Sentences with phrase «for synaptic function»

This damages nerve cells by blocking their ability to make the proteins needed for synaptic function and leads to the death of neurons in the brain and spinal cord.

In nerve cells, ribosomes are also found close to the synapses of the dendrites, thus enabling proteins that are required for synaptic function to be produced close to their sites of action.

Not exact matches

Thus, synaptobrevin 2 may function in catalyzing fusion reactions and stabilizing fusion intermediates but is not absolutely required for synaptic fusion.

These genes are believed to be essential for the normal function of nerve cells, and previous studies have linked these mutations to problems with synaptic function — how neurons communicate with each other.

This regulation is spectacularly apparent in the exquisite speed and precision of synaptic exocytosis, where synaptotagmin (the calcium - ion sensor for fusion) cooperates with complexin (the clamp activator) to control the precisely timed release of neurotransmitters that initiates synaptic transmission and underlies brain function.

The structure of synaptophysin suggests that the protein may function as a channel in the synaptic vesicle membrane, with the carboxyl terminus serving as a binding site for cellular factors.

«The appropriate balance of synapses strengthening and weakening, collectively termed synaptic plasticity, is critical for appropriate brain function.

Closer inspection of neuronal activity did reveal that reducing BACE1 activity did not completely restore synaptic functions and the researchers do suggest that caution is still warranted as the enzyme does seem to be fundamental for optimal cognitive function.

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.

Neuralized 1 activates CPEB3: A function for nonproteolytic ubiquitin in synaptic plasticity... Lire la suite

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).

Important aspects are how nerve endings provide glutamate for synaptic release and how they recover released glutamate for reuse, as well as how synapses provide energy for synaptic transmission and how astrocytes can modulate neuronal 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.

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 diseasFor 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 diseasfor 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 diseases.

Maternal care and hippocampal plasticity: evidence for experience - dependent structural plasticity, altered synaptic functioning, and differential responsiveness to glucocorticoids and stress.