1,721,019 research outputs found
The mGluR2/3 agonist LY379268 blocks the effects of GLT-1 up-regulation on prepulse inhibition of the startle reflex in adult rats
No full textThe main glutamate transporter GLT-1 is responsible for clearing synaptically released glutamate from the extracellular space and contributes to shape glutamatergic transmission. Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 up-regulation is associated to an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction of hippocampal mGluR2/3-dependent long term depression (LTD). Here, we tested the hypothesis that administration of the mGluR2/3 agonist LY379268 blocks the effect of GLT-1 up-regulation on PPI of the startle. We showed that LY379268 (1 mg/Kg) administration prevented PPI alterations associated to GLT-1 up-regulation, suggesting that CEF-induced PPI impairment was mGluR2/3-dependent. In addition, we demonstrated that CEF-induced GLT-1 up-regulaton did not alter the expression of mGluR2/3, and that it occurred at sites of mGluR2/3 expression. These results indicate a novel mechanism by which GLT-1 up-regulation modulates PPI of the startle
Structural synaptic plasticity across sleep and wake
Full text linkSleep-dependent synaptic plasticity is crucial for optimal cognition. However, establishing the direction of synaptic plasticity during sleep has been particularly challenging since data in support of both synaptic potentiation and depotentiation have been reported. This review focuses on structural synaptic plasticity across sleep and wake and summarizes recent developments in the use of 3-dimensional electron microscopy as applied to this field
The role of sleep and wakefulness in myelin plasticity
Full text linkMyelin plasticity is gaining increasing recognition as an essential partner to synaptic plasticity, which mediates experience-dependent brain structure and function. However, how neural activity induces adaptive myelination and which mechanisms are involved remain open questions. More than two decades of transcriptomic studies in rodents have revealed that hundreds of brain transcripts change their expression in relation to the sleep–wake cycle. These studies consistently report upregulation of myelin-related genes during sleep, suggesting that sleep represents a window of opportunity during which myelination occurs. In this review, we summarize recent molecular and morphological studies detailing the dependence of myelin dynamics after sleep, wake, and chronic sleep loss, a condition that can affect myelin substantially. We present novel data about the effects of sleep loss on the node of Ranvier length and provide a hypothetical mechanism through which myelin changes in response to sleep loss. Finally, we discuss the current findings in humans, which appear to confirm the important role of sleep in promoting white matter integrity
Sleep quality relates to emotional reactivity via intracortical myelination
Full text linka good quality and amount of sleep are fundamental to preserve cognition and affect. New evidence also indicates that poor sleep is detrimental to brain myelination. In this study, we test the hypothesis that sleep quality and/or quantity relate to variability in cognitive and emotional function via the mediating effect of interindividual differences in proxy neuroimaging measures of white matter integrity and intracortical myelination. by employing a demographically and neuropsychologically well-characterized sample of healthy people drawn from the human connectome project (n = 974), we found that quality and amount of sleep were only marginally linked to cognitive performance. In contrast, poor quality and short sleep increased negative affect (i.e. anger, fear, and perceived stress) and reduced life satisfaction and positive emotionality. at the brain level, poorer sleep quality and shorter sleep duration related to lower intracortical myelin in the mid-posterior cingulate cortex (p = 0.038), middle temporal cortex (p = 0.024), and anterior orbitofrontal cortex (OFC, p = 0.034) but did not significantly affect different measures of white matter integrity. finally, lower intracortical myelin in the OFC mediated the association between poor sleep quality and negative emotionality (p < 0.05). we conclude that intracortical myelination is an important mediator of the negative consequences of poor sleep on affective behavior
Synaptic localization of GLT-1a in the rat somatic sensory cortex
No full textGLT-1a, the major glutamate transporter, plays an important role in both physiological and pathological conditions. Uncertainty regarding its localization in the cerebral cortex prompted us to re-examine its cellular and subcellular localization in the rat somatic sensory cortex. GLT-1a detection was sensitive to fixation; in optimal conditions approximately 25% of GLT-1a+ profiles were axon terminals. GLT-1a/VGLUT1 double-labeling and pre-embedding electron microscopy studies showed that approximately 50% of GLT-1a+ profiles were in the vicinity of asymmetric synapses. Using pre-embedding electron microscopy, we found that approximately 70% of GLT-1a located in the vicinity of asymmetric synapses was astrocytic and approximately 30% was neuronal. Post-embedding immunogold studies showed that the density of gold particles coding for GLT-1a was much higher in astrocytic processes than in axon terminals, and that in the latter they were never at the active zone. In both astrocytic processes and axon terminals most gold particles were localized in a membrane region extending for about 250 nm from active zone margin, with a peak at 140 nm for astrocytic processes and at 80 for axon terminals. We conclude that, although GLT-1a is expressed by both astrocytes and axon terminals, astrocytic GLT-1a predominates at asymmetric synapses, and that the perisynaptic localization of GLT-1a in cortex is well-suited to modulate Glu concentrations at the cleft and also to restrict Glu spillover
Cellular and Synaptic Localization of EAAT2a in Human Cerebral Cortex
No full textWe used light and electron microscopic immunocytochemical techniques to analyze the distribution, cellular and synaptic localization of EAAT2, the main glutamate transporter, in normal human neocortex. EAAT2a-immunoreactivity (ir) was in all layers and consisted of small neuropilar puncta and rare cells. In white matter EAAT2a+ cells were numerous. Electron microscopic studies showed that in gray matter ∼77% of immunoreactive elements were astrocytic processes, ∼14% axon terminals, ∼2.8% dendrites, whereas ∼5% were unidentifiable. In white matter, ∼81% were astrocytic processes, ∼17% were myelinated axons, and ∼2.0% were unidentified. EAAT2a-ir was never in microglial cells and oligodendrocytes. Pre-embedding electron microscopy showed that ∼67% of EAAT2a expressed at (or in the vicinity of) asymmetric synapses was in astrocytes, ∼17% in axon terminals, while ∼13% was both in astrocytes and in axons. Post-embedding electron microscopy studies showed that in astrocytic processes contacting asymmetric synapses and in axon terminals, gold particle density was ∼25.1 and ∼2.8 particles/μm(2), respectively, and was concentrated in a membrane region extending for ∼300 nm from the active zone edge. Besides representing the first detailed description of EAAT2a in human cerebral cortex, these findings may contribute to understanding its role in the pathophysiology of neuropsychiatric diseases
GLT-1 up-regulation enhances the effect of PCP on prepulse inhibition of the startle reflex in adult rats
No full textNo abstract availabl
The role of angular momentum transfer to determine the mass ratio of binaries
No full textA thermodynamical approach to the problem of star formation, presented in a previous paper, shows how the characteristics of the outcomes depend on the initial conditions and on the distribution of the angular momentum among the various parts of the system. In the case of a binary outcome, the distribution can be profitably expressed in terms of two parameters, roughly corresponding to (1) the spin ratio as function of the mass ratio and (2) the fraction of angular momentum involved in the orbital motion
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