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Brain Motor Centers and Pathways
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Stellate cells, so called because of their star-like shape, are approximately 16 times as numerous as Purkinje cells. Those that are located more superficially in the molecular layer have cell bodies 5–9 µm in diameter, few dendrites, and short axons. More deeply located stellate cells are larger, have more elaborate dendritic trees and axons that extend transversely for up to a few hundred µm. The axons of stellate cells terminate on smooth Purkinje cell dendrites. The cell bodies of basket cells, which are approximately six times as numerous as Purkinje cells, are located in the lower part of the molecular layer. Their axons extend in the transverse direction and give off collaterals that reach a block of up to 10 Purkinje cells transversely on either side of the basket cell and up to 6 Purkinje cells on either side of the transversely oriented axon. Each Purkinje cell receives input from 20–50 basket cells, partly on the smooth Purkinje cell dendrites close to the cell body, but mostly in the form of a basket-like network, hence the name basket cell, around the lower cell body and initial segment of the Purkinje cell. Collaterals of Purkinje cell axons terminate on Golgi and basket cells (Figure 12.11) and to a lesser extent on stellate cells as well as on other Purkinje cells. The somas of basket cells are contacted by axons of other basket cells, and the somas of stellate cells are contacted by axons of other stellate cells.
inHEART Models software – novel 3D cardiac modeling solution
Published in Expert Review of Medical Devices, 2023
Leah A. John, Brett Tomashitis, Zain Gowani, Dan Levin, Chau Vo, Ian John, Jeffrey R. Winterfield
A 61-year-old man with ICM presented in cardiogenic shock from an ST elevation myocardial infarction. This was complicated by monomorphic VT storm refractory to both antiarrhythmic medications and stellate ganglion block. He required mechanical support to stabilize his cardiac output. He underwent a cardiac CT prior to a planned VT ablation to assist in preoperative planning. During the procedure, a large area of scar was noted extending along the left ventricular (LV) septum from base to apex. The clinical VT morphology was suggestive of an inferoseptal exit, which correlated with scar border zone area of wall thinning on the cardiac CT (Figure 1). Ablation at this site terminated the VT, and he has remained without VT since his ablation.
Simplified cerebellum-like spiking neural network as short-range timing function for the talking robot
Published in Connection Science, 2018
Hardware limitations with the Xilinx SP-605 FPGA board used in this study meant that some parts of the cerebellum was ignored such as stellate cells and basket cells, reducing the plausibility of a bio-realistic neural network. Moreover, the robot was only tested with single vowel sounds. The next step will be to conduct a sequence of sounds or a sentence. In future, we plan to improve the design by using more advanced FPGA boards and faster servo motors to improve the neural network system. The success of this study opens the opportunity for the talking robot to be a test system for an articulatory speech-prosthesis system for animals or humans.
The role of low-level vagus nerve stimulation in cardiac therapy
Published in Expert Review of Medical Devices, 2019
Yuhong Wang, Sunny S. Po, Benjamin J. Scherlag, Lilei Yu, Hong Jiang
Many studies have shown the antiarrhythmic effect of LL-VNS. In 2009, Li et al [6] first reported paradoxical effects of VNS in that cervical LL-VNS administered 1 V below the threshold that slowed the sinus rate or AV conduction, significantly increased the effective refractory period (ERP), suppressed atrial fibrillation (AF) inducibility and shortened the AF duration at all pulmonary veins and atrial sites. Furthermore, the results of neural recordings indicated that LL-VNS could inhibit the neural activity of GP, thereby suppressing AF [18]. Studies on ambulatory dogs by Shen et al [19] demonstrated that LL-VNS could inhibit left stellate ganglion (LSG) activity and reduce sympathetic nerve density in the LSG, thereby suppressing paroxysmal atrial tachyarrhythmias. These findings indicated that LL-VNS was both anticholinergic and antiadrenergic, which may account for its antiarrhythmic effects. Other studies also showed the anticholinergic and antiadrenergic effects of LL-VNS [20]. Moreover, if LL-VNS was initiated simultaneously with rapid atrial pacing, electrical remodeling such as shortening of ERP and increases in ERP dispersion could be prevented, indicating that if LL-VNS can be started immediately after AF initiation, atrial electrical remodeling may be prevented [21,22]. LL-VNS not only reversed atrial electrical remodeling but also suppressed autonomic remodeling [23]. Noninvasive LL-TS was demonstrated to reverse atrial electrical remodeling and inhibit AF inducibility in anesthetized dogs [24]. Preventing the loss of atrial connexin 40 and connexin 43 may be an important reason for the protective effects of LL-TS [25]. Moreover, LL-TS was demonstrated to play an important role in the acute stage of AF induced by obstructive sleep apnea [26]. LL-TS could significantly prolong atrial and ventricular ERP, decrease the window of vulnerability, and decrease the activity of the cardiac intrinsic and extrinsic nervous systems [26].