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A C Spector

Publications and source records attributed to A C Spector.

At least 37 records · Page 2Linked to original sources

Amiloride disrupts NaCl versus KCl discrimination performance: implications for salt taste coding in rats.

Amiloride, an epithelial sodium channel blocker, suppresses the responsiveness of narrowly tuned sodium-responsive taste afferents when orally applied in the rat. Broadly tuned salt-responsive taste afferents, which respond to sodium and nonsodium salts and acids, are relatively unaffected by the drug. We used amiloride treatment to examine the consequences of the specific removal of input from narrowly tuned sodium-responsive afferents on taste discrimination. Five water-restricted rats were trained in a gustometer to press one lever after licking NaCl and another lever after licking KCl across a range of concentrations (0.05, 0.1, and 0.2 M). Correct responses were rewarded with brief water access, and incorrect responses were punished with a time-out. After training, animals averaged about 90% correct responses and maintained competent performance during subsequent control sessions. Amiloride was then placed in all solutions at a given concentration (1-100 microM) for single test sessions. Control sessions were interposed between amiloride sessions. At high amiloride concentrations, overall responding was reduced to 50% correct and progressively improved as the drug concentration was lowered. The sigmoidal dose-response functions corresponded quantitatively with electrophysiological findings. Performance deficits occurred primarily with NaCl and were concentration dependent; performance during KCl trials was relatively undisturbed by amiloride adulteration. At high amiloride concentrations, rats treated NaCl as if it were KCl. Given that amiloride is tasteless to the rat, these results provide convincing evidence of the importance of narrowly tuned afferents in the discrimination between sodium and nonsodium salts and suggest that this is a general coding principle in the gustatory system.

Amiloride↗

Combined glossopharyngeal and chorda tympani nerve transection elevates quinine detection thresholds in rats (Rattus norvegicus).

Using a conditioned shock avoidance procedure, behavioral quinine hydrochloride thresholds were measured before and after glossopharyngeal (GLX), chorda tympani (CTX), or combined glossopharyngeal and chorda tympani (GLX + CTX) transection, as well as after sham surgery. In Experiment 1, thresholds in the sham, CTX, and GLX rats (Rattus norvegicus) either improved (lowered) or remained the same after surgery. In Experiment 2, GLX + CTX caused a pronounced 1.5 log10 unit increase in presurgically measured thresholds. Neither the glossopharyngeal nor the chorda tympani nerve is necessary for normal sensitivity to low quinine concentrations provided the other is intact. When both of these nerve are transected, however, the remaining afferent input is not sufficient to maintain normal detection performance.

Animals↗

The consequences of gustatory nerve transection on taste-guided licking of sucrose and maltose in the rat.

Lick responses to sucrose and maltose (0.01-1.0 M) were measured in nondeprived rats during brief-access taste trials before and after histologically confirmed gustatory neurotomy. Pronounced decreases in sugar responsiveness occurred after combined section of the chorda tympani (CT) and greater superficial petrosal nerves. The additional section of the glossopharyngeal nerve (GL) flattened the sucrose concentration-response function. Extirpation of the sublingual and submaxillary salivary glands also attenuated sugar responsiveness. Section of the CT or GL alone or in combination caused less severe or no decreases in sugar licking. There were signs of licking impairments after some of these neurotomies, but the data suggest that changes in sugar responsiveness were not solely motor in origin. Thus the 7th nerve is necessary and most likely sufficient for the maintenance of normal unconditioned appetitive responsiveness to sucrose and maltose.

Animals↗

Gustatory parabrachial lesions disrupt taste-guided quinine responsiveness in rats.

This study examined the effects of electrophysiologically placed electrolytic lesions in the gustatory zone of the parabrachial nuclei (PBN) on the rat's taste-guided unconditioned licking of quinine hydrochloride during repeated 10-s trials. Concentration-response functions measured in water-deprived rats before and after surgery significantly shifted to the right as a result of the bilaterally placed lesions. These same rats were tested on their ability to acquire a lithium chloride (LiCl)-based conditioned taste aversion (CTA) to 0.1 M sucrose. Although the largest lesions severely affected performance in both tasks, there was only a modest correlation (r = -.447) between the extent of the lesion-induced shift in the quinine concentration-response curves and the degree of sucrose intake suppression after the first CTA conditioning trial. Thus, PBN lesions can disrupt performance on both tasks, but it appears that the neural processes governing unconditioned responsiveness to quinine may be to some extent dissociable from those subserving acquisition of a sucrose LiCl-based CTA.

Animals↗

Salt discriminability is related to number of regenerated taste buds after chorda tympani nerve section in rats.

Transection of the chorda tympani nerve (CTX) impairs taste-guided discrimination of NaCl from KCl in rats. We wanted to determine whether this discrimination recovers after chorda tympani regeneration. Experiment 1 showed that few taste buds regenerated 14 days after CTX, whereas substantial regeneration occurred 42 days after surgery. Experiment 2 demonstrated that rats trained before CTX could clearly discriminate the two salts when tested starting 49 days after surgery, whereas rats tested starting 8 days after surgery were severely impaired in this task. Rats tested starting 28 days after CTX were unimpaired, moderately impaired, or severely impaired on the discrimination task. Overall, discrimination performance was significantly related to the number of regenerated taste buds. Unilaterally transected rats tested shortly after surgery were nearly as competent as controls. These results indicate that rats can recover the ability to discriminate NaCl from KCl after regeneration of anterior tongue taste buds.

Animals↗

Glossopharyngeal nerve transection does not compromise the specificity of taste-guided sodium appetite in rats.

The chorda tympani nerve (CT) has been shown to be critical in the sodium-specific drinking behavior of sodium-depleted rats, but the role of other gustatory nerves and the contribution of the major salivary glands remain to be elucidated. In this study, rats received either bilateral section of the CT (CTX) or the glossopharyngeal nerve (GLX), extirpation of the sublingual and submaxillary salivary glands (DSAL), or sham surgery. After recovery, rats were sodium depleted with furosemide and tested for their licking responses to 0.05 and 0.3 M NaCl, KCl, CaCl2, and NH4Cl, as well as distilled water in an automated gustometer. Rats that received GLX maintained a specific sodium appetite comparable to controls despite denervation of approximately 64% of the taste buds. In contrast, compared with control rats, CTX and DSAL rats had altered response profiles, showing much smaller differences in licking to NaCl relative to the other stimuli. This was accompanied by a substantially lower lick rate in DSAL rats, raising the possibility that general licking impairments contributed to the decreased NaCl responsiveness in these rats. These findings imply that the CT, but not the glossopharyngeal nerve, is necessary for the maintenance of normal sodium-specific, taste-guided behavior under sodium deplete conditions.

Animals↗

Sodium specificity of salt appetite in Fischer-344 and Wistar rats is impaired by chorda tympani nerve transection.

Unlike other rat strains, the sodium-replete Fischer-344 (F344) strain shows no innate preference for NaCl and displays more aversive and fewer ingestive oral motor responses to orally infused NaCl when tested in sodium balance. Despite these differences, F344 rats show an increase in preference for NaCl in response to sodium depletion. The present study was designed to determine whether the salt appetite of sodium-depleted F344 rats is cation specific and whether such selectivity is mediated in part by an intact chorda tympani nerve. Sodium-depleted (10 mg furosemide) F344 (n = 13) and Wistar (n = 16) rats were permitted repeated access to nine stimuli (water, and 0.05 and 0.3 M NaCl, KCl, NH4Cl, and CaCl2), presented randomly in 10-s trials. One-half of the rats had their chorda tympani nerve sectioned (CTX). Under conditions of sodium depletion, both strains discriminated NaCl from other chloride salts. CTX significantly impaired the selectivity of the licking behavior in both strains, suggesting that sodium-specific licking is partially mediated by anterior tongue taste receptors. These findings suggest that both sodium-depleted F344 and Wistar rats are comparable in their abilities to recognize NaCl, to distinguish it from other salts, and to respond selectively to it, despite the fact that sodium-replete F344 and Wistar rats differ greatly in their NaCl preference.

Animals↗

Gustatory detection thresholds after parabrachial nuclei lesions in rats.

Rats with either electrolytic (Experiment 1) or excitotoxic lesions (Experiment 2) that had been electrophysiologically centered in the gustatory zone of the parabrachial nuclei (PBN) were tested for sucrose and NaCl taste detection thresholds in a conditioned avoidance task. With 1 exception, all of these rats had previously shown severe deficits in acquiring an LiCl-based conditioned taste aversion (CTA) to sucrose, NaCl, or alanine. The rats with excitotoxic lesions also had failed to express a depletion-induced sodium appetite. Despite the uniformity of these deficits, the rats with lesions exhibited varied performance in the detectability task. Roughly 1/3 of the rats did not perform competently, 1/3 had elevated thresholds, and 1/3 showed no or only marginal impairments in taste detectability. These findings demonstrate that the elimination of CTA following PBN lesions is not necessarily linked to an impairment in taste signal detection. Thus, PBN-induced deficits on 1 taste-related task do not entirely correspond with impairments on another.

Animals↗

Excitotoxic lesions of the parabrachial nuclei prevent conditioned taste aversions and sodium appetite in rats.

Electrolytic lesions of the parabrachial nuclei (PBN) disrupt conditioned taste aversion (CTA) in the rat, but it is not known whether this effect is due to damaging axons of passage or to destruction of intrinsic neurons. We tested 10 rats with electrophysiologically guided, ibotenic acid lesions of the PBN (PBNx) to determine whether they could acquire a LiCl-induced CTA to l-alanine (0.3 M) or demonstrate a sodium appetite following furosemide treatment and overnight access to sodium deficient chow. Vehicle-treated and nonsurgical controls were included in the design. PBNx rats failed to develop a CTA, even after 3 conditioning trials. Moreover, more than 8 months later, a subset of the PBNx rats were again unable to learn a CTA using NaCl as the conditional stimulus (CS). After the furosemide treatment, the control rats drank an average of 20.3 ml of strong salt in 24 hr. The PBNx rats drank virtually no NaCl during the first 2 hr and averaged only 4.0 ml in 24 hr. In the PBN, damage to neuronal somata is more critical than interrupting fibers of passage for producing deficits in taste-guided behaviors.

Afferent Pathways↗

Reversal of dexfenfluramine-induced anorexia and c-Fos/c-Jun expression by lesion in the lateral parabrachial nucleus.

The external subdivision of the lateral parabrachial nucleus (LPBE) shows strong Fos-like immunoreactivity (FLI) following anorectic doses of the indirect serotonin agonist dexfenfluramine (DFEN). In an effort to determine the contribution of the LPBE to DFEN-induced anorexia, bilateral ibotenate lesions were made in the LPBE, and the effects of the lesion on DFEN-induced anorexia and FLI as well as c-Jun-like immunoreactivity (JLI) were examined. It was found that LPBE lesion significantly attenuated DFEN anorexia: in a 1-h food intake test following 24-h food deprivation, DFEN (2 mg/kg) suppressed food intake by 60% in intact rats but only 34% in rats with LPBE lesions. In addition to this behavioral change, LPBE lesion completely abolished DFEN-induced FLI and JLI in the lateral subdivision of the central nucleus of the amygdala (CeL) and laterodorsal subdivision of the bed nucleus of stria terminalis (BSTLD), both of which showed strong FLI and JLI in intact rats. DFEN-induced FLI and JLI in other brain regions were not affected by LPBE lesion, including the ventromedial and lateral hypothalamus, caudate-putamen, and the nucleus of the solitary tract (NST). The parallel loss of DFEN-induced anorexia and FLI/JLI following LPBE lesion raises the novel possibility that LPBE-CeL/BSTLD pathway may be involved in DFEN anorexia.

Animals↗

Combined, but not single, gustatory nerve transection substantially alters taste-guided licking behavior to quinine in rats.

On the basis of electrophysiological studies, the glossopharyngeal nerve (GL) is far more responsive to quinine than the chorda tympani (CT) or greater superficial petrosal (GSP) nerves. The licking behavior of water-deprived rats to quinine (0.03-3.0 mM) and distilled water (10-s trails) was tested before and after various nerve transections. GL+CT section caused a substantial reduction in responsiveness. GSP+CT section had a moderate effect, and GL section alone produced only marginal impairments. Control, partially desalivated, and CT-sectioned rats were unaffected. Thus, the GL is not necessary for normal unconditioned taste-guided appetitive responsiveness to quinine, but the collective input from the GSP and CT is necessary and most likely sufficient. These data suggest that the quinine-evoked input of the GL and CT converge centrally.

Animals↗

Lesions of the pontine parabrachial nuclei eliminate successive negative contrast effects in rats.

Rats shifted from a high to a low concentration of sucrose make fewer licks for the low concentration than rats that experience only the low concentration of sucrose. This phenomenon, referred to as successive negative contrast, is eliminated after bilateral electrolytic lesions of the amygdala. Because the amygdala receives direct projections from the gustatory zone of the parabrachial nuclei of the pons (PBN), this experiment was designed to examine this phenomenon in rats with electrophysiologically guided bilateral electrolytic lesions of the PBN. The results of this experiment showed that lesions of the PBN fully prevent contrast in rats shifted from the high to the low concentration of sucrose. Thus, an intact PBN is essential for the occurrence of successive negative contrast effects in rats.

Amygdala↗

Concentration-dependent licking of sucrose and sodium chloride in rats with parabrachial gustatory lesions.

The medial zone of parabrachial nuclei (PBN) serves as an obligatory synapse in the central gustatory system in rodents. Lesions in the PBN impair taste aversion learning and depletion-induced sodium appetite in rats, and also alter the ingestion of sapid stimuli. Interpretation of these lesion-induced behavioral deficits requires an evaluation of whether taste function is compromised. The present study examined whether rats with PBN lesions could show normal concentration-dependent changes in licking behavior to very small volumes of NaCl and sucrose. Physiological state was also varied; taste responsivity was examined in water-deprived and nondeprived rats. In a specially designed gustometer, nine rats with electrophysiologically guided lesions in the PBN and five surgical controls were trained to lick a drinking spout to receive 10-s access to various concentrations of NaCl (0.03-1.0 M) and sucrose (0.01-1.0 M) during 30-min sessions. Water-deprived control rats progressively decreased their responses compared with water as the concentration of NaCl was raised. In contrast, water-deprived PBNX rats did not decrease their licking responses to NaCl relative to water until the concentration reached 1.0 M. In the nondeprived state, control and PBNX rats decreased their responsiveness as a function of NaCl concentration, and the two groups did not differ. The licking responses of water-deprived PBNX rats did not differ from control rats when sucrose was the stimulus. In the nondeprived condition, both groups monotonically increased their licking to sucrose as a function of concentration, but PBNX rats were significantly less responsive than controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Microstructural analysis of successive negative contrast in free-feeding and deprived rats.

Rats shifted from 1.0 M to 0.1 M sucrose lick at lower rates for the weaker solution than rats that have continual access to the 0.1 M sucrose solution only. This effect, referred to as successive negative contrast, has been investigated primarily in food-deprived rats and, in all cases, using total licks or total volume consumed as the dependent measure. The present experiment used a microstructural analysis of licking patterns to examine the changes in behavior that constitute the contrast effect in total licks in both deprived and free-feeding rats. Although the magnitude of the effect was similar, deprived rats recovered from contrast more rapidly than free-feeding rats. Furthermore, the patterns of licking behavior associated with contrast differed under the two deprivation conditions. Specifically, when compared with the unshifted controls, the contrast effect in deprived rats was accomplished through a decrease in the number of licks per burst, an increase in the number of bursts initiated, a brief increase in the length of the interburst intervals, and no change in length of the interlick intervals. In free-feeding animals, contrast was associated with a decrease in the number of licks per burst, a brief increase in the length of the interburst interval, and no changes in either the number of bursts initiated or in the length of the interlick intervals. Together, these data demonstrate that patterns of licking behavior are differentially affected by solution concentration, deprivation state, and relative aspects of reward value.

Animals↗

Taste receptors on the anterior tongue and nasoincisor ducts of rats contribute synergistically to behavioral responses to sucrose.

In four groups of rats, behavioral responsiveness to sucrose was tested by allowing them to lick solutions in a computer-controlled gustometer (10-s trials; 0.01-1.0 M). Rats with cautery lesions of the nasoincisor ducts (NID) behaved no differently from controls. After bilateral chorda tympani nerve (CT) section, which removes taste input from the anterior tongue (AT), rats demonstrated a marginal attenuation in their responsiveness to sucrose. Combining the two lesions, however, had the greatest effect on the concentration-response curve. By shifting the curve to the right and lowering the asymptotic licking rate, the combined lesion reduced the area under the curve by one third. The effects of the combined treatments were larger than would be predicted from the sum of either one alone. This presumably reflects the central convergence of primary afferent axons from the NID and AT. Neurophysiological data have demonstrated such convergence within the nucleus of the solitary tract.

Afferent Pathways↗

Lick rate analysis of sodium taste-state combinations.

The combined effects of taste and physiological state on lick rate for NaCl were systematically evaluated in two experiments. In experiment 1 the lick rates of six groups of rats (Sprague-Dawley) were recorded during the first 3 min of a NaCl drinking bout, where each group received a different concentration. Half of the rats were depleted by injections of the diuretic-natriuretic furosemide (10 mg ip), whereas the other half were not. The inverted U-shaped concentration-response functions for sodium-replete rats peaked approximately at isotonicity. The replete lick rate function was uniformly elevated for rats examined in the sodium-depleted state. In experiment 2 each rat received access to all six solutions within a 40-min test session. Rats were tested twice, once in positive and once in negative sodium balance. The solutions were repeatedly presented in counterbalanced order in a series of 10-s exposures. The replete and deplete functions of the within-group study closely resembled those of the between-group study. When the deplete rats' function was divided into three segments coinciding with the beginning, middle, and end of the 40-min session, the functions were shifted down vertically but retained their shape. In general, sodium-state level dramatically affected the absolute lick rates but did not appear to shift the location of the concentration-response function along the horizontal (i.e., concentration) axis. The form of the function appears to have been determined by oral factors alone.

Analysis of Variance↗

Chorda tympani section decreases the cation specificity of depletion-induced sodium appetite in rats.

Rats depleted of sodium by diuretic treatment were tested for their ability to respond selectively to NaCl after chorda tympani nerve (CTn) section (CTX). A variety of chloride salts (NaCl, KCl, NH4Cl, CaCl2) at two concentrations (0.05 and 0.3 M) were presented semirandomly to sodium-deplete rats in repeated single-stimulus trials (10 s). The responses of sodium-depleted surgical control rats (n = 8) were highly cation specific. These rats licked substantially more for both sodium stimuli than for any other chloride salt. On the other hand, the licking responses of CTX sodium-depleted rats (n = 8) were less cation selective. These rats licked NaCl and 0.05 M KCl at comparable rates. For both NaCl concentrations, CTX rats had significantly lower lick rates than controls. In addition, the difference between the lick rate for NaCl and that for the other salts was much greater for control rats than for CTX rats. Although CTn section did not entirely eliminate the high levels of responsivity to NaCl observed in the intact sodium-depleted rat, it did substantially compromise the selectivity of the behavior, which suggests that the input of the CTn is critical for taste-guided sodium specific behaviors.

Animals↗