Neuroreport
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Clinical Trial
Decreased calmodulin-NR1 co-assembly as a mechanism for focal epilepsy in cortical dysplasia.
The NMDA receptor is one of the ionotropic glutamate receptors essential for excitatory neurotransmission. The NMDAR1 subunit is inactivated by direct interaction with calmodulin. ⋯ In all patients, the co-assembly of calmodulin and NMDAR1 was decreased in epileptogenic dysplastic cortex compared with normal appearing non-epileptogenic cortex, while there was no significant difference in the total protein levels of calmodulin or NMDAR1 between the two EEG groups. These results suggest that decreased calmodulin-NMDAR1 co-assembly is a cellular mechanism that contributes to hyperexcitability in dysplastic cortical neurons and in focal seizure onsets.
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Ts65Dn mice have an extra chromosome that contains a segment of chromosome 16 homologous to the Down syndrome 'critical region' of human chromosome 21. Since pain transmission and expression may be limited in people with mental disabilities, including Down syndrome, responsiveness to nociception in Ts65Dn mice was compared with that in their control litter-mates. ⋯ In the hot-plate test, no changes were observed in escape latencies during the first exposure, but Ts65Dn mice showed smaller tendency to lick. The results indicate that trisomic mice present an overall depressed responsiveness to nociceptive stimulation.
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Clinical Trial
Plasticity in the motor system related to therapy-induced improvement of movement after stroke.
Neuroplasticity might play a beneficial role in the recovery of function after stroke but empirical evidence for this is lacking thus far. Constraint-induced (CI) therapy was used to increase the use of a paretic upper extremity in four hemiparetic stroke patients. ⋯ The source locations associated with affected hand movement were unusual at follow-up because activation of the ipsilateral hemisphere was found in the absence of mirror movements of the unaffected hand. This long-term change may be considered as an initial demonstration of large-scale neuroplasticity associated with increased use of the paretic limb after application of CI therapy.
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Cortical activity can be substantially changed by the type of anaesthetic used, and by its dose level. For easy monitoring of depth of anaesthesia we describe the changes in electroencephalogram and electrocardiogram accompanying changes in depth of anaesthesia in the cat. Anaesthesia was induced by the volatile anaesthetic isoflurane. ⋯ The electrocardiogram also shows substantial changes in contamination due to muscle fasciculations with anaesthesia level. Fasciculations appear as noise in the electrocardiogram. The amplitude of the electrical muscle activity contaminating the ECG can be easily used for the maintainance of a constant level of anaesthesia during a neurophysiological experiment.
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In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. ⋯ CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons.