[Behavior of the receptors in the foliate papillae after colchicine treatment of the glossopharyngeal nerve in the rabbit].
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The cause of the initial hyperventilation, which occurs on exposure to O2 at high pressure (o.h.p.), has been investigated by measuring tidal volume (VT), frequency of breathing (f) and hence ventilation (VE) in thirty-six barbiturate-anaesthetized rats, with or without their glossopharyngeal (IX) nerves sectioned, during 30-60 min of exposure to o.h.p. at 4, 6 or 8 atm absolute. In intact rats the rates of rise of VT, f and VE with time during exposure to o.h.p. were smallest at 4 and greatest at 8 atm absolute. In IX-sectioned rats the rates of rise of VT at 4, 6 and 8 atm absolute and of f at 4 atm absolute were similar to those of intact rats. At 6 atm absolute and even more so at 8 atm absolute, however, f decreased. Hence the slope of VE in IX-sectioned compared with intact rats was similar at 4 atm absolute but smaller at 6 and 8 atm absolute. In fact at 8 atm absolute VE remained constant in IX-sectioned rats. Since the slope of VE versus time in intact rats was steeper the greater the pressure and since the removal of carotid bodies in IX-sectioned rats reduced the VE slope at 6 and 8 atm absolute, the stimulus to the hyperventilation induced by o.h.p. cannot be an accumulation of CO2 in the brain resulting from the lack of O2 desaturation of haemoglobin. This theory would predict that VE should be identical at all pressures above 3.5 atm absolute. The findings in the IX-sectioned rats indicate a major contribution of the carotid bodies to the f increase in o.h.p. They may be stimulated by a histotoxic hypoxia induced by early O2 poisoning. Since the VT increase on exposure to o.h.p. was both large and fairly similar in intact and IX-sectioned rats, it is suggested that a large part of the VT increase was caused by stimulation of the central chemoreceptors by lactic acidosis induced by an o.h.p.-induced histotoxic hypoxia of the brain.
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The cerebellum receives information from many kinds of sensory organs (muscle, somatosensory, auditory, vestibular, visual) as well as from the autonomic system. The cerebellum presumably has a role in the control of tongue movement and salivary secretion. However, the relationship between cerebellar neuron activity and tongue sensation has not been investigated previously. In the present study, negative cerebellar field potentials in the molecular layer and single unit responses of Purkinje cells induced by electrical stimulation of the bullfrog glossopharyngeal (IXth) nerve or tongue surface were investigated. The interaction between IXth nerve stimulation and natural (taste and touch) stimulation of the tongue in their effects on cerebellar neuron activity were investigated. The negative field potentials were potentiated by a brief train of electrical pulses to the tongue or IXth nerve. With electrical stimulation of the tongue surface, several fungiform papillae were needed to elicit cerebellar field potentials. The latency of Purkinje cells following IXth nerve stimulation was 44.4-53.6 msec for complex spikes, whereas for simple spikes two maxima were seen, with mean values at 33.9-36 msec and 96.8 msec. A preceding electrical stimulation of the IXth nerve depressed the negative field potentials or Purkinje cell complex spike responses induced by test stimulation of the IXth nerve. These depressive effects were also seen following a preceding natural stimulation of the tongue and were dependent upon the type of preceding stimulation. The depressive effects were produced by preceding stimulation with NaCl, CaCl2, water, and touch, but not with quinine and acetic acid stimulation. These results clearly demonstrate that gustatory and tactile signals from the tongue can influence cerebellar neuron activity.
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The authors report 14 cases of idiopathic glossopharyngeal neuralgias surgically treated and followed over a mean 3.5 year period. The series consisted of 7 females and 7 males, 66 years old on average. The pain was located on the left side in 13 out of the 14 cases. A trigeminal neuralgia was associated to the glossopharyngeal pain (on the same side) in 4 cases. The vertebral angiogram evidenced a megadolicho-artery in 6 cases and was considered normal in 8 cases. The surgical treatment was a percutaneous thermocoagulation of the Andersh ganglion in 3 case (the thermolesion could not be completed in one of these cases due to the onset of coronarian ischemia). A microsurgical vascular decompression was carried out 9 times, alone in 8 cases, associated with a radicotomy in one case. A mere radicotomy was performed in 2 other cases, because of no finding vascular compression. Total pain relief was achieved in the 2 cases of completed thermocoagulation and in all the 11 cases of direct approach. The thermocoagulations, as well as the radicotomies, of the IX and anterior rootlets of the X produced in each case permanent deficits in the IX and X territories, whilst the side-effects of the decompression procedure were only mild or transient. Therefore microsurgical vascular decompression is preferred by the authors everytime the age, general conditions and the patient's acceptance authorize it.
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Anterograde transport of horseradish peroxidase (HRP) along the bullfrog IXth nerve was studied 6-16 days after application of HRP to the cut end of either the IXth nerve trunk or its distal 2 branches. The jugular and IXth nerve ganglia attached to the rhombencephalon were removed after fixation and serial sections of 50 microns in thickness were stained by the Graham and Karnovsky method. Of all the primary afferent neurons in the IXth nerve, 62% of the cell bodies were distributed within the IXth nerve ganglion, the remaining 38%, within the jugular ganglion. Similar distribution was found with the cells belonging to each of the IXth nerve branches. A part of the transganglionic IXth nerve fibers entering the medulla oblongata ascended to the cerebellar peduncle while the majority descended along the fasciculus solitarius. Some of the descending fibers in the fasciculus extended to the dorsal field of the spinal cord at the third spinal nerve, while some others run to join the descending tract of trigeminal nerve.
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