Use of dexamethasone with TTX block of nerve conduction shows that muscle membrane properties are fully controlled by evoked activity

1997 ◽  
Vol 770 (1-2) ◽  
pp. 242-247 ◽  
Author(s):  
Efrem Pasino ◽  
Mario Buffelli ◽  
Giuseppe Busetto ◽  
Alberto Cangiano
Author(s):  
Agnes Witt ◽  
Hugh Bostock ◽  
Werner J. Z'Graggen ◽  
S. Veronica Tan ◽  
Alexander Gramm Kristensen ◽  
...  

2016 ◽  
Vol 54 (2) ◽  
pp. 249-257 ◽  
Author(s):  
S. Veronica Tan ◽  
Werner J. Z'graggen ◽  
Delphine Boërio ◽  
Christopher Turner ◽  
Michael G. Hanna ◽  
...  

2013 ◽  
Vol 110 (4) ◽  
pp. 999-1008 ◽  
Author(s):  
Anne E. Takesian ◽  
Vibhakar C. Kotak ◽  
Neeti Sharma ◽  
Dan H. Sanes

Sensory deprivation, such as developmental hearing loss, leads to an adjustment of synaptic and membrane properties throughout the central nervous system. These changes are thought to compensate for diminished sound-evoked activity. This model predicts that compensatory changes should be synergistic with one another along each functional pathway. To test this idea, we examined the excitatory thalamic drive to two types of cortical inhibitory interneurons that display differential effects in response to developmental hearing loss. The inhibitory synapses made by fast-spiking (FS) cells are weakened by hearing loss, whereas those made by low threshold-spiking (LTS) cells remain strong but display greater short-term depression ( Takesian et al. 2010 ). Whole-cell recordings were made from FS or LTS interneurons in a thalamocortical brain slice, and medial geniculate (MG)-evoked postsynaptic potentials were analyzed. Following hearing loss, MG-evoked net excitatory potentials were smaller than normal at FS cells but larger than normal at LTS cells. Furthermore, MG-evoked excitatory potentials displayed less short-term depression at FS cells and greater short-term depression at LTS cells. Thus deprivation-induced adjustments of excitatory synapses onto inhibitory interneurons are cell-type specific and parallel the changes made by the inhibitory afferents.


2011 ◽  
Vol 106 (3) ◽  
pp. 1443-1453 ◽  
Author(s):  
Jan Walcher ◽  
Benjamin Hassfurth ◽  
Benedikt Grothe ◽  
Ursula Koch

Interaural intensity differences are analyzed in neurons of the lateral superior olive (LSO) by integration of an inhibitory input from the medial nucleus of the trapezoid body (MNTB), activated by sound from the contralateral ear, with an excitatory input from the ipsilateral cochlear nucleus. The early postnatal refinement of this inhibitory MNTB-LSO projection along the tonotopic axis of the LSO has been extensively studied. However, little is known to what extent physiological changes at these inputs also occur after the onset of sound-evoked activity. Using whole-cell patch-clamp recordings of LSO neurons in acute brain stem slices, we analyzed the developmental changes of inhibitory synaptic currents evoked by MNTB fiber stimulation occurring after hearing onset. We compared these results in gerbils and mice, two species frequently used in auditory research. Our data show that neither the number of presumed input fibers nor the conductance of single fibers significantly changed after hearing onset. Also the amplitude of miniature inhibitory currents remained constant during this developmental period. In contrast, the kinetics of inhibitory synaptic currents greatly accelerated after hearing onset. We conclude that tonotopic refinement of inhibitory projections to the LSO is largely completed before the onset of hearing, whereas acceleration of synaptic kinetics occurs to a large part after hearing onset and might thus be dependent on proper auditory experience. Surprisingly, inhibitory input characteristics, as well as basic membrane properties of LSO neurons, were rather similar in gerbils and mice.


Critical Care ◽  
2014 ◽  
Vol 18 (4) ◽  
Author(s):  
Karin A Ackermann ◽  
Hugh Bostock ◽  
Lukas Brander ◽  
Ralph Schröder ◽  
Siamak Djafarzadeh ◽  
...  

Author(s):  
Belén Rodriguez ◽  
Karin Jost ◽  
Lotte Hardbo Larsen ◽  
Hatice Tankisi ◽  
Werner J. Z’Graggen

Abstract Purpose In neuropathic postural tachycardia syndrome, peripheral sympathetic dysfunction leads to excessive venous blood pooling during orthostasis. Up to 84% of patients report leg pain and weakness in the upright position. To explore possible pathophysiological processes underlying these symptoms, the present study examined muscle excitability depending on body position in patients with neuropathic postural tachycardia syndrome and healthy subjects. Methods In ten patients with neuropathic postural tachycardia syndrome and ten healthy subjects, muscle excitability measurements were performed repeatedly: in the supine position, during 10 min of head-up tilt and during 6 min thereafter. Additionally, lower leg circumference was measured and subjective leg pain levels were assessed. Results In patients with neuropathic postural tachycardia syndrome, muscle excitability was increased in the supine position, decreased progressively during tilt, continued to decrease after being returned to the supine position, and did not completely recover to baseline values after 6 min of supine rest. The reduction in muscle excitability during tilt was paralleled by an increase in lower leg circumference as well as leg pain levels. No such changes were observed in healthy subjects. Conclusions This study provides evidence for the occurrence of orthostatic changes in muscle excitability in patients with neuropathic postural tachycardia syndrome and that these may be associated with inadequate perfusion of the lower extremities. Insufficient perfusion as a consequence of blood stasis may cause misery perfusion of the muscles, which could explain the occurrence of orthostatic leg pain in neuropathic postural tachycardia syndrome.


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