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R J Contreras

Publications and source records attributed to R J Contreras.

At least 19 recordsLinked to original sources

Altered NaCl taste responses precede increased NaCl ingestion during Na(+) deprivation.

It has been suggested that Na(+) deficiency alters the sensitivity of taste receptors, thereby rendering NaCl solutions more palatable or preferred and more likely to be ingested. Increased ingestion of concentrated NaCl solutions by rats during dietary Na(+) deprivation occurs only after approximately 8-10 days. To determine whether changes in gustatory responses mediate the deprivation-induced NaCl ingestion (salt appetite), we evaluated taste responses to a range of NaCl concentrations before, during, and after dietary Na(+) deprivation. Rats were trained to lick rapidly in short-duration (10 s) tests by mixing NaCl solutions in a dilute sucrose solution. This method elicited consistent, interpretable rates of licking, even of normally avoided NaCl concentrations, without the necessity of depriving the rats of water. The licking rate increased after dietary Na(+) deprivation of only 2 days, increased further after 5 days of Na(+) deprivation and, after 10 days, was not different from that after 2 days. These results suggest that a change in the response to NaCl taste, as evidenced by increased rates of licking during short-access tests, occurred after 2 days of dietary Na(+) deprivation. In contrast, a significant increase in the 24-h ingestion of a concentrated NaCl solution occurred only after approximately 1 week of maintenance on Na(+)-deficient chow. Thus, it is unlikely that a delayed change in the response to NaCl taste to more palatable or preferred underlies the delayed increase in 24-h NaCl intake during dietary Na(+) deprivation.

Animals↗

Gustatory neuron types in rat geniculate ganglion.

We used extracellular single-cell recording procedures to characterize the chemical and thermal sensitivity of the rat geniculate ganglion to lingual stimulation, and to examine the effects of specific ion transport antagonists on salt transduction mechanisms. Hierarchical cluster analysis of the responses from 73 single neurons to 3 salts (0.075 and 0.3 M NaCl, KCl, and NH(4) Cl), 0.5 M sucrose, 0.01 M HCl, and 0.02 M quinine HCl (QHCl) indicated 3 main groups that responded best to either sucrose, HCl, or NaCl. Eight narrowly tuned neurons were deemed sucrose-specialists and 33 broadly tuned neurons as HCl-generalists. The NaCl group contained three identifiable subclusters: 18 NaCl-specialists, 11 NaCl-generalists, and 3 QHCl-generalists. Sucrose- and NaCl-specialists responded specifically to sucrose and NaCl, respectively. All generalist neurons responded to salt, acid, and alkaloid stimuli to varying degree and order depending on neuron type. Response order was NaCl > HCl = QHCl > sucrose in NaCl-generalists, HCl > NaCl > QHCl > sucrose in HCl-generalists, and QHCl = NaCl = HCl > sucrose in QHCl-generalists. NaCl-specialists responded robustly to low and high NaCl concentrations, but weakly, if at all, to high KCl and NH(4) Cl concentrations after prolonged stimulation. HCl-generalist neurons responded to all three salts, but at twice the rate to NH(4) Cl than to NaCl and KCl. NaCl- and QHCl-generalists responded equally to the three salts. Amiloride and 5-(N,N-dimethyl)-amiloride (DMA), antagonists of Na(+) channels and Na(+)/H(+) exchangers, respectively, inhibited the responses to 0.075 M NaCl only in NaCl-specialist neurons. The K(+) channel antagonist, 4-aminopyridine (4-AP), was without a suppressive effect on salt responses, but, when applied alone in solution, it evoked a response in many HCl-generalists and one QHCl-generalist neuron so tested. Of the 39 neurons tested for their sensitivity to temperature, 23 responded to cooling and chemical stimulation, and 20 of these neurons were HCl-generalists. Moreover, the responses to the four standard stimuli were reduced progressively at lower temperatures in HCl- and QHCl-generalist neurons, but not in NaCl-specialists. Thus sodium channels and Na(+)/H(+) exchangers appear to be expressed exclusively on the membranes of receptor cells that synapse with NaCl-specialist neurons. In addition, cooling sensitivity and taste-temperature interactions appear to be prominent features of broadly tuned neuron groups, particularly HCl-generalists. Taken all together, it appears that lingual taste cells make specific connections with afferent fibers that allow gustatory stimuli to be parceled into different input pathways. In general, these neurons are organized physiologically into specialist and generalist types. The sucrose- and NaCl-specialists alone can provide sufficient information to distinguish sucrose and NaCl from other stimuli, respectively.

Animals↗

Responses of single lingual nerve fibers to thermal and chemical stimulation.

The goals of this study were to characterize the responses of: (1) thermally-sensitive fibers of the lingual branch of the trigeminal nerve to cooling from 35 degrees to 10 degrees C at a rate of 1 degrees C/s; and (2) these neurons to a mid-range concentration of NaCl (150 mM), glucose (150 mM), citric acid (0.3 mM), and quinine-HCl (3 mM) at 35 degrees and 25 degrees C. A cluster analysis of 47 neurons' responses to cooling revealed two major groups and one minor group. Group 1 neurons (n=19) had a shorter latency, exhibited faster time-to-peak activity, and responded over a smaller range of temperature compared to Group 2 neurons (n=22). Group 3 neurons (n=6) exhibited the longest response latency and responded over a wider cooler range of temperature. Twenty-five out of thirty-one thermally-sensitive, non-tactile lingual neurons responded weakly to at least one chemical stimulus, with some neurons responding to 2, 3, or all 4 chemical stimuli. Group 1 neurons responded to more chemical stimuli at 35 degrees C, while Group 2 neurons responded more at 25 degrees C. Under their optimal temperature conditions, Group 1 and Group 2 neurons responded most often to citric acid and least often to glucose, with NaCl and Q-HCl eliciting an intermediate number of responses. As a whole, the responses of thermally-sensitive fibers to chemical stimulation were modest at best with an absence of chemical specificity. There was no evidence of a 'best' stimulus, although there was a suggestion of temporal coding.

Action Potentials↗

Temperature and amiloride alter taste nerve responses to Na+, K+, and NH+4 salts in rats.

The effects of adaptation/stimulus temperature (25 degrees C vs. 35 degrees C) on taste nerve responses to salt stimulation and amiloride suppression were assessed in rats. We measured the integrated responses of the chorda tympani nerve to 500 mM concentrations of NaCl, Na2SO4, sodium acetate (NaAc), KCl, K2SO4, potassium acetate (KAc), NH4Cl, (NH4)2SO4, and ammonium acetate (NH4Ac) mixed with or without 100 microM amiloride hydrochloride at 35 degrees C. Taste nerve responses to all Na+ and NH4+ salts, but not K/ salts, were significantly smaller at 25 degrees C than at 35 degrees C. Amiloride significantly suppressed taste nerve responses to all salts (Na+ salts > K+ salts > NH4+ salts); amiloride suppression of Na+ and NH4+ salts was significantly greater at 25 degrees C than at 35 degrees C. Benzamil-HCl, a more potent Na+ channel blocker compared to amiloride, strongly suppressed taste nerve responses to NaCl and KCl, but not to NH4Cl. Amiloride and benzamil suppression of NaCl responses were similar; however, amiloride suppressed KCl responses more than did benzamil. The results suggest that: (1) amiloride-sensitive Na+ channels are involved to varying degrees in the transduction of sodium and potassium salt taste, and (2) amiloride may inhibit membrane proteins other than passive Na+ channels during stimulation with potassium and ammonium salts.

Acetates↗

Role for epithelial Na+ channels and putative Na+/H+ exchangers in salt taste transduction in rats.

The effects of the epithelial Na+ channel antagonists amiloride and benzamil and the Na+/H+ exchange antagonist 5-(N,N-dimethyl)-amiloride (DMA)-Cl on the integrated responses of the chorda tympani nerve to 30, 75, 150, 300, and 500 mM concentrations of NaCl, KCl, and NH4Cl were assessed in male Sprague-Dawley rats. Based on evidence from other systems, 1 and 25 microM amiloride and benzamil were chosen to selectively inhibit epithelial Na+ channels and 1 microM DMA was chosen to selectively inhibit Na+/H+ exchange. When added to stimulating salt solutions, amiloride, benzamil, and DMA were each effective in inhibiting responses to all three salts. The degree of inhibition varied with drug, salt, and salt concentration, but not drug dose. Amiloride suppressed NaCl responses to a greater degree than KCl and NH4Cl responses, whereas DMA suppressed NH4Cl responses to a greater degree than NaCl and KCl responses. In all but one case (25 microM amiloride added to KCl), drug suppression of taste nerve responses decreased with an increase in salt concentration. The present results suggest that 1) epithelial Na+ channels in rat taste receptor cells may play a role in KCl and NH4Cl taste transduction; 2) a Na+/H+ exchange protein may be present in taste receptor cells, representing a putative component, in addition to epithelial Na+ channels, in salt taste transduction; and 3) salt taste detection and transduction may depend on the utilization of a combination of common and distinct transcellular pathways.

Amiloride↗

Amiloride inhibits taste nerve responses to NaCl and KCl in Sprague-Dawley and Fischer 344 rats.

In a two-bottle test, Sprague-Dawley rats preferentially consume a greater amount of hypotonic and isotonic NaCl solutions relative to water, whereas inbred Fischer 344 (F344) rats fail to prefer NaCl solutions at any concentration relative to water. To determine whether taste contributes to this strain difference, we measured the integrated neural responses of the chorda tympani nerve to a concentration range of NaCl and KCl solutions. The amiloride-sensitive component of the taste nerve response was assessed by adding amiloride during salt stimulation in Experiment 1, and by pretreating the taste receptors with amiloride prior to salt stimulation in Experiment 2. Adding amiloride to NaCl during sustained neural activity suppressed chorda tympani nerve responses more than pretreating the tongue with amiloride. Adding amiloride during salt stimulation also partially suppressed chorda tympani neuron responses to KCl, a presumed control stimulus. The neural responses of the chorda tympani nerve to NaCl and KCl were similar for salt-avoiding F344 and salt-preferring Sprague-Dawley rats. However, amiloride pretreatment suppressed the taste nerve responses to NaCl significantly less in F344 rats than in Sprague-Dawley rats. The strain difference in the amiloride-sensitive component of the taste response may contribute to the difference in NaCl preference.

Amiloride↗

Tongue adaptation temperature influences lingual nerve responses to thermal and menthol stimulation.

Menthol, a tangible substance present in many orally administered products, can produce a powerful influence on the perceived intensity of subsequent thermal stimulation in humans as well as the response magnitudes of thermally sensitive neurons in rats. However, there are no prior studies examining the influence of adaptation temperature on perceived intensity and/or response magnitudes of thermally sensitive neurons to subsequent menthol stimulation. We identified 32 thermally sensitive neurons that increased their discharge rate to a gradual temperature decrement beginning from 35 degrees C and dropping to 10 degrees C at 1 degree C/s. Based on their response threshold, time-to-peak, and range of sensitivity, these thermally sensitive lingual neurons were found to be divisible into two distinct groups. Group 1 neurons (n = 21) responded best to the upper cool range (34-15 degrees C) of the temperature decrement, whereas Group 2 neurons (n = 11) responded to the lower cold range (32-10 degrees C) of the temperature decrement. Our Group 1 and Group 2 neurons may be analogous to low threshold and high threshold cold receptors identified previously in primates. We also examined the responses of lingual neurons to 0%, 25%, 50% and 75% dilution's of a stock menthol concentration (1.28 mM) at 25 and 35 degrees C adaptation temperatures. Menthol responses across all concentrations were far larger after adaptation to 35 degrees C compared to 25 degrees C. Furthermore, only during 35 degrees C adaptation did responses to menthol stimulation persist during the ensuing 20 s after menthol off-set and water on-set.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Sodium intake linked to amiloride-sensitive gustatory transduction in C57BL/6J and 129/J mice.

Mice of 129/J and C57BL/6J inbred strains received two-bottle, 48-h preference tests of NaCl solutions vs. distilled water. 129/J mice exhibited a greater preference for 0.08 M NaCl than did C57BL/6J mice. To determine if this strain difference was mediated by taste, the integrated neural responses of the chorda tympani nerve to a concentration range of NaCl and KCl were examined. Gustatory neural responses to NaCl were similar for 129/J and C57BL/6J mice. However, lingual application of 0.5 mM amiloride hydrochloride significantly suppressed chorda tympani responses to a range of NaCl concentrations in C57BL/6J mice but did not do so consistently in 129/J mice. Amiloride failed to significantly suppress responses to a range of KCl concentrations in both mouse strains. The results suggest that for 129/J mice, sodium reception and transduction are primarily amiloride insensitive, whereas for C57BL/6J mice, both amiloride-sensitive and amiloride-insensitive components are present. The strain difference in NaCl intake may be mediated, in part, through gustatory mechanisms, with reduced preference for NaCl influenced by amiloride-sensitive sodium transduction mechanisms.

Amiloride↗

A novel psychophysical procedure for bitter taste assessment in rats.

A persistent problem with attempts to examine bitter taste mechanisms has been the lack of adequate behavioral methodology providing data which parallels that obtained from physiological investigations. We developed a brief contact procedure to assess the ability of rats to detect the presence of a weak bitter compound dissolved in a strong sucrose solution. Male Fischer 344 rats were trained to drink immediately to multiple 10-s presentations of acetaminophen (2, 8, 32, 128 mM), chlorpheniramine maleate (1, 3, 9, 27 mM) L-tryptophan (13.5, 27, 54, 108 mM), pseudoephedrine hydrochloride (1, 4, 16, 64 mM) and quinine hydrochloride (0.008, 0.04, 0.2, 1.0 mM) dissolved in 0.8 M sucrose. The number of licks to sucrose and water were also measured. A microcomputer controlled stimulus presentations and measured the animal's licks of each solution during each 10-s presentation. The responses to the bitter+sucrose mixture were significantly decreased at most concentrations with increasing levels of the bitter component. This was true for all five bitter-tasting compounds, but over different concentration ranges relatively unique to each compound. The present study is the first to characterize the sensory effects of acetaminophen, pseudoephedrine, and chlorpheniramine maleate, all purported to taste bitter to humans. These results demonstrate rats' acute ability to discriminate by taste not only the presence but the concentration of a dilute bitter compound dissolved in a strong sucrose solution.

Acetaminophen↗

Neural responses of thermal-sensitive lingual fibers to brief menthol stimulation.

The addition of the coolant menthol to several oral and facial products is to increase their attractiveness and commercial value. Little is, however, known about the physiological basis of menthol's sensory effects. We studied the electrophysiological responses of 45 thermal-sensitive lingual fibers to anterior tongue stimulation (10 s) with menthol in male Sprague-Dawley rats. Menthol responses were unlike the responses to cold water. Cold water (6 degrees C, 15 degrees C) elicited an immediate sustained increase in impulse frequencies of thermal-sensitive fibers adapted to room temperature water (22-24 degrees C). Inhibitory off-responses followed cold water stimulation. Depending on the concentration and time of measurement, menthol stimulation either excited, inhibited, or had no effect on impulse frequencies of thermal-sensitive fibers. Strong menthol (0.64 mM, 1.28 mM) unequivocally excited thermal-sensitive fibers with a response latency of 4-6 s. In most cases after menthol stimulation, the impulse frequencies returned to baseline; there were no off-responses. Weak menthol (0.0128 mM, 0.064 mM, 0.128 mM) inhibited impulse frequencies of 14 thermal-sensitive fibers and excited impulse frequencies of 6 fibers primarily during the first 2 s of stimulation. Menthol responses were also unlike responses to stimulation with taste solutions. Most taste solutions (30 and 100 mM NaCl, 0.3 and 1 mM quinine-HCl, 0.3 mM citric acid) significantly inhibited impulse frequencies but only during the first 2-5 s of stimulation. The effect of NaCl was biphasic with the initial inhibitory phase followed by an excitatory phase during the second 5 s of stimulation. An excitatory off-response followed quinine stimulation. While considered principally a coolant, menthol elicits a unique pattern of responses from trigeminal and taste nerve endings quite unlike those of conventional thermal and taste stimuli.

Animals↗

Amiloride alters lick rate responses to NaCl and KCl in rats.

The role of cation channels on taste cell membranes to salt taste sensation was assessed in rats. We measured the number of licks during multiple 10-s presentations of NaCl and KCl concentrations (0.05, 0.09, 0.16, 0.28, 0.5 M) dissolved in either water or in 100 microM amiloride, a sodium-channel blocker. The number of licks to water and 0.3 M sucrose was also measured. The number of licks to NaCl was significantly lower and the number of licks to KCl was significantly higher when these test solutions were dissolved in amiloride than in water. There were no differences in lick responses to water and sucrose. These results suggest that amiloride may have altered the taste of NaCl and KCl. The results are discussed in relationship to prior electrophysiological studies characterizing the effect of amiloride in blocking salt responses of the chorda tympani nerve.

Amiloride↗

Taste prestimulation increases the chorda tympani nerve response to menthol.

Electrophysiological recordings of the summated response of the chorda tympani nerve to menthol stimulation of the tongue were obtained from 15 adult Sprague-Dawley rats. The chorda tympani nerve response to menthol was of short duration, ending within 2.5 s after stimulus onset, leaving the receptors in a state of insensitivity to subsequent menthol stimulation. Rinse durations with deionized-distilled water up to 10 min failed to bring the receptors back to their original prestimulus state. Although stimulation with menthol prevented taste receptors from responding to subsequent presentations of menthol, the chorda tympani nerve would respond normally to NaCl, NH4Cl, KCl, sodium acetate, glucose, citric acid, and quinine-HCl solutions. Prior stimulation with one of these taste solutions resulted in the recovery of the menthol response. The magnitude of the recovered menthol response depended on the magnitude of the phasic response elicited by the preceding taste stimulus. A general explanation involving possible reception and transduction mechanisms was offered to account for menthol's unexpected stimulatory effects on the chorda tympani nerve.

Animals↗

High NaCl intake of rat dams alters maternal behavior and elevates blood pressure of adult offspring.

The present study investigated whether differences in maternal NaCl intake altered 1) maternal-pup behavior and 2) the development of dietary obesity and blood pressure level of adult Sprague-Dawley rats maintained on a palatable high-fat/milk (HF/M) diet. Thirteen dams fed high (3%) NaCl and 12 dams fed basal (0.12%) NaCl were observed on postnatal days 2-21 for differences in the number of times spent 1) nursing, 2) in contact with or licking, sniffing, and carrying pups, and 3) in nest building. The offspring were continued on their respective NaCl diets to 30 days postpartum, and then both NaCl groups were fed an intermediate (1%) NaCl diet thereafter. Beginning at 60 days of age, the offspring from each maternal NaCl condition were fed either Agway R-M-H 1000 pelleted food or a HF/M diet for 14 wk. Dams fed 3% NaCl spent significantly more time licking their pups than did dams fed 0.12% NaCl. The adult offspring of dams fed 3% NaCl had a significantly higher level of systolic blood pressure and consumed more calories of sweetened condensed milk on the HF/M diet than did rats raised on 0.12% NaCl. Dietary-induced obesity did not magnify the increase in systolic blood pressure from high maternal NaCl intake. The present results raise the possibility that increased maternal licking may contribute to the increased blood pressure and solution intake that follows from high maternal NaCl intake.

Animals↗

Sex difference in blood pressure of spontaneously hypertensive rats influenced by perinatal NaCl exposure.

Our prior study showed that the basal blood pressure level and pressor response to peripheral angiotensin II of adult Sprague-Dawley rats were enhanced by perinatal exposure to a high NaCl diet. The purpose of the present study was to assess further the relationship between NaCl-sensitivity of blood pressure and perinatal NaCl exposure. We tested the hypothesis that the basal blood pressure level and pressor responses to angiotensin II could be increased by perinatal exposure to high NaCl in NaCl-resistant spontaneously hypertensive rats (SHR-R). Adult female SHR-R were maintained on a diet containing either basal 1% or high 8% NaCl throughout pregnancy and lactation. The offspring were continued on these same diets to 30 days postpartum. Thereafter, all offspring were maintained on a diet containing 1% NaCl. After being adapted to restraint, systolic blood pressure was measured indirectly by the tail-cuff procedure when the rats were 30, 44, and 58 days of age. Subsequently, baseline mean arterial pressure (MAP) and pressor responses to intravenous administration of angiotensin II (20, 40, 80, and 120 ng/kg body weight) were obtained from the catheterized femoral artery in conscious unrestrained rats. The MAP levels of adult female SHR-R exposed perinatally to 8% NaCl were significantly greater than those of females exposed to 1% NaCl. This elevated blood pressure was accompanied by an elevation in plasma osmolality. Perinatal exposure to 8% NaCl did not raise the blood pressure and plasma osmolality levels of adult male SHR-R, but did enhance pressor responses to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

Dietary obesity and weight cycling in rats: a model of stress-induced hypertension?

The present study was designed to reproduce the mild hypertension seen in dietary obese weight-cycled rats [P. Ernsberger and D. O. Nelson. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R47-R55, 1988] and determine whether this mild hypertension was associated with changes in sodium excretion and pressor responsiveness to angiotensin II (ANG II). Male Sprague-Dawley rats were fed pelleted chow (Pellet group) or chow plus sweetened condensed milk (Milk group) or were exposed to four cycles of a 4-day fast alternated with 2 wk of refeeding of pelleted chow and sweetened condensed milk (Cycled group). Blood pressure and heart rate were measured by tail cuff at the onset and last day of each fast and after 3 days of refeeding. During fasting, urine sodium excretion was measured. Mean arterial pressure and heart rate responses to intravenous administration of ANG II (40, 80, and 120 ng/kg), metoprolol (1 mg/kg), and methyl scopolamine (2 mg/kg) were obtained from the femoral artery in awake unrestrained rats. Weight cycling did not lead to mild hypertension or increased bradycardic response to sympathetic blockade with metoprolol. ANG II-elicited pressor responses were similar for Pellet, Milk, and Cycled groups. Sodium excretion did not change with fasting. Mild hypertension developed when obese weight-cycled rats were housed together in groups and not when housed individually. Our preliminary data are consistent with the notion that stress associated with group housing may be a factor in the mild hypertension of obese weight-cycled rats.

Animals↗

Perinatal exposure to a high NaCl diet increases the NaCl intake of adult rats.

To determine the effect of differences in perinatal NaCl exposure on NaCl intake, adult Sprague-Dawley female rats were maintained on diets containing either 0.12, 1.0, or 3% NaCl throughout pregnancy and lactation. The offspring were continued on the these same diets to 30 days postpartum. Thereafter, all offspring were fed the same basal diet containing 1% NaCl. At 90 days of age, the adult offspring were placed in metabolism cages for 7 days and fed 1% NaCl chow for days 1-2, and 0% NaCl chow for days 3-7. On days 6-7, the animals were free to consume both water and 0.3 M NaCl. When dietary NaCl was available, adult rats exposed perinatally to the high NaCl diet excreted significantly more sodium on days 1-2 and 6-7 than did the rats exposed to either the mid or low NaCl diets. There were no differences in sodium excretion during sodium deprivation on days 3-5. The 0.3 M NaCl intake of the high NaCl-exposed rats was also significantly greater than the intake of the mid and low NaCl-exposed rats. In another group of adult rats, exposed perinatally to either a low or high NaCl diet, the spontaneous 24-hr intake of water and 0.3 M NaCl was measured after repeated episodes of acute sodium depletion. Sodium depletion was induced by 48 hr of dietary sodium deprivation combined with a single subcutaneous injection of 5 mg furosemide. Acute sodium depletion was found to augment existing differences in NaCl intake between low and high NaCl-exposed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Dissociation of autonomic controls of heart rate in weaning-aged borderline hypertensive rats by perinatal NaCl.

The ontogeny of functional sympathetic neural, adrenal medullary, and extra-adrenal components of adrenergic control of heart rate was investigated in borderline hypertensive rats exposed to either high or low sodium chloride (NaCl) from conception through weaning. Borderline hypertensive rats were produced by mating spontaneously hypertensive females with normotensive Wistar-Kyoto males. Females were maintained on diets containing either low (0.12% NaCl) or high (3% NaCl) dietary NaCl throughout pregnancy and lactation. At 28 days of age, baseline heart rates recorded from awake and unrestrained pups did not differ between low and high NaCl-exposed pups. Overall sympathetic tone, inferred from heart rate change after beta 1-adrenergic blockade with atenolol, did not differ between high and low NaCl-exposed pups. Early NaCl exposure did not alter the neural component of sympathetic control of heart rate as inferred from heart rate decrease after bretylium tosylate. Parasympathetic nervous system control, as reflected by tachycardic response to muscarinic receptor blockade with atropine methyl nitrate was also unchanged by early NaCl exposure. The adrenal catecholamine component of sympathetic control of heart rate was inferred from bradycardia following administration of the ganglion blocking agent, chlorisondamine, to pups pretreated with bretylium and atropine methyl nitrate. Pups exposed to low NaCl showed increased adrenal control of heart rate compared to high NaCl-exposed pups. The influence of residual catecholamines on heart rate was inferred from bradycardia following administration of the beta 1-adrenergic receptor blocking agent, atenolol, in pups pretreated with bretylium, atropine methyl nitrate, and chlorisondamine. Residual catecholamine influence was greater in rats exposed to high NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗

Deficits in conditioned heart rate and taste aversion in area postrema-lesioned rats.

Previous studies have shown that area postrema (AP) lesions cause deficits in conditioned taste aversion in the rat. They also lead to chronically lowered heart rate which can be reversed by the animals' increased appetite for and ingestion of hypertonic saline. Although not previously examined in conditioned taste aversion, changes in autonomic nervous system activity as reflected in heart rate may be an important aspect of conditioning. The present study investigated the effects of AP lesions on heart rate conditioned responses (CRs) and unconditioned responses (UCRs). Two groups of AP lesioned and sham-operated rats, one that did and one that did not drink saline solution to raise heart rate, were studied. Both LiCl and scopolamine, which have opposite effects on heart rate, were the unconditioned stimulus (UCS) agents in two separate studies. In intact rats, LiCl-mediated conditioned taste aversion was associated with decreased conditioned stimulus (CS) intake and decreased heart rate Both effects were blunted by AP lesions, although all rats displayed heart rate UCRs to LiCl. The AP rats that drank saline behaved like intact rats exhibiting both a conditioned taste aversion and conditioned heart rate responses to the CS. Although CS intake decreased, no heart rate CRs developed with scopolamine. Scopolamine-mediated conditioned taste aversion was attenuated in both saline and non-saline drinking AP-lesioned groups. Thus, when conditioned taste aversion was associated with heart rate CRs, the AP lesion-induced deficit was counteracted by saline ingestion. Conversely, when there were no heart rate CRs, conditioned taste aversion was disrupted by the lesion regardless of saline ingestion.

Animals↗