The synapse is an incredibly specialized structure that allows for the coordinated communication of information from one neuron to another. When assembled into circuits, steady streams of excitatory and inhibitory syn...The synapse is an incredibly specialized structure that allows for the coordinated communication of information from one neuron to another. When assembled into circuits, steady streams of excitatory and inhibitory synaptic activity shape neural outputs. At the organismal level, ensembles of neural networks underlie behavior, emotion and memory. Disorder or dysfunctions of synapses, a synaptopathy, may underlie a host of developmental and degenerative neurological conditions. There is a possibility that amyotrophic lateral sclerosis may be a result of a synaptopathy within the neuromotor system. To this end, particular attention has been trained on the excitatory glutamatergic synapses and their morphological proxy, the dendritic spine. The extensive detailing of these dysfunctions in vulnerable neuronal populations, including corticospinal neurons and motor neurons, has recently been the subject of original research in rodents and humans. If amyotrophic lateral sclerosis is indeed a synaptopathy, it is entirely consistent with other proposed pathogenic mechanisms – including glutamate excitotoxicity, accumulation of misfolded proteins and mitochondrial dysfunction at distal axon terminals(cortico-motor neuron and neuromuscular). Further, although the exact mechanism of disease spread from region to region is unknown, the synaptopathy hypothesis is consistent with emerging die-forward evidence and the prion-like propagation of misfolded protein aggregates to distant neuronal populations. Here in this mini-review, we focus on the timeline of synaptic observations in both cortical and spinal neurons from different rodent models, and provide a conceptual framework for assessing the synaptopathy hypothesis in amyotrophic lateral sclerosis.展开更多
The paper introduces a monitoring system of muscle relaxant actionduring the anaesthesia operation,which is based on measurement of acceleration.The monitor consists of an acceleration transducer,a nerve stimlation an...The paper introduces a monitoring system of muscle relaxant actionduring the anaesthesia operation,which is based on measurement of acceleration.The monitor consists of an acceleration transducer,a nerve stimlation and a microcomputer unit.The transducer can be fastened to the thumb,and the signal of thethumb movement in response to ulnar nerve stimulation is measured and registeredin the computing unit. In daily clinical practice it has proved possible,using this newapparatus, to achieve reliable evaluation of nuromuscular transimission functionand to contribute to improve anesthesia quality and patient care.展开更多
1 Introduction Sea anemone toxins are polypeptide neurotoxins. The symptoms of the toxic animals exhibits contracture and paralysis of their limbs. It is evident that the peripheral nerve and muscle are important targ...1 Introduction Sea anemone toxins are polypeptide neurotoxins. The symptoms of the toxic animals exhibits contracture and paralysis of their limbs. It is evident that the peripheral nerve and muscle are important targets of the toxin. Up to now, it is still a controversial topic about which part of the N-M preparation is affected. Shapiro considered that the venom from Condylactic gigantea was active on crayfish nerve but not on muscle membrane. Metezeau et al. used curarized and denervated frog sartofius muscles, and found that ATX-Ⅱ from Anemonia sulcata acted on motor nerve terminals but not directly on muscle fibres. Erxleben et al. proved that ATX-Ⅱ could act on frog skeletal muscle directly展开更多
文摘The synapse is an incredibly specialized structure that allows for the coordinated communication of information from one neuron to another. When assembled into circuits, steady streams of excitatory and inhibitory synaptic activity shape neural outputs. At the organismal level, ensembles of neural networks underlie behavior, emotion and memory. Disorder or dysfunctions of synapses, a synaptopathy, may underlie a host of developmental and degenerative neurological conditions. There is a possibility that amyotrophic lateral sclerosis may be a result of a synaptopathy within the neuromotor system. To this end, particular attention has been trained on the excitatory glutamatergic synapses and their morphological proxy, the dendritic spine. The extensive detailing of these dysfunctions in vulnerable neuronal populations, including corticospinal neurons and motor neurons, has recently been the subject of original research in rodents and humans. If amyotrophic lateral sclerosis is indeed a synaptopathy, it is entirely consistent with other proposed pathogenic mechanisms – including glutamate excitotoxicity, accumulation of misfolded proteins and mitochondrial dysfunction at distal axon terminals(cortico-motor neuron and neuromuscular). Further, although the exact mechanism of disease spread from region to region is unknown, the synaptopathy hypothesis is consistent with emerging die-forward evidence and the prion-like propagation of misfolded protein aggregates to distant neuronal populations. Here in this mini-review, we focus on the timeline of synaptic observations in both cortical and spinal neurons from different rodent models, and provide a conceptual framework for assessing the synaptopathy hypothesis in amyotrophic lateral sclerosis.
文摘The paper introduces a monitoring system of muscle relaxant actionduring the anaesthesia operation,which is based on measurement of acceleration.The monitor consists of an acceleration transducer,a nerve stimlation and a microcomputer unit.The transducer can be fastened to the thumb,and the signal of thethumb movement in response to ulnar nerve stimulation is measured and registeredin the computing unit. In daily clinical practice it has proved possible,using this newapparatus, to achieve reliable evaluation of nuromuscular transimission functionand to contribute to improve anesthesia quality and patient care.
基金Project supported by the National Natural Science Foundation of China
文摘1 Introduction Sea anemone toxins are polypeptide neurotoxins. The symptoms of the toxic animals exhibits contracture and paralysis of their limbs. It is evident that the peripheral nerve and muscle are important targets of the toxin. Up to now, it is still a controversial topic about which part of the N-M preparation is affected. Shapiro considered that the venom from Condylactic gigantea was active on crayfish nerve but not on muscle membrane. Metezeau et al. used curarized and denervated frog sartofius muscles, and found that ATX-Ⅱ from Anemonia sulcata acted on motor nerve terminals but not directly on muscle fibres. Erxleben et al. proved that ATX-Ⅱ could act on frog skeletal muscle directly
