scholarly journals THE EFFECT OF DEPRIVATION OF GLUCOSE ON THE ULTRASTRUCTURE AND FUNCTION OF THE SUPERIOR CERVICAL GANGLION OF THE RAT IN VITRO

1966 ◽  
Vol 29 (2) ◽  
pp. 267-285 ◽  
Author(s):  
P. Nicolescu ◽  
M. Dolivo ◽  
C. Rouiller ◽  
C. Foroglou-Kerameus

The superior cervical sympathetic ganglion of the rat kept in vitro in a bicarbonate-buffered Krebs' solution retains its capacity for synaptic transmission and axonal conduction during more than 36 hr. After glucose withdrawal, synaptic transmission is lost in 2½ hr and this loss is irreversible; on the other hand, axonal conduction can still be measured on the postganglionic nerve for more than 24 hr after glucose deprivation. Electrophysiological measurements as well as electron microscope studies revealed specific changes at the level of the presynaptic terminal processes, while the ganglion cells and the satellite cells remained relatively unaltered. The presynaptic lesion due to lack of glucose can be prevented by keeping the preparation in vitro at 6°C. This strongly suggests that this lesion results from a major disturbance of the metabolism of the presynaptic fibers.

2019 ◽  
Vol 317 (2) ◽  
pp. C375-C389
Author(s):  
Rachel A. Fischer ◽  
Abigail L. Roux ◽  
Lauren K. Wareham ◽  
Rebecca M. Sappington

Glaucoma is the leading cause of blindness worldwide, resulting from degeneration of retinal ganglion cells (RGCs), which form the optic nerve. Prior to structural degeneration, RGCs exhibit physiological deficits. Müller glia provide homeostatic regulation of ions that supports RGC physiology through a process called K+ siphoning. Recent studies suggest that several retinal conditions, including glaucoma, involve changes in the expression of K+ channels in Müller glia. To clarify whether glaucoma-related stressors directly alter expression and function of K+ channels in Müller glia, we examined changes in the expression of inwardly rectifying K+ (Kir) channels and two-pore domain (K2P) channels in response to elevated intraocular pressure (IOP) in vivo and in vitro in primary cultures of Müller glia exposed to elevated hydrostatic pressure. We then measured outcomes of cell health, cation homeostasis, and cation flux in Müller glia cultures. Transcriptome analysis in a murine model of microbead-induced glaucoma revealed pressure-dependent downregulation of Kir and K2P channels in vivo. Changes in the expression and localization of Kir and K2P channels in response to elevated pressure were also found in Müller glia in vitro. Finally, we found that elevated pressure compromises the plasma membrane of Müller glia and induces cation dyshomeostasis that involves changes in ion flux through cation channels. Pressure-induced changes in cation flux precede both cation dyshomeostasis and membrane compromise. Our findings have implications for Müller glia responses to pressure-related conditions, i.e., glaucoma, and identify cation dyshomeostasis as a potential contributor to electrophysiological impairment observed in RGCs of glaucomatous retina.


1992 ◽  
Vol 70 (S1) ◽  
pp. S27-S31 ◽  
Author(s):  
M. Bachoo ◽  
C. Polosa

A stimulus train to preganglionic axons produces long-term potentiation (LTP) of population responses of sympathetic ganglion cells evoked by the same or by other converging axons. The present study shows that preganglionic axons emerging from the spinal cord in different thoracic rami, and converging onto a common pool of ganglion cells that innervate a single target, differ in their ability to induce LTP. In anesthetized cats under partial nicotinic block with hexamethonium, the nictitating-membrane (NM) contraction evoked by stimulation of the first (T1) and third (T3) thoracic white rami (WR) was recorded. Each ramus produced a contraction of similar amplitude. In contrast, the homosynaptic potentiation produced by a 40-Hz 10-s train differed markedly. T1WR produced a potentiation of duration comparable to that produced by stimulation of the cervical sympathetic trunk, while T3WR produced either no potentiation or a potentiation of much shorter duration. The NM response evoked by T3WR, however, was potentiated by similar extent and duration as was the response evoked by T1WR when the train was applied to T1WR (heterosynaptic LTP). This suggests that the ganglionic synapses made by T3WR possess the mechanism for expressing LTP. Conversely, T3WR was ineffective at potentiating heterosynaptically the NM response evoked by T1WR. These results suggest that the ability to produce or release the LTP inducer varies markedly among sympathetic preganglionic neurons.Key words: preganglionic neuron heterogeneity, long-term potentiation induction, synaptic transmission, neuropeptides.


1968 ◽  
Vol 25 (5-6) ◽  
pp. 381-407 ◽  
Author(s):  
G. Siegrist ◽  
M. Dolivo ◽  
Y. Dunant ◽  
C. Foroglou-Kerameus ◽  
Fr. de Ribaupierre ◽  
...  

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