Repeated sodium depletion affects gustatory neural responses in the nucleus of the solitary tract of rats

1997 ◽  
Vol 273 (4) ◽  
pp. R1381-R1391 ◽  
Author(s):  
Ryoi Tamura ◽  
Ralph Norgren
Keyword(s):  
The Other ◽  
Dietary Sodium ◽  
Gustatory System ◽  
Solitary Tract ◽  
Sodium Restriction ◽  
Neural Responses ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
The Third ◽  
Quinine Hydrochloride

Furosemide sodium depletions were induced repeatedly to determine the effects on gustatory neural responses in the nucleus of the solitary tract (NST) of chronically prepared, but lightly anesthetized, rats. Sodium-replete and sodium-deplete conditions were alternated four times in each rat. When rats were under depleted conditions, the responses to NaCl were significantly greater than in sodium-replete conditions. This effect was attributable primarily to an increase in the magnitude of response of those neurons that responded better to NaCl than to the other standard stimuli (sucrose, citric acid, and quinine hydrochloride). In addition, the largest change in responsiveness of the NaCl-best neurons occurred during the third and fourth sodium depletions. These results are essentially opposite to those reported for NST neurons when sodium appetite is induced by dietary sodium restriction. This suggests that the coding of intensity in the gustatory system is dependent not only on the animal’s deprivation condition, but also the method through which the deprivation is produced.

Intracranial renin alters gustatory neural responses in the nucleus of the solitary tract of rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1108-R1118 ◽  
Author(s):  
R. Tamura ◽  
R. Norgren
Keyword(s):  
Neural Activity ◽  
Renin Angiotensin System ◽  
Intracerebroventricular Injection ◽  
Solitary Tract ◽  
Neural Responses ◽  
Angiotensin System ◽  
Sodium Appetite ◽  
Similar Tendency ◽  
Quinine Hydrochloride ◽  
The Brain

Activation of the renin-angiotensin system in the brain is considered important in the arousal and expression of sodium appetite. To clarify the effects of directly activating this hormonal cascade, taste neurons in the nucleus of the solitary tract of rats were tested with a battery of sapid stimuli after intracerebroventricular injection of renin or its vehicle. The rats were chronically prepared but lightly anesthetized during the recording procedure. Eighty-five taste neurons were tested: 46 after renin injections and 39 after vehicle. Neural activity was counted for 5.0-s periods without stimulation (spontaneous) and during stimulation with water and sapid chemicals. The averaged responses to each of the standard stimuli (0.1 M NaCl, 0.3 M sucrose, 0.01 M citric acid, and 0.01 M quinine hydrochloride) did not differ significantly between the two conditions. When the rats were tested with a concentration range of NaCl, however, after renin the average responses to the hypertonic 0.3 and 1.0 M stimuli were reduced to 74 and 70%, respectively, compared with those after vehicle injections. A similar tendency was evident for the subsample of neurons that responded best to NaCl, but the effect was smaller. These data are consistent with, but not as dramatic as, those reported after dietary-induced sodium appetite.

scholarly journals Parabrachial and hypothalamic interaction in sodium appetite

2011 ◽  
Vol 300 (5) ◽  
pp. R1091-R1099 ◽  
Author(s):  
S. Dayawansa ◽  
S. Peckins ◽  
S. Ruch ◽  
R. Norgren
Keyword(s):  
Weight Loss ◽  
Lateral Hypothalamus ◽  
Ibotenic Acid ◽  
The Other ◽  
Salt Appetite ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
Parabrachial Nuclei ◽  
Bilateral Lesions

Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN.

THE ROLE OF A FEEDBACK MECHANISM IN THE REGULATION OF ALDOSTERONE SECRETION IN THE RAT

1973 ◽  
Vol 73 (2) ◽  
pp. 282-288
Author(s):  
L. Debreceni ◽  
B. Csete
Keyword(s):  
Marked Decrease ◽  
Feedback Regulation ◽  
Feedback Mechanism ◽  
The Other ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Aldosterone Production

ABSTRACT The effect of prolonged aldosterone and DOC treatment in the in vitro aldosterone production was studied in the rat. When the animals were supplied with food containing 16.5 mEq./100 g of sodium, both aldosterone and DOC treatment led to a marked decrease in aldosterone production. On the other hand, under dietary sodium restriction both aldosterone and DOC treatment failed to induce a suppression of the elevated aldosterone production. On the basis of these findings, it seems that a sufficient sodium supply of the organism is necessary for the control of aldosterone secretion either by an increase of aldosterone production or DOC treatment if any feedback regulation is involved in the mechanism controlling aldosterone secretion.

scholarly journals Brain serotonin depletion enhances the sodium appetite induced by sodium depletion or beta-adrenergic stimulation

2004 ◽  
Vol 76 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Hawlinston R. C. Lima ◽  
Haerishton R. Cavalcante-Lima ◽  
Pedro L. Cedraz-Mercez ◽  
Ricardo H. Costa-E-Sousa ◽  
Emerson L. Olivares ◽  
...  
Keyword(s):  
Systemic Administration ◽  
Brain Serotonin ◽  
Control Group ◽  
Sodium Depletion ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Serotonin Depletion ◽  
Sodium Appetite ◽  
The Third ◽  
Observation Period

We investigate the influence of brain serotonin depletion on the sodium appetite. Rats depleted of serotonin through the systemic administration of p-chlorophenylalanine (300 mg/kg, ip, for 2 days) showed an intense natriorexigenic response induced by sodium depletion (furosemide, 20 mg/kg, sc, 24 h before water and 1.8% NaCl presentation). Intake of 1.8% NaCl was always higher than that observed for the control group (12.9 ± 1.4 and 21.4 ± 3.0 mL vs 5.7 ± 1.2 and 12.7 ± 1.6 mL, 30 and 300 min after water and saline presentation). After 24 h, the natriorexigenic response continued to be significantly higher compared to control (33.6±5.1 vs 21.9±3.6 mL,P <0.05). Fourteen days after p-chlorophenylalanine administration, 1.8% NaCl intake did not differ from controls. Serotonin-depleted rats expressed an early natriorexigenic response after isoproterenol administration on the third day after the first injection of p-chlorophenylalanine. An increase in 1.8% NaCl intake was first observed at 120 min (1.9 ± 0.2 vs 0.45 ± 0.3 mL,P <0.05) and remained high up to the end of the 24-h observation period (17.3±3.2 vs 1.1±0.5 mL,P <0.05). After 7 and 14 days, the natriorexigenic response became comparable to that of control animals. Present results show that brain serotonin depletion exaggerates the sodium appetite induced by the paradigm of sodium depletion or after beta-adrenergic stimulation.

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

2004 ◽  
Vol 287 (4) ◽  
pp. R706-R714 ◽  
Author(s):  
Young K. Cho ◽  
Michael E. Smith ◽  
Ralph Norgren
Keyword(s):  
Sucrose Concentration ◽  
Solitary Tract ◽  
Neural Responses ◽  
Original Experiment ◽  
Sodium Appetite ◽  
Nacl Concentration ◽  
Effect Of Treatment ◽  
Sensory Neural ◽  
Gustatory Neurons ◽  
Concentration Series

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.

Bulbar gustatory responses to anterior and to posterior tongue stimulation in the rat

1965 ◽  
Vol 209 (1) ◽  
pp. 105-110 ◽  
Author(s):  
Bruce P. Halpern ◽  
Linda M. Nelson
Keyword(s):  
Active Zone ◽  
The Other ◽  
Anterior Region ◽  
Reference Standard ◽  
Neural Responses ◽  
Quinine Hydrochloride ◽  
Posterior Tongue ◽  
Stimulation Of

Amplitudes of neural responses in the nucleus of the fasciculus solitarius to stimulation of the tongue with quinine hydrochloride were analyzed using the response to NaCl as a reference standard. Three distinguishable areas were observed within the gustatory response zone of the nucleus. One area, responsive only to stimulation of the anterior region of the tongue, was at the anterolateral limit of the active zone. A second area, caudal and medial to the first, responded to both anterior and posterior tongue-region stimulation, the latter region yielding larger responses. Medial to both of the other areas was a third, highly responsive area, which responded only to posterior tongue-region stimulation.

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