Species differences in the taste qualities mediated through the glossopharyngeal nerve.
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Cobaltic-lysine complex was used to label the afferent and efferent components of the glossopharyngeal nerve in the ganglion and brainstem of the Mexican salamander, axolotl (Ambystoma mexicanum). The distribution of afferent cell bodies in the combined glossopharyngeal-vagus ganglion (the IX-X ganglion) was reconstructed from serial sections, and the sizes of the cell bodies were measured. The central projection of afferents and the location of efferent cell bodies were determined by the tracer. The afferent cell bodies in the ganglion were medium-sized (ca. 25 microns). Cell bodies with a single process were seen. The ganglion was not clearly divided into superior and inferior ganglia, as is observed in mammals and frogs, but comprised a single ganglion. Labelled cells were diffusely distributed in the rostral part of the IX-X ganglion. A few labelled cells also were seen in the caudal part, where the vagus nerve fibers and cell bodies were mainly distributed. Double labellings of the glossopharyngeal and vagus nerves with HRP and cobaltic-lysine demonstrated that the ganglion cells of each nerve are not clearly separated in the IX-X ganglion. In the brainstem, the majority of afferent fibers formed thick ascending and descending limbs in the solitary fasciculus. The remaining afferent fibers formed a thin bundle in the spinal tract of the trigeminal nerve, which had a short ascending limb and a long descending limb. These two bundles had terminal areas in the ipsilateral brainstem: in the dorsal gray matter for the solitary fasciculus and in the lateral funiculus for the spinal tract of the trigeminal nerve, respectively. The cell bodies of the efferent neurons possessed developed dendritic arborizations in the ventrolateral white matter, and formed a longitudinal cell column in the ventrolateral margin of the gray matter. Thus, the glossopharyngeal nerve system in the axolotl assumes a primordial form in its ganglions, but its topographical organization in the brainstem is basically similar to that in anurans.
Unitary discharges from single water fibers of the frog glossopharyngeal nerve, caused by stimulation with 0.02-5 mM CaSO4, were recorded from fungiform papillae with a suction electrode. NiSO4 at concentrations of 0.2-2 mM, namely, at concentrations that are barely effective in producing impulses, had a dual action on the Ca2+ response: NiSO4 caused both inhibition and enhancement of the Ca2+ response. In the present study, this dual action of Ni2+ ions on the Ca2+ response was investigated in detail. Single water fibers yielded a saturation type of concentration-response curve for CaSO4, which suggested that sulfate ions do not affect the Ca2+ response. Thus, sulfates were used as test salts in the present study. At low concentrations of Ca2+ ions, Ni2+ ions inhibited the Ca2+ response, but at higher concentrations of Ca2+ ions they enhanced it. The results can be explained quantitatively by the hypothesis that Ni2+ ions inhibit the Ca2+ response by competing with Ca2+ ions for the Ca2+ receptor (XCa) that is responsible for the Ca2+ response and that Ni2+ ions enhance the Ca2+ response by acting on a membrane element that interacts with XCa. Double-reciprocal plots of the data indicate that the enhancing action of Ni2+ ions is saturated at 1-2 mM Ni2+ ions and that Ni2+ ions at these concentrations increase the maximal response of the Ca2+ response by 182%. Dissociation constants for the Ca-XCa complex and the Ni-XCa complex were 4.2 x 10(-5) M and 7.6 x 10(-5) M, respectively. The analysis suggests that Ni2+ ions enhance the Ca2+ response by affecting the Ca-XCa complex without altering the affinity of XCa for Ca2+ ions.
Fibers of the frog glossopharyngeal nerve (water fibers) that are sensitive to water also respond to CaCl2, MgCl2 and NaCl. In the present study, interaction among cations (Ca2+, Mg2+ and Na+) on taste cell membrane in frogs was studied using transition metals (NiCl2, CoCl2 and MnCl2), which themselves are barely effective in producing neural response at concentrations below 5 mM. Unitary discharges from single water fibers were recorded from fungiform papillae with suction electrode. Transition metal ions (0.05-5.0 mM) had exclusively enhancing effects on the responses to 50 mM Ca2+, 100 mM Mg2+ and 500 mM Na+. The effects of transition metal ions were always reversible. The rank order of effectiveness of transition metals at 1 mM in the enhancement of the responses to 50 mM CaCl2, 100 mM MgCl2 and 500 mM NaCl was NiCl2 > CoCl2 > MnCl2. The concentration of transition metal ions effective to enhance salt response was almost the same among Ca2+, Mg2+ and Na+ responses. The results suggest that a common mechanism is involved in the enhancement of Ca2+, Mg2+ and Na+ taste responses. The enhanced Mg2+ response and the enhanced Na+ response were greatly inhibited by the addition of Ca2+ ions, and the enhanced Ca2+ response was inhibited by the addition of Mg2+ or Na+ ions, suggesting that competitive antagonism occurs between Ca2+ and Mg2+ ions and between Ca2+ and Na+ ions in the presence of Ni2+ ions. Ni2+ ions had a dual effect on the Ca2+ response induced by low concentration (0.1 mM) of CaCl2: enhancement at lower concentrations (0.02-0.1 mM) of NiCl2 and inhibition at higher concentrations (0.5-5 mM) of NiCl2. The present results suggest that transition metal ions do not affect the receptor-antagonist complex, but affect only the receptor-agonist complex.
Central distribution of efferent and afferent components of the glossopharyngeal (IX) nerve in the cat was studied by applying horseradish peroxidase (HRP) to the lesser petrosal nerve (LPN), carotid sinus nerve (CSN) or cervical trunk (CT) distal to the branching point of the CSN. After applying HRP to the LPN or CT, HRP-labeled neurons were distributed ipsilaterally in the lateral regions of the reticular formation from the caudalmost levels of the facial nerve genu to the rostral levels of the solitary nucleus. HRP-labeled axons of these neurons ran dorsomedially and then medially along the ventral borders of the medial vestibular nucleus and the facial nerve genu, to form a small genu rostrally at the regions medial to the facial genu and caudally at the medial tip of the medial vestibular nucleus. Subsequently, the labeled axons coursed ventrolaterally to exit from the brain stem with other IX nerve components. After HRP application to the CT, labeled neurons were also seen ipsilaterally within the rostral most levels of the nucleus ambiguous, and labeled fibers were traced ipsilaterally to the medial and interstitial subnuclei of the solarity nucleus, dorsolateral portions of the spinal trigeminal nucleus at the caudalmost levels of the alaminar parts, and ventrolateral regions of the medial cuneate nucleus. Afferent components of the CSN ended ipsilaterally in the medial subnucleus, and bilaterally in the commissural subnucleus of the solitary nucleus; within the medial subnucleus, the CSN terminals located more dorsolaterally than the CT terminals. No efferent components were found in the CSN.
Electrical stimulation of the frog glossopharyngeal (GP) nerve evoked slow hyperpolarizing potentials (HPs) in taste cells. This study aimed to clarify whether slow HPs were postsynaptically induced in taste cells. The slow HPs were recorded intracellularly with a microelectrode. When Ca2+ concentration in the blood plasma was decreased to approximately 0.5 mM, the amplitude of slow HPs reduced and their latency lengthened. When the Ca2+ concentration was increased to approximately 20 mM, the amplitude of slow HPs increased and their latency shortened. Addition of Cd2+ to the plasma greatly reduced the amplitude of slow HPs and lengthened their latency. These data suggest that the slow HPs are dependent on presynaptic activities in the GP nerve terminals in the taste disk. Of various antagonists injected intravenously for blocking receptors of neurotransmitter biogenic amines and peptides, only antagonists for substance P blocked the slow HPs at 2-4 mg/kg body wt. Application of substance P of 2 mg/kg to the plasma induced hyperpolarizing responses in taste cells, whose amplitude was the same as that of the slow HPs induced by GP nerve stimulation. Application of a nonselective cation channel antagonist, flufenamic acid, to the plasma blocked the slow HPs. These results suggest that the slow HPs are generated by closing the nonselective cation channels in the postsynaptic membrane of taste cells following possible release of substance P from the GP nerve terminals in the taste disk.
20 adult dogs were classified into five groups; in two animals of each group hypoglossa-glossopharyngeal suturing was done. In the other two animals glossopharyngeal nerve transection with concomitant central segment avulsion was done and these two animals were used as controls. The animals of the five groups were sacrified at 4-week intervals starting by the first group on the 4th post-operative week and ending by the fifth group on the 20th week; the circumvallate papillae were studied. On the 4th week following either operative procedure, few taste buds persisted on the circumvallate papillae. Invasion of the papillae by regenerating hypoglossal fibres from the 8th week onwards was not followed by any appreciable increase in the number of taste buds. The difference in number of taste buds between hypoglossal-glossopharyngeal suture and glossopharyngeal avulsion procedures was not statistically significant. from the 8th weeks following cross-innervation the reaction for acetylcholinesterase was more intense than in denervated papillae which showed a persistent weakly positive reaction up to the 20th post-operative week.
A new technique for blocking the glossopharyngeal nerve is described using ultrasound guidance. It is felt this technique will decrease the incidence of complications and increase the efficacy of this block for pain relief in cancer patients. The pertinent anatomic and technical considerations are discussed.
Behavioral studies on the effects of bilateral glossopharyngeal nerve (GL) transection on quinine responsiveness have yielded mixed results. These differences may be explained by the presence or absence of presurgical exposure with the tastant. In the present experiment we measured unconditioned licking to quinine in rats that had no exposure to quinine before surgery. Rats were water deprived and trained to lick water during 10 s trials in an automated gustometer. Next, they were divided into groups that received either GL transection or sham surgery (CON). Following recovery, the water-deprived rats were presented with seven concentrations of quinine hydrochloride (0.003-3 mM) and distilled water. The number of licks to each tastant was averaged over three days of testing. Rats with GL transection licked significantly more to the higher concentrations of quinine relative to CON rats, resulting in a 0.44 log10 unit shift in the quinine concentration-response curve. These results when considered with prior work suggest that experience before nerve transection may have a small protective effect on taste-guided behavioral responsiveness to quinine in rats.
Our study was aimed to examine the anatomic relationships of the tympanic branch of the glossopharyngeal nerve (GPN), namely the Jacobson's nerve (JN). The JN is the first branch of the GPN after having passed the jugular foramen. It contributes to the tympanic plexus on the promontory. It transmits secretory innervation to the parotid gland. Its possible role in the regulation of the middle ear pressure has also been hypothesized in terms of animal studies. Using microdissection techniques and high-resolution computed tomography (HRCT) scanning, the anatomic relationships and course of the JN were examined in eight formalin-preserved cadavers (16 sides). A morphometric analysis related to the JN was also performed both in the 16 cadavers and 40 dry-skull specimens. The JN emerged from the inferior ganglion of the GPN in all specimens. The mean distance between the ganglion and the genu of the GPN was 11.3 mm. The inferior 2/3 of the tympanic canal (TC) followed a vertical course, and then it ran anteromedially with an angle of 160 degrees to 170 degrees. The mean length of the TC was 9.5 mm. The TC was well-defined in all axial HRCT scans. In 2 cases the JN was entirely encased in a bony canal in the middle ear. A double JN was observed in one case. This study gives an additional information regarding the anatomy of the JN.
Glossopharyngeal afferents may be the neural channel by which immune challenge of the posterior oral cavity conveys information to the brain. If this is the case, then bilateral transection of the glossopharyngeal nerves (GLOx) should disrupt this communication. Injection of lipopolysaccharide (LPS) or interleukin (IL)-1beta into the soft palate (ISP) of sham-operated rats induced a dose-related febrile response. GLOx significantly attenuated the febrile response induced by ISP injection of both LPS and IL-1beta. In contrast, GLOx did not affect the febrile response when LPS or IL-1beta were injected intraperitoneally, indicating that the effect of GLOx is not systemic. These results provide experimental evidence for a novel neural pathway for immune-to-brain communication.
Single fibers of the frog glossopharyngeal nerve respond to MgCl2 at concentrations exceeding 10 mM. NiCl2 at 1 mM enhanced the Mg2+ response. CaCl2 at 0.5-2 mM induced an inhibition of the Ni(2+)-enhanced response to Mg2+ ions. A quantitative explanation for these results is provided by the hypothesis that Ni2+ ions secondarily affect a magnesium receptor (designated X*Mg) that is responsible for the Mg2+ response and that Ca2+ ions inhibit the Ni(2+)-enhanced response to Mg2+ ions by competing with Mg2+ ions for X*Mg. Double-reciprocal plots of the experimental data indicate that Ni2+ ions do not affect the affinities of X*Mg for both Mg2+ ions (agonist) and Ca2+ ions (competitive antagonist) appreciably, and that Ni2+ ions at 1 mM enhanced the maximal response to Mg2+ ions by 270%. It appears that a magnesium receptor interacts with an Ni(2+)-binding element that is affected by Ni2+ ions and, thus, Ni2+ ions can induce an enhancement of the Mg2+ response.
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