In order to encode spatial locations or sequences of multiple items and to guarantee a defined temporal order of memory processing, synchron…
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Neuroplasticity after spinal cord injury and training: an emerging paradigm shift in rehabilitation and walking recovery.
Physical rehabilitation after spinal cord injury has been based on the premise that the nervous system is hard-wired and irreparable. Upon this assumption, clinicians have compensated for irremediable sensorimotor deficits using braces, assistive devices, and wheelchairs to achieve upright and seated mobility. Evidence from basic science, however, demonstrates that the central nervous system after injury is malleable and can learn, and this evidence has challenged our current assumptions. The evidence is especially compelling concerning locomotion. The purpose of this perspective article is to summarize the evidence supporting an impending paradigm shift from compensation for deficits to rehabilitation as an agent for walking recovery. A physiologically based approach for the rehabilitation of walking has developed, translating evidence for activity-dependent neuroplasticity after spinal…
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Soliman F, Glatt CE, Bath KG, Levita L, Jones RM, Pattwell SS, Jing D, Tottenham N, Amso D, Somerville LH, Voss HU, Glover G, Ballon DJ, Liston C, Teslovich T, Van Kempen T, Lee FS, Casey BJ (2010)cohort or longitudinalMEDLINE-indexed journal, not yet read by usScience (New York, N.Y.)448 citations A genetic variant BDNF polymorphism alters extinction learning in both mouse and human.
Mouse models are useful for studying genes involved in behavior, but whether they are relevant to human behavior is unclear. Here, we identified parallel phenotypes in mice and humans resulting from a common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, which is involved in anxiety-related behavior. An inbred genetic knock-in mouse strain expressing the variant BDNF recapitulated the phenotypic effects of the human polymorphism. Both were impaired in extinguishing a conditioned fear response, which was paralleled by atypical frontoamygdala activity in humans. Thus, this variant BDNF allele may play a role in anxiety disorders showing impaired learning of cues that signal safety versus threat and in the efficacy of treatments that rely on extinction mechanisms, such as exposure therapy.
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The antidepressant fluoxetine restores plasticity in the adult visual cortex.
We investigated whether fluoxetine, a widely prescribed medication for treatment of depression, restores neuronal plasticity in the adult visual system of the rat. We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pa…
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Importance of the brain corticosteroid receptor balance in metaplasticity, cognitive performance and neuro-inflammation.
Bruce McEwen's discovery of receptors for corticosterone in the rat hippocampus introduced higher brain circuits in the neuroendocrinology of stress. Subsequently, these receptors were identified as mineralocorticoid receptors (MRs) that are involved in appraisal processes, choice of coping style, encoding and retrieval. The MR-mediated actions on cognition are complemented by slower actions via glucocorticoid receptors (GRs) on contextualization, rationalization and memory storage of the experience. These sequential phases in cognitive performance depend on synaptic metaplasticity that is regulated by coordinate MR- and GR activation. The receptor activation includes recruitment of coregulators and transcription factors as determinants of context-dependent specificity in steroid action; they can be modulated by genetic variation and (early) experience. Interestingly, inflammatory respon…
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