Francis W. Flynn

Sodium depletion enhances salt palatability in rats.

Sterotyped fixed action patterns (FAPs) are elicited in rats by oral infusions of taste solutions. These taste-elicited FAPs can be classified as either ingestive or aversive. They reflect the palatability of the taste and can be modified by learning and by the physiological state of the animal. These studies demonstrated that when the physiological state of the rat is altered by sodium depletion, the pattern of FAPs elicited by oral infusions of 0.5 M NaCl shifts from a mixture of ingestive and aversive components (while sodium replete) to exclusively ingestive ones (while sodium deplete). This shift in taste reactivity occurred the first time the rats were made sodium deplete. A similar shift was not observed to accompany infusions of 0.01 M HCl, a taste solution that also elicited mixed ingestive and aversive FAPs. This result suggests that the shift in response to NaCl is not due to a general change in ingestive bias or to a general taste deficit. On the basis of the change in FAPs, it is concluded that the palatability of highly concentrated salt solutions increases in sodium-deplete rats. Such a shift in salt palatability may be instrumental in directing the appetitive behavior of the animal.

Central Gustatory Lesions: II. Effects on Sodium Appetite, Taste Aversion Learning, and Feeding Behaviors

Intake and taste reactivity tests were used to determine the effects of bilateral lesions of the gustatory portions of the nucleus of the solitary tract (NST), the parabrachial nucleus (PBN), and the ventral posteromedial nucleus of the thalamus (VPMpc) on several complex ingestive behaviors. In the 1st experiment, lesions of the PBN and the NST blocked, and VPMpc lesions impaired, the behavioral expression of salt appetite. In the 2nd experiment, alanine was paired with injections of LiCl. Control rats as well as rats with NST and VPMpc lesions acquired the taste aversion, but rats with PBN lesions did not. In the 3rd experiment, all animals increased their food intake after injections of 2 U/kg insulin and 250 mg/kg 2-deoxy-D-glucose, and their food intake was suppressed after nutritive stomach loads.

Central gustatory lesions. I : Preference and taste reactivity tests

Bilateral electrophysiologically guided lesions were placed in the nucleus of the solitary tract (NST), the parabrachial nucleus (PBN), and the ventral posteromedial thalamic nucleus (VPMpc) of rats, and 15-min intake and taste reactivity (TR) responses elicited by 3 concentrations each of sucrose, NaCl, HCl, and quinine (Q) HCl were subsequently measured. Compared with controls, NST lesions had no significant effects on intake, and rats with PBN lesions consumed significantly more QHCl, sucrose, NaCl, and HCl. Thalamic lesions decreased sucrose intake. Analysis of TR responses showed that the QHCl threshold for aversive responses increased after VPMpc, PBN, and NST lesions. Rats with NST or PBN lesions were unresponsive to increasing sucrose concentration. TR responses elicited by NaCl and HCl were similar across the groups.

Intraoral intake and taste reactivity responses elicited by sucrose and sodium chloride in chronic decerebrate rats.

The oral stimulating effects of sucrose and sodium chloride (NaCl) were assessed in chronic decerebrate and pair-fed intact control rats by measuring both oral motor taste-reactivity responses and intraoral intake volume. Taste-reactivity responses were videotaped during the first minute of the intraoral taste infusion. The infusion continued until the taste solution was rejected from the mouth, and the intake volume was computed accordingly. The number of ingestive taste-reactivity responses and the volume of intraoral intake consumed by pair-fed control and decerebrate rats increased with increasing sucrose concentration. Sucrose intake increased as concentration increased to 0.1 M, then plateaued between 0.3, 1.3, and 2.0 M sucrose for both groups. For control rats, intraoral NaCl elicited an inverted U-shaped function for both taste-reactivity responses and intake. Taste-reactivity responses of chronic decerebrate rats varied with NaCl concentration. In contrast to control rats, intake of NaCl did not differ from that of water for decerebrate rats. These data indicate that caudal brain-stem mechanisms are sufficient to control sucrose intake but are not adequate for the concentration dependent intake of NaCl. Second, these data also indicate that it is possible for taste-elicited oral motor responses to be dissociated from intake. The different roles of taste and postingestive factors in sucrose and NaCl intake are discussed.

Sodium homeostasis in chronic decerebrate rats

Physiological and behavioral concomitants of sodium need were studied in supracollicularly transected and pair-fed intact rats. Chronic decerebrate rats, like intact rats, reduced their urine sodium output when placed on a sodium-deficient diet. Similarly, 24 hr after sodium loading, decerebrate and intact rats excreted comparable levels of the excess sodium. In the 2 hr immediately following the loading, decerebrate rats excreted less sodium. In contrast, behavioral aspects of sodium homeostasis were completely absent in chronic decerebrate rats. In separate experiments, intraoral intake, and taste-reactivity responses, elicited by intraoral infusions of NaCl were measured during sodium-replete and sodium-deficient conditions. In response to oral infusions of NaCl, intact rats consumed significantly more and produced greater numbers of ingestive taste-reactivity responses when they were sodium deficient than when they were sodium replete. The same sodium-depletion treatments in chronic decerebrate rats, however, altered neither the intraoral intake of NaCl nor the frequency of NaCl-elicited ingestive taste-reactivity responses. These results suggest that the behavioral compensatory responses that follow changes in the internal sodium state are dependent upon forebrain mechanisms.

Fourth ventricular phlorizin dissociates feeding from hyperglycemia in rats.

The effects of 4th ventricular injections of phlorizin and 5-thioglucose (5-TG) on feeding, plasma glucose, and plasma insulin levels were determined. Fourth ventricular applications of phlorizin (13 micrograms) and 5-TG (150 and 210 micrograms) were equally effective in stimulating feeding. Systemic injections of phlorizin (13 micrograms) did not stimulate feeding. In the absence of food, hyperglycemia was elicited by 4th ventricular injections of 5-TG. In contrast, the dose of phlorizin that stimulated feeding, did not produce hyperglycemia. Basal plasma insulin levels were not affected by either of the 4th ventricular injections. These data indicate that activation of caudal brainstem metabolic interoceptors provides an afferent limb for the production of compensatory responses and that behavioral and autonomic compensatory responses can be activated independently. The glucodynamic action of phlorizin appears selective for that mechanism mediating the behavioral compensatory response of feeding in contrast to the dual effects produced by 5-TG. These and other data suggest that different caudal brainstem mechanisms control behavioral and autonomic compensatory responses.

Chronic voluntary nicotine drinking enhances nicotine palatability in rats

The response of rats to nicotine solutions was examined with the brief-exposure, taste reactivity test and a two-bottle, 24-hr preference test. In Experiment 1, naive nondeprived rats were administered intraoral infusions (0.8 ml infused during 1 min) of distilled water and 1 microgram/ml, 5 micrograms/ml, 10 micrograms/ml, 25 micrograms/ml, 50 micrograms/ml, and 100 micrograms/ml nicotine. The oral motor, taste reactivity (TR) responses of the rats were recorded during the infusion. Nicotine solutions up to a concentration of 50 micrograms/ml elicited a number of ingestive TR responses similar to that by water. Ingestive responses significantly decreased and aversive TR responses significantly increased in response to 100 micrograms/ml nicotine. On the basis of these results, two-bottle preferences for water versus 1 microgram/ml, 5 micrograms/ml, and 0 microgram/ml (water control group) nicotine were measured in three groups of naive rats. Rats initially showed an equal preference for 0 microgram/ml and 1 microgram/ml nicotine. After 16 days of exposure, however, rats developed a significant preference for 1 microgram/ml nicotine. The preference ratio for 5 micrograms/ml nicotine significantly increased during the experiment, but the preference ratio remained significantly less than that for 1 microgram/ml and 0 microgram/ml nicotine solutions. Last, TR responses elicited by intraoral infusions of 1 microgram/ml and 5 micrograms/ml nicotine were then measured in these rats having had the two-bottle experience. Rats showing a two-bottle preference for the 1 microgram/ml nicotine solution displayed significantly more ingestive TR responses to 1 microgram/ml and 5 micrograms/ml nicotine than did the control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Potency of food deprivation intensity cues as discriminative stimuli.

Rats were trained to use stimuli arising from 0 and 24 hr without food as discriminative signals for shock. In Experiment 1, one group was shocked under 0-hr food deprivation and not shocked under 24-hr food deprivation. Another group received the reverse contingency. The groups received only 3 training trials under each deprivation level. Learning was revealed in a test phase when greater extinction of freezing was observed under the nonshocked than under the shocked deprivation level for both groups. A similar pattern of results was obtained in Experiment 2 when auditory cues were also relevant throughout training. Furthermore, prior training with food deprivation cues seemed to reduce learning about auditory cues subsequently trained in compound with deprivation stimuli. The results indicate that food deprivation intensity cues can be potent discriminative stimuli. The idea that deprivation cues function as conditioned modulatory stimuli cues is also discussed.

Cardiovascular alteration and treatment of hypertension: do men and women differ?

Cardiovascular disease is one of the most common causes of mortality affecting both men and women in industrialized nations. Sex-related differences have been well established with regard to heart and vascular function as well as cardiovascular disease processes. Nevertheless, the precise mechanisms of action behind these gender-related differences are poorly understood. Premenopausal women have a relatively lower arterial blood pressure compared to age-matched men and post-menopausal women, suggesting a role of ovarian hormones in blood pressure regulation. Sex-related differences in vasculature and neuroendocrine systems are also present that can affect hemostasis, vascular reactivity, and vascular tone. Treatment for cardiovascular disease and hypertension has been challenging and unsatisfactory. Men and women may require different antihypertensive regimens due to differences in the progression and presentation of hypertension. Additionally, hormone replacement therapy in postmenopausal women has been controversial, producing both beneficial and detrimental effects. Therefore, this review will focus on sex-related differences in the heart and vasculature, and treatments for cardiovascular disease, such as hypertension.

Distribution of fos‐like immunoreactivity within the rat brain following intraventricular injection of the selective NK3 receptor agonist senktide

Neurokinin B (NKB) is one member of an evolutionarily conserved family of neuropeptides, the tachykinins. Preferential binding of NKB to endogenous NK3 receptors affects a variety of biological and physiological processes, including endocrine secretions, sensory transmission, and fluid and electrolyte homeostasis. In light of its widespread biological actions, immunohistochemical detection of the c‐Fos protein product was used to study the distribution of neuronal activation in the rat brain caused by intraventricular (icv) injections of the selective NK3 receptor agonist (succinyl‐[Asp6, N‐Me‐Phe8] substance P [6–11]), senktide. Quantitative analysis revealed that treatment with isotonic saline or 200 ng senktide resulted in the differential expression of Fos‐like immunoreactivity (FLI) throughout the brain. Senktide induced the highest number of FLI neurons in the lateral septum, bed nucleus of the stria terminalis, amygdala, paraventricular nucleus of the hypothalamus, median preoptic nucleus, organum vasculosum of the lamina terminalis, supraoptic nucleus, periaqueductal gray, and medial nucleus of the solitary tract compared to isotonic saline controls. Additional regions that contained elevated FLI following icv injection of senktide, relative to saline injection, included the cerebral cortex, lateral hypothalamic nucleus, suprachiasmatic nucleus, ventral tegmental area, substantia nigra, inferior colliculus, locus coeruleus, zona incerta, and arcuate nucleus. Our data indicate that activation of NK3 receptors induces the expression of FLI within circumscribed regions of the rat brain. This pattern of neuronal activation overlaps with nuclei known to regulate homeostatic processes, such as endocrine secretion, cardiovascular function, salt intake, and nociception. J. Comp. Neurol. 426:413–428, 2000.