Medullary taste responses are modulated by the bed nucleus of the stria terminalis

Previous studies have shown a modulatory influence of limbic forebrain areas, such as the central nucleus of the amygdala and lateral hypothalamus, on the activity of taste-responsive cells in the nucleus of the solitary tract (NST). The bed nucleus of the stria terminalis (BST), which receives gustatory afferent information, also sends descending axons to the NST. The present studies were designed to investigate the role of the BST in the modulation of NST gustatory activity. Extracellular action potentials were recorded from 101 taste-responsive cells in the NST of urethane-anesthetized hamsters and analyzed for a change in excitability following bilateral electrical stimulation of the BST. The response of NST taste cells to stimulation of the BST was predominately inhibitory. Orthodromic inhibitory responses were observed in 29 of 101 (28.7%) NST taste-responsive cells, with four cells inhibited bilaterally. An increase in excitability was observed in seven of the 101 (6.9%) NST taste cells. Of the 34 cells showing these responses, 25 were modulated by the ipsilateral BST and 15 by the contralateral; four were inhibited bilaterally and two inhibited ipsilaterally and excited contralaterally. The duration of inhibitory responses (mean = 177.9 ms) was significantly longer than that of excitatory responses (35.4 ms). Application of subthreshold electrical stimulation to the BST during taste trials inhibited or excited the taste responses of every BST-responsive NST cell tested with this protocol. NST neurons that were most responsive to sucrose, NaCl, citric acid or quinine hydrochloride were all affected by BST stimulation, although citric acid-best cells were significantly more often modulated and NaCl-best less often modulated than expected by chance. These results combine with excitatory and inhibitory modulation of NST neurons by the insular cortex, lateral hypothalamus and central nucleus of the amygdala to demonstrate extensive centrifugal modulation of brainstem gustatory neurons.     

Efferent projection from the bed nucleus of the stria terminalis suppresses activity of taste-responsive neurons in the hamster parabrachial nuclei

Although the reciprocal projections between the bed nucleus of the stria terminalis (BNST) and the gustatory parabrachial nuclei (PbN) have been demonstrated neuroanatomically, there is no direct evidence showing that the projections from the PbN to the BNST carry taste information or that descending inputs from the BNST to the PbN modulate the activity of PbN gustatory neurons. A recent electrophysiological study has demonstrated that the BNST exerts modulatory influence on taste neurons in the nucleus of the solitary tract (NST), suggesting that the BNST may also modulate the activity of taste neurons in the PbN. In the present study, we recorded from 117 taste-responsive neurons in the PbN and examined their responsiveness to electrical stimulation of the BNST bilaterally. Thirteen neurons (11.1%) were antidromically invaded from the BNST, mostly from the ipsilateral side (12 cells), indicating that a subset of taste neurons in the PbN project their axons to the BNST. The BNST stimulation induced orthodromic responses on most of the PbN neurons: 115 out of 117 (98.3%), including all BNST projection units. This descending modulation on the PbN gustatory neurons was exclusively inhibitory. We also confirmed that activation of this efferent inhibitory projection from the BNST reduces taste responses of PbN neurons in all units tested. The BNST is part of the neural circuits that involve stress-associated feeding behavior. It is also known that brain stem gustatory nuclei, including the PbN, are associated with feeding behavior. Therefore, this neural substrate may be important in the stress-elicited alteration in ingestive behavior.     

Gustatory projections from the nucleus of the solitary tract to the parabrachial nuclei in the hamster.

Taste-responsive cells in the nucleus of the solitary tract (NST) either project to the parabrachial nuclei (PbN) of the pons, through which taste information is transmitted to forebrain gustatory nuclei, or give rise to axons terminating locally within the medulla. Numerous anatomical studies clearly demonstrate a substantial projection from the rostral NST, where most taste-responsive cells are found, to the PbN. In contrast, previous electrophysiological studies in the rat have shown that only a small proportion (21-45%) of taste-responsive NST cells are antidromically activated from the PbN, suggesting that less than half the cells recorded from the NST are actually involved in forebrain processing of gustatory information. In the present experiment we investigated the projections from the NST to the PbN electrophysiologically in urethane anesthetized hamsters. Responses of 101 single neurons in the rostral NST were recorded extracellularly following lingual stimulation with 32 mM NaCl, sucrose and quinine hydrochloride (QHCl) and 3.2 mM citric acid. The taste-responsive region of the PbN was identified electrophysiologically and stimulated with a concentric bipolar electrode to antidromically activate each NST cell. Of the 101 taste-responsive NST cells, 81 (80.2%) were antidromically activated from the ipsilateral PbN. The mean firing rates to taste stimulation and the spontaneous activity of these projection neurons were significantly greater than those of non-projecting cells. Every sucrose-best neuron in the sample projected to the PbN. The mean conduction velocity of the 23 QHCl-best neurons was significantly lower than that of the other 58 PbN projection neurons, suggesting that the most QHCl-responsive cells are a subset of smaller neurons. These data show that a large majority of NST cells responsive to taste stimulation of the anterior tongue project to the gustatory subdivisions of the PbN and that these cells have the most robust responses to gustatory stimulation.     

The number and location of Fos-like immunoreactive neurons in the central gustatory system following electrical stimulation of the parabrachial nucleus in conscious rats

Electrical stimulation of the waist area (W) of the parabrachial nucleus (PBN) in conscious rats elicits stereotypical oromotor behaviors (Galvin et al. 2004). To identify neurons possibly involved in these behavioral responses, we used Fos immunohistochemistry to locate populations of neurons within central gustatory and oromotor centers activated by PBN stimulation. Dramatic increases in the numbers of Fos-like immunoreactive neurons were observed in the ipsilateral PBN, nucleus of the solitary tract (NST), and central amygdala. The increase in neurally-activated cells within the ventral subdivision (V) of the rostral NST is particularly noteworthy because of its projections to medullary oromotor centers. A modest increase in labeled neurons occurred bilaterally within the gustatory cortex. Although there were trends for an increase in Fos-labeled neurons in the gustatory thalamus and medullary reticular formation, most changes in labeled neurons in these areas were not statistically significant. Linear regression analysis revealed a relationship between the number of taste reactivity (TR) behaviors performed during PBN stimulation and the number of Fos-like immunoreactive neurons in the caudal PBN and V of the rostral NST. These data support a role for neurons in W of the PBN and the ventral rostral NST in the initiation of TR behaviors.     

Forebrain neurons that project to the gustatory parabrachial nucleus in rat lack glutamic acid decarboxylase

Evidence suggests that GABA might mediate the inhibitory influence of centrifugal inputs on taste-evoked responses in the parabrachial nucleus (PBN). Previous studies show that activation of the gustatory cortex (GC), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CeA), and lateral hypothalamus (LH) inhibits PBN taste responses, GABAergic neurons are present in these forebrain regions, and GABA reduces the input resistance of PBN neurons. The present study investigated the expression of glutamic acid decarboxylase immunoreactivity (GAD_67 ir) in GC, BNST, CeA, and LH neurons that project to the PBN in rats. After anesthesia (50 mg/kg ip Nembutal), injections of the retrograde tracer Fluorogold (FG) were made in the physiologically defined gustatory PBN. Brain tissue containing the above forebrain structures was processed and examined for FG and GAD_67 ir. Similar to previous studies, each forebrain site contained retrogradely labeled neurons. Our results suggest further that the major source of input to the PBN taste region is the CeA (608 total cells) followed by GC (257 cells), LH (106 cells), and BNST (92 cells). This suggests a differential contribution to centrifugal control of PBN taste processing. We further show that despite the presence of GAD_67 neurons in each forebrain area, colocalization was extremely rare, occurring only in 3 out of 1,063 FG-labeled cells. If we assume that the influence of centrifugal input is mediated by direct projections to the gustatory region of the PBN, then GABAergic forebrain neurons apparently are not part of this descending pathway.     

Taste-responsive neurons in the nucleus of the solitary tract receive gustatory information from both sides of the tongue in the hamster

Taste receptors on the left and right sides of the anterior tongue are innervated by chorda tympani (CT) fibers, which carry taste information to the ipsilateral nucleus of the solitary tract (NST). Although the anterior tongue is essential for taste, patients with unilateral CT nerve damage often report no subjective change in their taste experience. The standing theory that explains the taste constancy is the "release of inhibition", which hypothesizes that within the NST there are inhibitory interactions between inputs from the CT and glossopharyngeal nerves and that the loss of taste information from the CT is compensated by a release of inhibition on the glossopharyngeal nerve input. However, the possibility of compensation by taste input from the other side of the tongue has never been investigated in rodents. We recorded from 95 taste-responsive neurons in the NST and examined their responsiveness to stimulation of the contralateral CT. Forty-six cells were activated, mostly with excitatory responses (42 cells). Activation of NST cells induced by contralateral CT stimulation was blocked by microinjection of lidocaine into the contralateral NST but was not affected by anesthetization of the contralateral parabrachial nuclei (PbN). In addition, the NST cells that were activated by contralateral CT stimulation showed reduced responsiveness to taste stimulation after microinjection of lidocaine into the contralateral NST. These results demonstrate that nearly half of the taste neurons in the NST receive gustatory information from both sides of the tongue. This "cross talk" between bilateral NST may also contribute to the "taste constancy".     

Integration of gastric distension and gustatory responses in the parabrachial nucleus

Palatable gustatory stimuli promote feeding, whereas gastric distension generally inhibits this behavior. We explored a neural basis for integration of these opposing sensory signals by evaluating the effect of gastric distension on gustatory responses in the parabrachial nucleus (PBN) of anesthetized rats. Sixteen percent of 92 taste cells were coactivated; they responded to independent taste or gastric distension stimulus application. Modulation of taste responses by distension was more prevalent; taste responses declined 37% in response to distension in 25% of the cells and increased by 46% in 10% of cells. Across the whole population, however, the suppressive effect of distension on taste responses was small (6%). The incidence of modulation did not vary as a simple hedonic function of gustatory sensitivity, i.e., similar proportions of sucrose-, citric-acid-, and QHCl-best, but not NaCl-best, neurons were modulated by gastric distension. Coactivated, modulated, and nonmodulated gustatory-responsive cells were intermingled in the gustatory zone of the caudal PBN. The suppression of PBN taste responses by visceral stimulation may reflect a mechanism for satiation and further implicates the PBN in the control of ingestive function.     

Tonic GABAergic inhibition of taste-responsive neurons in the nucleus of the solitary tract

The effects of gamma-aminobutyric acid (GABA) and the GABAA receptor antagonist bicuculline methiodide (BICM) on the activity of taste- responsive neurons in the nucleus of the solitary tract (NST) were examined electrophysiologically in urethane-anesthetized hamsters. Single neurons in the NST were recorded extracellularly and drugs (21 nl) were microinjected into the vicinity of the cell via a multibarrel pipette. The response of each cell was recorded to lingual stimulation with 0.032 M NaCl, 0.032 M sucrose, 0.0032 M citric acid and 0.032 M quinine hydrochloride (QHCl). Forty-six neurons were tested for the effects of GABA; the activity of 29 cells (63%) was inhibited by 5 mM GABA. Whether activity was elicited in these cells by repetitive anodal current stimulation (25 microA, 0.5 s, 0.1 Hz) of the tongue (n = 13 cells) or the cells were spontaneously active (n = 13 cells), GABA produced a dose-dependent (1, 2 and 5 mM) decrement in activity. Forty- seven NST neurons were tested for the effects of BICM on their responses to chemical stimulation of the tongue; the responses of 28 cells (60%) were enhanced by 10 mM BICM. The gustatory responses of 26 of these cells were tested with three concentrations (0.2, 2 and 10 mM) of BICM, which produced a dose-dependent increase in both spontaneous activity and taste-evoked responses. Nine of these neurons were sucrose- best, seven were NaCl-best, eight were acid-best and two responded best to QHCl. The responses to all four tastants were enhanced, with no difference among neuron types. For 18 cells that were tested with two or more gustatory stimuli, BICM increased their breadth of responsiveness to their two most effective stimuli. These data show that approximately 60% of the taste-responsive neurons in the rostral NST are inhibited by GABA and/or subject to a tonic inhibitory influence, which is mediated by GABAA receptors. The modulation of these cells by GABA provides a mechanism by which the breadth of tuning of the cell can be sharpened. Modulation of gustatory activity following a number of physiological changes could be mediated by such a GABAergic circuit.      

Low-dose furosemide modulates taste responses in the nucleus of the solitary tract of the rat

Taste-evoked neural responses in the nucleus of the solitary tract (NST) are subject to both excitatory and inhibitory modulation by physiological conditions that influence ingestion. Treatments that induce sodium appetite predominantly reduce NST gustatory responsiveness to sapid stimuli. When sodium appetite is aroused with 10 mg of the diuretic furosemide (Furo), however, NST gustatory neurons exhibit an enhanced responsiveness to NaCl. In addition to inducing a sodium appetite, 10 mg Furo supports a conditioned taste aversion (CTA). A lower, 2-mg dose of Furo induces an equivalent sodium appetite, but not a CTA. To determine whether the anomalous electrophysiological results reflected the adverse effects of the 10-mg dose, we replicated the original experiment but instead used 2 mg of Furo. In chronically prepared, lightly anesthetized rats, the responses of 49 single NST neurons to 12 taste stimuli were recorded after subcutaneous injections of either 2 mg Furo or saline. There was no effect of treatment on NST neural responses to the four standard taste stimuli. In the NaCl concentration series, however, 2 mg Furo evoked significantly higher responses to the two highest concentrations of NaCl. There was no effect of treatment in the sucrose concentration series. Thus, unlike other methods that induce a sodium appetite, Furo increases NST neural responsiveness to NaCl. At least as far as the first central relay, sodium appetite apparently does not depend on specific changes in the sensory neural code for taste.     

电损毁大鼠杏仁中央核对脑桥臂旁核味觉神经元的影响

应用细胞外记录的电生理学方法,在乌拉坦麻醉的大鼠观察了电损毁双侧杏仁中央核前后脑桥臂旁核味觉神经元对四种基本味觉刺激(即氯化钠、盐酸、奎宁和蔗糖)反应的变化。根据对味觉刺激的优势反应,29个记录的味觉神经元中,有14个NaCl优势、9个HCl优势、3个QH2SO4优势和3个蔗糖优势反应神经元。损毁杏仁中央核明显增强臂旁核味觉神经元对盐酸和硫酸奎宁的反应(P＜0．01)。氯化钠优势、盐酸优势和奎宁优势反应神经元对盐酸和硫酸奎宁的反应在电损毁杏仁中央核后也明显增强。在破坏杏仁中央核后,臂旁核味觉神经元对氯化钠和硫酸奎宁苦味的分辨能力降低。以上结果提示,杏仁中央核在大鼠脑桥水平的味觉编码中发挥重要作用,它可能是通过参与对味觉的影响来调节机体的摄食行为。     

阻断大鼠杏仁中央核AMPA受体对臂旁核味觉反应的影响

以往的研究表明,电刺激或损毁杏仁中央核明显改变臂旁核味觉神经元的活动。为了研究杏仁中央核内的兴奋性受体是否参与此调节,本实验应用细胞外记录方法,在乌拉坦麻醉的大鼠观察了杏仁中央核内微量注射6-氰基-7-硝基喹喔啉-2,3- 二酮(CNQX)前后臂旁核味觉神经元对四种基本味觉刺激反应的变化。结果表明,杏仁中央核内注射 CNQX 对 30% 的臂旁核神经元产生时间依赖性的抑制作用,此抑制作用以对盐酸和盐酸奎宁刺激引起的反应尤为明显(P<0.05)。根据对味觉刺激的优势反应,40% 的NaCl优势、30% 的HCl优势和20% 的奎宁优势反应神经元在注射CNQX 后对至少一种味觉刺激的反应降低;盐酸优势和奎宁优势反应神经元对各自的优势反应在杏仁中央核内注药后均明显降低(P<0.01)。相关性分析表明,在注射 CNQX 后,臂旁核味觉神经元对 NaCl 和其它三种味觉刺激物之间的分辨能力降低。以上结果表明,杏仁中央核内的AMPA 受体可能参与杏仁核对臂旁核味觉神经元的下行调控。     

Diverse bitter stimuli elicit highly similar patterns of Fos-like immunoreactivity in the nucleus of the solitary tract

Previous studies have demonstrated that oral stimulation with quinine elicits Fos-like immunoreactivity in the first-order gustatory nucleus, the NST, with a different topographic distribution than sucrose or citric acid. However, it is unknown whether the quinine pattern is unique to this alkaloid or common across bitter stimuli with different chemical structures. Indeed, recent physiological experiments suggest that taste receptor cells and primary afferent neurons may exhibit selectivity for various bitter tastants. The present investigation compared the distribution of FLI in NST following stimulation with three bitter chemicals: QHCl, denatonium and propylthiouracil, stimuli that evoked Ca(2+) currents in almost entirely different sets of receptor cells. The results demonstrate that the quinine pattern is not idiosyncratic but instead generalizes to the other two tastants. Although it remains possible that intermingled but different NST neurons are activated by these stimuli, these data suggest that a specialized region in the NST is preferentially involved in processing a common aspect of bitter tastants. In contrast to citric acid, quinine, denatonium and propylthiouracil all elicited vigorous oromotor rejection responses, consistent with our earlier hypothesis that the medial third of the NST may be an afferent trigger zone for oromotor rejection.     

Central gustatory projections and side-specificity of operant antennal muscle conditioning in the honeybee

Gustatory stimuli to the antennae, especially sucrose, are important for bees and are employed in learning paradigms as unconditioned stimulus. The present study identified primary antennal gustatory projections in the bee brain and determined the impact of stimulation of the antennal tip on antennal muscle activity and its plasticity. Central projections of antennal taste hairs contained axons of two morphologies projecting into the dorsal lobe, which is also the antennal motor centre. Putative mechanosensory axons arborised in a dorso-lateral area. Putative gustatory axons projected to a ventro-medial area. Bees scan gustatory and mechanical stimuli with their antennae using variable strategies but sensory input to the motor system has not been investigated in detail. Mechanical, gustatory, and electrical stimulation of the ipsilateral antennal tip were found to evoke short-latency responses in an antennal muscle, the fast flagellum flexor. Contralateral gustatory stimulation induced smaller responses with longer latency. The activity of the fast flagellum flexor was conditioned operantly by pairing high muscle activity with ipsilateral antennal sucrose stimulation. A proboscis reward was unnecessary for learning. With contralateral antennal sucrose stimulation, conditioning was unsuccessful. Thus, muscle activity induced by gustatory stimulation was important for learning success and conditioning was side-specific.     

The influence of GABA on cells in the gustatory region of the hamster solitary nucleus

A brainstem slice preparation was used to investigate GABA-inducedresponses in the gustatory region of the nucleus of the solitarytract (NST) of the hamster. The baseline activities of 91 cellsin the rostral NST were examined extracellularly; 59 cells werelocated in the rostral central (RC), 21 in the rostral lateral(RL), six in the ventral (V) and five in the medial (M) subdivisionof the NST. Of the 80 cells in the gustatory region of the NST(RC and RL subdivisions), application of GABA produced dose-dependentinhibition in 55 (69%), excitation in 9 (11%) and no effectin 16 cells (22%). In contrast, only nine cells were responsiveto baclofen, a GABA^B agonist. In all subdivision of the rostralNST, 57 cells were inhibited by GABA and the responses of 48of these were blocked by the specific GABA^A antagonist, bicucullinemethiodide (BICM). Application of BICM alone often yielded anexcitatory burst of impulses; this effect was eliminated whensynaptic release was blocked by perfusion with a high magnesiumphysiological saline solution (PSS/Mg⁺⁺). The GABA^A-responsivecells were distributed predominantly within the RC subdivision,whereas the GABA^B-responsive neurons were mostly in the RL subdivisionof the NST. The influences of GABA on the membrane properties of cells withinthe gustatory region (RC and RL subdivisions) of the NST wererecorded using conventional intracellular (16 cells) or whole-cellpatch (17 cells) recording methods. Intracellular recordingrevealed that GABA produced hyperpolarisation of the membrane,decreased the firing frequency, and increased the membrane conductance.In the patch-clamp experiments, the application of GABA evokedboth inward and outward currents, and an increase in membraneconductance. The reversal potential produced by GABA was closeto the Cl– equilibrium potential. The effects of GABAwere blocked by BICM. These results suggest that (i) GABA hasa strong inhibitory influence on rostral NST neurons, whichin the majority of cells is mediated through GABA^A, receptors;and (ii) the gustatory region of the NST may contain a tonicallyactive GABAergic netw     

EFFECTS OF ELECTRICAL STIMULATION OF CHORDA TYMPANI ON GLOSSOPHARYNGEAL NERVE RESPONSE TO THE FOLIATE PAPILLAE STIMULATION

The foliate papillae of the rat are dually innervated by thechorda tympani and the glossopharyngeal nerves. The effectsof electrical stimulation of the distal end of the cut chordatympani on the spontaneous discharges and the gustatory responsesof the glossopharyngeal nerve fibers were examined in the ratwhile gustatory stimuli were applied to the foliate papillae.Activities of 5 out of 35 taste units in the glossopharyngealnerve were influenced by this procedure. Three units showedan inhibitory effect, 1 unit showed an excitatory effect and1 unit changed its firing pattern. These facts may be derivedfrom alterations of the blood circulation in the vicinity ofthe taste receptor cells innervated by the glossopharyngealnerve fibers.     

Gustatory neural responses to umami taste stimuli in C57BL/6ByJ and 129P3/J mice

In long-term two-bottle tests, mice from the C57BL/6ByJ (B6) strain drink more monosodium L-glutamate (MSG) and inosine-5'-monophosphate (IMP) compared with mice from the 129P3/J (129) strain. The goal of this study was to assess the role of afferent gustatory input in these strain differences. We measured integrated responses of the mouse chorda tympani and glossopharyngeal nerves to lingual application of compounds that evoke umami taste in humans: MSG, monoammonium L-glutamate (NH(4) glutamate), IMP and guanosine-5'-monophosphate (GMP) and also to other taste stimuli. Chorda tympani responses to MSG and NH(4) glutamate were similar in B6 and 129 mice. Chorda tympani responses to IMP and GMP were lower in B6 than in 129 mice. Responses to umami stimuli in the glossopharyngeal nerve did not differ between the B6 and 129 strains. Responses to MSG, IMP and GMP were not affected by sodium present in these compounds because B6 and 129 mice had similar neural taste responses to NaCl. This study has demonstrated that the increased ingestive responses to the umami stimuli in B6 mice are accompanied by either unchanged or decreased neural responses to these stimuli. Lack of support for the role of the chorda tympani or glossopharyngeal nerves in the enhanced consumption of MSG and IMP by B6 mice suggests that it is due to some other factors. Although results of our previous study suggest that postingestive effects of MSG can affect its intake, contribution of other gustatory components (e.g. greater superficial petrosal nerve or central gustatory processing) to the strain differences in consumption of umami compounds also cannot be excluded. Strain differences in gustatory neural responses to nucleotides but not glutamate suggest that these compounds may activate distinct taste transduction mechanisms.     

Local spiking interneurons controlling the equilibrium response in the crayfish Procambarus clarkii

1. In the crayfish brain, the responses of local spiking interneurons to body roll simulated by bending of statocyst hairs, were investigated with intracellular recording and staining techniques. The neurons had two separate branching portions in the protocerebrum and the deutocerebrum. They were named as type-I local neurons and further classified into 5 types (ac-U, vplc-U, vplc-B, vupc-U, vupc-B). 2. Vupc-U neurons showed excitatory responses and vplc-U neurons showed inhibitory responses to inward hair deflection of the statocyst ipsilateral to their deutocerebral branches. The other 3 types were of mixed populations of the interneurons showing either excitatory or inhibitory responses to the stimulation. 3. Of 10 type-I local neurons showing excitatory responses to inward hair deflection, 6 interneurons had output effects on oculomotor and/or descending neurons. All these 6 interneurons showed large EPSPs and much higher frequency of spikes to the hair stimulation than those of the other 4. All 8 type-I local neurons that showed inhibitory responses had no output effects. 4. Type-I local neurons controlled two equilibrium responses, compensatory eye movement and righting reflex, either simultaneously or independently.     

Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem

Consummatory responses to taste stimuli are modulated by visceral signals processed in the caudal nucleus of the solitary tract (cNST) and ventrolateral medulla. On the basis of decerebrate preparations, this modulation can occur through local brain stem pathways. Among the large number of neuropeptides and neuromodulators implicated in these visceral pathways is neuropeptide Y (NPY), which is oftentimes colocalized in catecholaminergic neurons themselves implicated in glucoprivic-induced feeding and satiety. In addition to the cNST and ventrolateral medulla, noradrenergic and NPY receptors are found in circumscribed regions of the medullary reticular formation rich in preoromotor neurons. To test the hypothesis that NPY may act as a neuromodulator on preoromotor neurons, we recorded the effects of bath application of NPY and specific Y1 and Y2 agonists on currents elicited from electrical stimulation of the rostral (taste) NST in prehypoglossal neurons in a brain stem slice preparation. A high proportion of NST-driven responses were suppressed by NPY, as well as Y1 and Y2 agonists. On the basis of paired pulse ratios and changes in membrane resistance, we concluded that Y1 receptors influence these neurons both presynaptically and postsynaptically and that Y2 receptors have a presynaptic locus. To test the hypothesis that NPY may act in concert with norepinephrine (NE), we examined neurons showing suppressed responses in the presence of a Y2 agonist and demonstrated a greater degree of suppression to a Y2 agonist/NE cocktail. These suppressive effects on preoromotoneurons may reflect a satiety pathway originating from A2 neurons in the caudal brain stem.     

Depression of gustatory receptor potential in frog taste cell by parasympathetic nerve-induced slow hyperpolarizing potential

Parasympathetic nerve (PSN) innervates taste cells of the frog taste disk, and electrical stimulation of PSN elicited a slow hyperpolarizing potential (HP) in taste cells. Here we report that gustatory receptor potentials in frog taste cells are depressed by PSN-induced slow HPs. When PSN was stimulated at 30 Hz during generation of taste cell responses, the large amplitude of depolarizing receptor potential for 1 M NaCl and 1 mM acetic acid was depressed by approximately 40% by slow HPs, but the small amplitude of the depolarizing receptor potential for 10 mM quinine-HCl (Q-HCl) and 1 M sucrose was completely depressed by slow HPs and furthermore changed to the hyperpolarizing direction. The duration of the depolarizing receptor potentials depressed by slow HPs prolonged with increasing period of PSN stimulation. As tastant-induced depolarizing receptor potentials were increased, the amplitude of PSN-induced slow HPs inhibiting the receptor potentials gradually decreased. The mean reversal potentials of the slow HPs were approximately -1 mV under NaCl and acetic acid stimulations, but approximately -14 mV under Q-HCl and sucrose stimulations. This implies that when a slow HP was evoked on the same amplitude of depolarizing receptor potentials, the depression of the NaCl and acetic acid responses in taste cells was larger than that of Q-HCl and sucrose responses. It is concluded that slow HP-induced depression of gustatory depolarizing receptor potentials derives from the interaction between gustatory receptor current and slow hyperpolarizing current in frog taste cells and that the interaction is stronger for NaCl and acetic acid stimulations than for Q-HCl and sucrose stimulations.     

Genetic tracing of the gustatory neural pathway originating from Pkd1l3-expressing type III taste cells in circumvallate and foliate papillae

Polycystic kidney disease 1-like 3 (Pkd1l3) is expressed specifically in sour-sensing type III taste cells that have synaptic contacts with afferent nerve fibers in circumvallate (CvP) and foliate papillae (FoP) located in the posterior region of the tongue, although not in fungiform papillae (FuP) or the palate. To visualize the gustatory neural pathways that originate from type III taste cells in CvP and FoP, we established transgenic mouse lines that express the transneuronal tracer wheat germ agglutinin (WGA) under the control of the mouse Pkd1l3 gene promoter/enhancer. The WGA transgene was accurately expressed in Pkd1l3-expressing type III taste cells in CvP and FoP. Punctate WGA protein signals appeared to be detected specifically in type III taste cells but not in other types of taste cells. WGA protein was transferred primarily to a subset of neurons located in close proximity to the glossopharyngeal (GL) nerve bundles in the nodose/petrosal ganglion (NPG). WGA signals were also observed in a small population of neurons in the geniculate ganglion (GG). This result demonstrates the anatomical connection between taste receptor cells (TRCs) in the FoP and the chorda tympani (CT) nerves. WGA protein was further conveyed to neurons in a rostro-central subdivision of the nucleus of the solitary tract (NST). These findings demonstrate that the approximately 10?kb 5'-flanking region of the mouse Pkd1l3 gene functions as a type III taste cell-specific promoter/enhancer. In addition, experiments using the pkd1l3-WGA transgenic mice reveal a sour gustatory pathway that originates from TRCs in the posterior region of the tongue.