Sentences with phrase «role in synaptic function»

NMDA - Rs are expressed in both neurons and glia (Conti et al., 1997; Verkhratsky and Kirchhoff, 2007), and selective genetic access to these cell classes in the brain could allow for dissection of their relative role in synaptic function.

Alpha - synuclein occurs naturally in the nervous system, where it plays an important role in synaptic function.

Not exact matches

The lipid type, ceramide, also has a functional role in various signaling pathways and affects synaptic function, although its primary role is not in the synapse, but providing structure in cell membranes.

We will explore the function of these genes in controlling synaptic homeostasis, develop novel imaging approaches to visualize homeostatic changes in real time, and systematically screen genes implicated in aging and longevity for roles in homeostatic plasticity.

He joined the Polleux lab in 2014 and studies the role of SRGAP2 in the evolution of human synaptic structure and function.

Dr. Mentis» publication highlights the importance of the role of synaptic functions and neurocircuits in SMA.

A role of glutamine has been defined for normal synaptic function (J Neurochem 2008) as well as dendritic retrograde signaling (Cereb Cortex 2009c), and a potential target uncovered in Alzheimer's disease (Neurochem Res 2008).

Wei - Chi She, Charles Quairiaux, Michael J. Albright, Yu - Chi Wang, Denisse E. Sanchez, Poh - Shing Chang, Egbert Welker, Hui - Chen Lu (2009) «Roles of mGluR5 in synaptic function and plasticity of the mouse thalamocortical pathway», European J. Neuroscience, 29: 1379 — 1396 (EJN featured article).

We will examine whether astrocytes play a role in loss of synaptic function as well as identifying the astrocyte - derived molecules that may regulate this process.

This powerful amino acid plays a role in synaptic maintenance and function and lends a hand in improving your learning and memory.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasein neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasein the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasein a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseaseIn addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasein most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseasein the treatment of convulsion diseases.

One final example is the prefrontal cortex, which is thought to play an important role in regulating behavior by suppressing impulses and emotions arising from the amygdala and other parts of the limbic system.50 — 52 In animal studies, exposure to chronic stress or glucocorticoids alters the synaptic connectivity within the prefrontal cortex, 52,53 and this may limit the ability of the prefrontal cortex to (1) suppress the impulsivity and aggression of the limbic system, and (2) execute adaptive responses (rather than maladaptive responses) to stress.54 — 56 Stress - induced changes in brain structure parallel the well - described impact of significant childhood adversity on a variety of brain functions, including the modulation of physiologic responses (hyper - responsive or chronically active stress response), learning (impaired memory), and the regulation of behavior (the ability to execute adaptive vs maladaptive responses to stress).3, 39,in regulating behavior by suppressing impulses and emotions arising from the amygdala and other parts of the limbic system.50 — 52 In animal studies, exposure to chronic stress or glucocorticoids alters the synaptic connectivity within the prefrontal cortex, 52,53 and this may limit the ability of the prefrontal cortex to (1) suppress the impulsivity and aggression of the limbic system, and (2) execute adaptive responses (rather than maladaptive responses) to stress.54 — 56 Stress - induced changes in brain structure parallel the well - described impact of significant childhood adversity on a variety of brain functions, including the modulation of physiologic responses (hyper - responsive or chronically active stress response), learning (impaired memory), and the regulation of behavior (the ability to execute adaptive vs maladaptive responses to stress).3, 39,In animal studies, exposure to chronic stress or glucocorticoids alters the synaptic connectivity within the prefrontal cortex, 52,53 and this may limit the ability of the prefrontal cortex to (1) suppress the impulsivity and aggression of the limbic system, and (2) execute adaptive responses (rather than maladaptive responses) to stress.54 — 56 Stress - induced changes in brain structure parallel the well - described impact of significant childhood adversity on a variety of brain functions, including the modulation of physiologic responses (hyper - responsive or chronically active stress response), learning (impaired memory), and the regulation of behavior (the ability to execute adaptive vs maladaptive responses to stress).3, 39,in brain structure parallel the well - described impact of significant childhood adversity on a variety of brain functions, including the modulation of physiologic responses (hyper - responsive or chronically active stress response), learning (impaired memory), and the regulation of behavior (the ability to execute adaptive vs maladaptive responses to stress).3, 39,57