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351 to 375 of 677Pedersen BK (2009)reviewMEDLINE-indexed journal, not yet read by usThe Journal of physiology376 citations The diseasome of physical inactivity--and the role of myokines in muscle--fat cross talk.
Type 2 diabetes, cardiovascular diseases, colon cancer, breast cancer, dementia and depression constitute a cluster of diseases, which defines 'a diseasome of physical inactivity'. Both physical inactivity and abdominal adiposity, reflecting accumulation of visceral fat mass, are associated with the occurrence of the diseases within the diseasome. Physical inactivity appears to be an independent and strong risk factor for accumulation of visceral fat, which again is a source of systemic inflammation. Chronic inflammation is involved in the pathogenesis of insulin resistance, atherosclerosis, neurodegeneration and tumour growth. Evidence suggests that the protective effect of exercise may to some extent be ascribed to the anti-inflammatory effect of regular exercise, which can be mediated via a reduction in visceral fat mass and/or by induction of an anti-inflammatory environment with eac…
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Social support and resilience to stress across the life span: a neurobiologic framework.
This review discusses selected neurobiologic and genetic factors-including noradrenergic and hypothalamic-pituitary-adrenal axis markers, oxytocin pathways, and serotonin transporter and brain-derived neurotrophic factor gene polymorphisms-in the context of resilience to stress, with an emphasis on social support. Social support's impact on medical and psychiatric health outcomes is reviewed, and putative mediators are discussed. The reviewed literature indicates that social support is exceptionally important to maintaining good physical and psychological health in the presence of genetic, developmental, and other environmental risks. Future studies should continue to explore the neurobiologic factors associated with social support's contribution to stress resilience.
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Adolescent cortical development: a critical period of vulnerability for addiction.
Cortical growth and remodeling continues from birth through youth and adolescence to stable adult levels changing slowly into senescence. There are critical periods of cortical development when specific experiences drive major synaptic rearrangements and learning that only occur during the critical period. For example, visual cortex is characterized by a critical period of plasticity involved in establishing visual acuity. Adolescence is defined by characteristic behaviors that include high levels of risk taking, exploration, novelty and sensation seeking, social interaction and play behaviors. In addition, adolescence is the final period of development of the adult during which talents, reasoning and complex adult behaviors mature. This maturation of behaviors corresponds with periods of marked changes in neurogenesis, cortical synaptic remodeling, neurotransmitter receptors and transpo…
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Grigoriadis S, Robinson GE (2007)reviewMEDLINE-indexed journal, not yet read by usAnnals of clinical psychiatry : official journal of the American Academy of Clinical Psychiatrists168 citations Gender issues in depression.
Background: Gender differences in depression have been documented for many years and thought to be insignificant to treatment selection until recently.
Methods: This article reviews gender differences in the prevalence, presentation, etiology, and antidepressant treatment of depressive disorders.
Results: The high female to male sex ratio in the prevalence of depression, especially during the reproductive years, is one of the most replicated findings in epidemiology. Women more often have a seasonal component, anxious and atypical depression. Explanations for the differences include psychological, neurochemical, anatomic, hormonal, genetic, and personality factors. Gender differences in antidepressant treatment response have not been found consistently. Hormonal status may be an important variable in addition to the effects of the menstrual cycle, pregnancy, perimenopause and menopause.
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New insights into BDNF function in depression and anxiety.
The 'neurotrophin hypothesis of depression' is based largely on correlations between stress or antidepressant treatment and down- or upregulation, respectively, of brain-derived neurotrophic factor (BDNF). Genetic disruption of the signaling pathways involving BDNF and its receptor, the tyrosine kinase TrkB, does not seem to cause depressive behaviors, but does hamper the effect of antidepressant drugs. Thus, BDNF may be a target of antidepressants, but not the sole mediator of depression or anxiety. Advances in BDNF cell biology, including its transcription through multiple promoters, trafficking and secretion, may provide new insights into its role in mood disorders. Moreover, as the precursor proBDNF and the mature protein mBDNF can elicit opposite effects on cellular functions, the impact of proBDNF and its cleavage on mood should be considered. Opposing influences of mBDNF and proBD…
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A neurotrophic model for stress-related mood disorders.
There is a growing body of evidence demonstrating that stress decreases the expression of brain-derived neurotrophic factor (BDNF) in limbic structures that control mood and that antidepressant treatment reverses or blocks the effects of stress. Decreased levels of BDNF, as well as other neurotrophic factors, could contribute to the atrophy of certain limbic structures, including the hippocampus and prefrontal cortex that has been observed in depressed subjects. Conversely, the neurotrophic actions of antidepressants could reverse neuronal atrophy and cell loss and thereby contribute to the therapeutic actions of these treatments. This review provides a critical examination of the neurotrophic hypothesis of depression that has evolved from this work, including analysis of preclinical cellular (adult neurogenesis) and behavioral models of depression and antidepressant actions, as well as …
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Oxidative Stress in Depression: The Link with the Stress Response, Neuroinflammation, Serotonin, Neurogenesis and Synaptic Plasticity.
Depression is a prevalent, complex, and highly debilitating disease. The full comprehension of this disease is still a global challenge. Indeed, relapse, recurrency, and therapeutic resistance are serious challenges in the fight against depression. Nevertheless, abnormal functioning of the stress response, inflammatory processes, neurotransmission, neurogenesis, and synaptic plasticity are known to underlie the pathophysiology of this mental disorder. The role of oxidative stress in disease and, particularly, in depression is widely recognized, being important for both its onset and development. Indeed, excessive generation of reactive oxygen species and lack of efficient antioxidant response trigger processes such as inflammation, neurodegeneration, and neuronal death. Keeping in mind the importance of a detailed study about cellular and molecular mechanisms that are present in depressi…
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The neurobiology of depression: An integrated view.
Major Depressive Disorder (MDD) is one of the most common and debilitating mental disorders; however, its etiology remains unclear. This paper aims to summarize the major neurobiological underpinnings of depression, synthesizing the findings into a comprehensive integrated view. A literature review was conducted using Pubmed. Search terms included "depression" or "MDD" AND "biology", "neurobiology", "inflammation", "neurogenesis", "monoamine", and "stress". Articles from 1995 to 2016 were reviewed with a focus on the connection between different biological and psychological models. Some possible pathophysiological mechanisms of depression include altered neurotransmission, HPA axis abnormalities involved in chronic stress, inflammation, reduced neuroplasticity, and network dysfunction. All of these proposed mechanisms are integrally related and interact bidirectionally. In addition, psyc…
matched on Neurogenesis (keyword), neuroplasticity (text)
Depression as a microglial disease.
Despite decades of intensive research, the biological mechanisms that causally underlie depression are still unclear, and therefore the development of novel effective antidepressant treatments is hindered. Recent studies indicate that impairment of the normal structure and function of microglia, caused by either intense inflammatory activation (e.g., following infections, trauma, stroke, short-term stress, autoimmune or neurodegenerative diseases) or by decline and senescence of these cells (e.g., during aging, Alzheimer's disease, or chronic unpredictable stress exposure), can lead to depression and associated impairments in neuroplasticity and neurogenesis. Accordingly, some forms of depression can be considered as a microglial disease (microgliopathy), which should be treated by a personalized medical approach using microglial inhibitors or stimulators depending on the microglial stat…
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Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity.
Cytokines are key regulatory mediators involved in the host response to immunological challenges, but also play a critical role in the communication between the immune and the central nervous system. For this, their expression in both systems is under a tight regulatory control. However, pathological conditions may lead to an overproduction of pro-inflammatory cytokines that may have a detrimental impact on central nervous system. In particular, they may damage neuronal structure and function leading to deficits of neuroplasticity, the ability of nervous system to perceive, respond and adapt to external or internal stimuli. In search of the mechanisms by which pro-inflammatory cytokines may affect this crucial brain capability, we will discuss one of the most interesting hypotheses: the involvement of the neurotrophin brain-derived neurotrophic factor (BDNF), which represents one of the …
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Modulation of learning and memory by cytokines: signaling mechanisms and long term consequences.
This review describes the role of cytokines and their downstream signaling cascades on the modulation of learning and memory. Immune proteins are required for many key neural processes and dysregulation of these functions by systemic inflammation can result in impairments of memory that persist long after the resolution of inflammation. Recent research has demonstrated that manipulations of individual cytokines can modulate learning, memory, and synaptic plasticity. The many conflicting findings, however, have prevented a clear understanding of the precise role of cytokines in memory. Given the complexity of inflammatory signaling, understanding its modulatory role requires a shift in focus from single cytokines to a network of cytokine interactions and elucidation of the cytokine-dependent intracellular signaling cascades. Finally, we propose that whereas signal transduction and transcr…
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Norepinephrine and serotonin are required for vagus nerve stimulation directed cortical plasticity.
Vagus nerve stimulation (VNS) paired with forelimb training drives robust, specific reorganization of movement representations in the motor cortex. This effect is hypothesized to be mediated by VNS-dependent engagement of neuromodulatory networks. VNS influences activity in the locus coeruleus (LC) and dorsal raphe nucleus (DRN), but the involvement of these neuromodulatory networks in VNS-directed plasticity is unknown. We tested the hypothesis that cortical norepinephrine and serotonin are required for VNS-dependent enhancement of motor cortex plasticity. Rats were trained on a lever pressing task emphasizing proximal forelimb use. Once proficient, all rats received a surgically implanted vagus nerve cuff and cortical injections of either immunotoxins to deplete serotonin or norepinephrine, or vehicle control. Following surgical recovery, rats received half second bursts of 0.8 mA or s…
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Mitochondrial Dysfunction in Depression.
Background: Depression is the most debilitating neuropsychiatric disorder with significant impact on socio-occupational and well being of individual. The exact pathophysiology of depression is still enigmatic though various theories have been put forwarded. There are evidences showing that mitochondrial dysfunction in various brain regions is associated with depression. Recent findings have sparked renewed appreciation for the role of mitochondria in many intracellular processes coupled to synaptic plasticity and cellular resilience. New insights in depression pathophysiology are revolving around the impairment of neuroplasticity. Mitochondria have potential role in ATP production, intracellular Ca2+ signalling to establish membrane stability, reactive oxygen species (ROS) balance and to execute the complex processes of neurotransmission and plasticity. So understanding the various conce…
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Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity.
In the mammalian central nervous system, reactive oxygen species (ROS) generation is counterbalanced by antioxidant defenses. When large amounts of ROS accumulate, antioxidant mechanisms become overwhelmed and oxidative cellular stress may occur. Therefore, ROS are typically characterized as toxic molecules, oxidizing membrane lipids, changing the conformation of proteins, damaging nucleic acids, and causing deficits in synaptic plasticity. High ROS concentrations are associated with a decline in cognitive functions, as observed in some neurodegenerative disorders and age-dependent decay of neuroplasticity. Nevertheless, controlled ROS production provides the optimal redox state for the activation of transductional pathways involved in synaptic changes. Since ROS may regulate neuronal activity and elicit negative effects at the same time, the distinction between beneficial and deleteriou…
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Mrachacz-Kersting N, Jiang N, Stevenson AJ, Niazi IK, Kostic V, Pavlovic A, Radovanovic S, Djuric-Jovicic M, Agosta F, Dremstrup K, Farina D (2016)MEDLINE-indexed journal, not yet read by usJournal of neurophysiology158 citations Efficient neuroplasticity induction in chronic stroke patients by an associative brain-computer interface.
Brain-computer interfaces (BCIs) have the potential to improve functionality in chronic stoke patients when applied over a large number of sessions. Here we evaluated the effect and the underlying mechanisms of three BCI training sessions in a double-blind sham-controlled design. The applied BCI is based on Hebbian principles of associativity that hypothesize that neural assemblies activated in a correlated manner will strengthen synaptic connections. Twenty-two chronic stroke patients were divided into two training groups. Movement-related cortical potentials (MRCPs) were detected by electroencephalography during repetitions of foot dorsiflexion. Detection triggered a single electrical stimulation of the common peroneal nerve timed so that the resulting afferent volley arrived at the peak negative phase of the MRCP (BCIassociative group) or randomly (BCInonassociative group). Fugl-Meyer…
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The beneficial effects of regular exercise on cognition in REM sleep deprivation: behavioral, electrophysiological and molecular evidence.
Inadequate sleep is prevalent in modern societies and is known to profoundly impair cognitive function. We examined the impact of 4 weeks of regular treadmill exercise on sleep deprivation induced spatial learning and memory, synaptic plasticity and related signaling molecules in area CA1 of the rat hippocampus. Rats were exercised on a treadmill and subsequently sleep-deprived for 24h using the modified multiple platform technique. Testing of learning and short-term memory performance in the radial arm water maze showed that although sedentary sleep deprived rats were severely impaired, exercised sleep deprived rats' performance was normal. Extracellular recording from area CA1 of anesthetized rats revealed that early phase LTP (E-LTP) was markedly impaired in the sedentary sleep deprived animals, but was normal in the exercised sleep deprived group. Additionally, immunoblot analysis of…
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Alhowail A (2021)reviewMEDLINE-indexed journal, not yet read by usMolecular medicine reports43 citations Molecular insights into the benefits of nicotine on memory and cognition (Review).
The health risks of nicotine are well known, but there is some evidence of its beneficial effects on cognitive function. The present review focused on the reported benefits of nicotine in the brain and summarizes the associated underlying mechanisms. Nicotine administration can improve cognitive impairment in Alzheimer's disease (AD), and dyskinesia and memory impairment in Parkinson's disease (PD). In terms of its mechanism of action, nicotine slows the progression of PD by inhibiting Sirtuin 6, a stress‑responsive protein deacetylase, thereby decreasing neuronal apoptosis and improving neuronal survival. In AD, nicotine improves cognitive impairment by enhancing protein kinase B (also referred to as Akt) activity and stimulating phosphoinositide 3‑kinase/Akt signaling, which regulates learning and memory processes. Nicotine may also activate thyroid receptor signaling pathways to impro…
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Mechanisms of systems memory consolidation during sleep.
Long-term memory formation is a major function of sleep. Based on evidence from neurophysiological and behavioral studies mainly in humans and rodents, we consider the formation of long-term memory during sleep as an active systems consolidation process that is embedded in a process of global synaptic downscaling. Repeated neuronal replay of representations originating from the hippocampus during slow-wave sleep leads to a gradual transformation and integration of representations in neocortical networks. We highlight three features of this process: (i) hippocampal replay that, by capturing episodic memory aspects, drives consolidation of both hippocampus-dependent and non-hippocampus-dependent memory; (ii) brain oscillations hallmarking slow-wave and rapid-eye movement sleep that provide mechanisms for regulating both information flow across distant brain networks and local synaptic plas…
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Multiple sclerosis and cognition: synaptic failure and network dysfunction.
Cognitive impairment is increasingly recognized to be a core feature of multiple sclerosis (MS), with important implications for the everyday life of individuals with MS and for disease management. Unfortunately, the exact mechanisms that underlie this cognitive impairment are poorly understood and there are no effective therapeutic options for this aspect of the disease. During MS, focal brain inflammatory lesions, together with pathological changes of both CNS grey matter and normal-appearing white matter, can interfere with cognitive functions. Moreover, inflammation may alter the crosstalk between the immune and the nervous systems, modulating the induction of synaptic plasticity and neurotransmission. In this Review, we examine the CNS structures and cognitive domains that are affected by the disease, with a specific focus on hippocampal involvement in MS and experimental autoimmune…
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Alcohol-dependent molecular adaptations of the NMDA receptor system.
Phenotypes such as motivation to consume alcohol, goal-directed alcohol seeking and habit formation take part in mechanisms underlying heavy alcohol use. Learning and memory processes greatly contribute to the establishment and maintenance of these behavioral phenotypes. The N-methyl-d-aspartate receptor (NMDAR) is a driving force of synaptic plasticity, a key cellular hallmark of learning and memory. Here, we describe data in rodents and humans linking signaling molecules that center around the NMDARs, and behaviors associated with the development and/or maintenance of alcohol use disorder (AUD). Specifically, we show that enzymes that participate in the regulation of NMDAR function including Fyn kinase as well as signaling cascades downstream of NMDAR including calcium/calmodulin-dependent protein kinase II (CamKII), the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AM…
matched on synaptic plasticity (text), Receptors, N-Methyl-D-Aspartate (mesh)
The influence of cannabinoids on learning and memory processes of the dorsal striatum.
Extensive evidence indicates that the mammalian endocannabinoid system plays an integral role in learning and memory. Our understanding of how cannabinoids influence memory comes predominantly from studies examining cognitive and emotional memory systems mediated by the hippocampus and amygdala, respectively. However, recent evidence suggests that cannabinoids also affect habit or stimulus-response (S-R) memory mediated by the dorsal striatum. Studies implementing a variety of maze tasks in rats indicate that systemic or intra-dorsolateral striatum infusions of cannabinoid receptor agonists or antagonists impair habit memory. In mice, cannabinoid 1 (CB1) receptor knockdown can enhance or impair habit formation, whereas Δ(9)THC tolerance enhances habit formation. Studies in human cannabis users also suggest an enhancement of S-R/habit memory. A tentative conclusion based on the available …
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Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders.
Half a century after the first formulation of the monoamine hypothesis, compelling evidence implies that long-term changes in an array of brain areas and circuits mediating complex cognitive-emotional behaviors represent the biological underpinnings of mood/anxiety disorders. A large number of clinical studies suggest that pathophysiology is associated with dysfunction of the predominant glutamatergic system, malfunction in the mechanisms regulating clearance and metabolism of glutamate, and cytoarchitectural/morphological maladaptive changes in a number of brain areas mediating cognitive-emotional behaviors. Concurrently, a wealth of data from animal models have shown that different types of environmental stress enhance glutamate release/transmission in limbic/cortical areas and exert powerful structural effects, inducing dendritic remodeling, reduction of synapses and possibly volumetr…
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Rewiring the brain: potential role of the premotor cortex in motor control, learning, and recovery of function following brain injury.
The brain is a plastic organ with a capability to reorganize in response to behavior and/or injury. Following injury to the motor cortex or emergent corticospinal pathways, recovery of function depends on the capacity of surviving anatomical resources to recover and repair in response to task-specific training. One such area implicated in poststroke reorganization to promote recovery of upper extremity recovery is the premotor cortex (PMC). This study reviews the role of distinct subdivisions of PMC: dorsal (PMd) and ventral (PMv) premotor cortices as critical anatomical and physiological nodes within the neural networks for the control and learning of goal-oriented reach and grasp actions in healthy individuals and individuals with stroke. Based on evidence emerging from studies of intrinsic and extrinsic connectivity, transcranial magnetic stimulation, functional neuroimaging, and expe…
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Dopamine D2 receptors in discrimination learning and spine enlargement.
Dopamine D2 receptors (D2Rs) are densely expressed in the striatum and have been linked to neuropsychiatric disorders such as schizophrenia1,2. High-affinity binding of dopamine suggests that D2Rs detect transient reductions in dopamine concentration (the dopamine dip) during punishment learning3-5. However, the nature and cellular basis of D2R-dependent behaviour are unclear. Here we show that tone reward conditioning induces marked stimulus generalization in a manner that depends on dopamine D1 receptors (D1Rs) in the nucleus accumbens (NAc) of mice, and that discrimination learning refines the conditioning using a dopamine dip. In NAc slices, a narrow dopamine dip (as short as 0.4 s) was detected by D2Rs to disinhibit adenosine A2A receptor (A2AR)-mediated enlargement of dendritic spines in D2R-expressing spiny projection neurons (D2-SPNs). Plasticity-related signalling by Ca2+/calmod…
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Penzo MA, Robert V, Tucciarone J, De Bundel D, Wang M, Van Aelst L, Darvas M, Parada LF, Palmiter RD, He M, Huang ZJ, Li B (2015)MEDLINE-indexed journal, not yet read by usNature431 citations The paraventricular thalamus controls a central amygdala fear circuit.
Appropriate responses to an imminent threat brace us for adversities. The ability to sense and predict threatening or stressful events is essential for such adaptive behaviour. In the mammalian brain, one putative stress sensor is the paraventricular nucleus of the thalamus (PVT), an area that is readily activated by both physical and psychological stressors. However, the role of the PVT in the establishment of adaptive behavioural responses remains unclear. Here we show in mice that the PVT regulates fear processing in the lateral division of the central amygdala (CeL), a structure that orchestrates fear learning and expression. Selective inactivation of CeL-projecting PVT neurons prevented fear conditioning, an effect that can be accounted for by an impairment in fear-conditioning-induced synaptic potentiation onto somatostatin-expressing (SOM(+)) CeL neurons, which has previously been…
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