Liquid diet preference in weanling rats with dorsomedial hypothalamic lesions.
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Publications and source records attributed to L L Bellinger.
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Weanling Sprague-Dawley rats received bilateral anodic electrolytic lesions with platinum-iridium (PtIr) electrodes in the ventromedial (VMN) and dorsomedial (DMN) hypothalamic areas. Sham-operated rats served as controls. The rats were maintained for 48 days (experiment 1) and 33 days (experiment 2) and food intake, body weight (b.w.), nose-tail length and obesity index were recorded. The data of both experiments indicate that all parameters change in the same direction, as they do when lesions are produced with anodic stainless steel electrodes: in the VMN-P-lesioned animals, b.w. gains and overall mean food intake were normal, carcass fat increased and linear growth was reduced. In experiment 2, however, there was a temporary hyperphagia during the 1st 2 weeks of the study. In the DMN-lesioned rats, both ponderal and linear growth and food intake were decreased but body composition was normal. Plasma obtained at sacrifice in experiment 2 showed slight but significant hyperinsulinemia in the VMN rats (p less than 0.02 vs control and p less than 0.05 vs DMN rats). Prolactin (PRL) levels, on the other hand, were higher in the DMN-lesioned rats (p less than 0.05 vs control and p less than 0.02 vs VMN rats). The data indicate that the changes characteristic of the weanling rat VMN and DMN syndrmes are due to 'true' tissue destruction rather than to artifactitious side effects of the lesions. They also suggest, therefore, than an 'irritative focus' hypothesis is not required to account for the observed alterations. They further suggest that the DMN may play role in the control of PRL release.
Weanling rats received bilateral electrolytic lesions in the dorsomedial (DMH) or ventromedial (VMH) hypothalamic areas destroying primarily the dorsomedial (DMN) or ventromedial (VMN) hypothalamic nuclei. Sham-operated rats served as controls. Lesions in the VMN and DMN, both of which have previously been shown to disrupt normal diurnal feeding rhythms, were also observed to disrupt normal plasma corticosterone rhythms in the present study. The a.m. values of plasma corticosterone in the DMN-lesioned rats were higher than the sham-operated controls. In the p.m., the values of both VMN- and DMN-lesioned rats were lower than those of the controls but unchanged in comparison to their own a.m. concentrations. This disruption of the normal diurnal plasma corticosterone rhythm persisted for at least 9 post-operative weeks.
The amount of food eaten in a two hour trial by male Sprague Dawley rats was recorded after periods of food deprivation up to 42 hr in length. Rats ate 50-78% more when refed during the dark phase than when refed during the light phase. This occurred even when light fed animals were fasted for longer periods than the dark fed animals. Rats eat in a rhythmic pattern after deprivation. These data are in good agreement with data previously reported and extend it by increasing the number of observations, increasing the length of deprivation, and comparing different age groups.
After rats had adapted to regular meal feeding in the morning they demonstrated an altered circadian rhythm of plasma corticosterone (B) even under the normal light-dark cycle. The altered daily rhythm of plasma B consisted of two peaks, with one peak at 08.00 h in anticipation of meal feeding and a second peak corresponding to the normal peak of plasma B prior to lights-off seen in ad libitum-fed animals. Neither peak of plasma B in the meal-fed animals achieved the magnitude of the single peak observed in control animals. In spite of some quantitative differences during certain periods of the day, after the animals had adapted to meal feeding there was no difference in the basic profile of the daily rhythm of plasma immunoactive growth hormone (GH).
Serial, apparently basal radio-immunoassayable plasma insulin and growth-hormone values were obtained when fast-knock down ether anesthesia was used. Radioimmunoassayable prolactin was elevated at the second, third, and fourth bleedings but cause no apparent increase in circulating insulin levels. The elevation in plasma glucose may also have been a transient effect of sympathetic stimulation which simultaneous inhibited insulin release.
We observed previously that totally liver denervated (TLD) rats consumed more of an imbalanced amino acid diet (IAAD) than sham-operated controls (CON). For the present study rats were either CON, TLD, had only the hepatic-vagal branch cut (HVX), or had all nerves on the hepatic artery and portal vein removed (HAPV) (n = 10-11). The rats were prefed a purified basal diet for 9 days then switched to an isoleucine IAAD for 7 days. On days 2-5 all experimental groups consumed more (p < 0.05) of the IAAD than the CON; they also showed less (p < 0.01) weight loss on days 3-7. This experiment showed that either total or partial liver denervations enhanced the intake of an IAAD compared to CON. However, when one considers the anatomical arrangement of the nerves and the surgery technique employed the vital neural pathway may involve the hepatic vagal branch.
Rats with dorsomedial hypothalamic lesions (DMN-L) or sham operations were injected IP with saline or the satiety peptide cholecystokinin (CCK) at 3.0 and 6.0 micrograms/kg at the onset of the dark phase. Food consumption was then measured 15, 30 and 60 min later. Compared to saline baseline intake, CCK suppressed feeding during the first 30 min following injection in the sham operated group but not in the DMN-L group. Bombesin (BBS), another satiety peptide was also injected (4.0 and 8.0 micrograms/kg) into the two groups. BBS produced significant and comparable suppression of feeding in both DMN-L and sham operated rats. In a third trial a large dose of CCK (12.0 micrograms/kg) was injected into the two groups as described above. The CCK suppressed feeding for 60 min in the control group. CCK also attenuated feeding in the DMN-L group, but for only 30 min. However, even this suppression was reduced compared to the control group. The data suggest that the DMN may play a role in CCK induced satiety.
Development of a new class of drugs designed to selectively inhibit the inducible cyclooxygenase isoenzyme, COX-2, was initially prescribed for individuals diagnosed with osteoarthritis or rheumatoid arthritis. Although these inflammatory disorders are more typically related to the joints of the knee, ankle, or hand, the temporomandibular joint (TMJ) plays a special role due to its involvement in our normal day-to-day activities of eating and communicating. The TMJ, unlike most of the other joints, contains some unique morphological characteristics that support various inflammatory disorders. An overview of these characteristics and the prospective use of the COX-2 inhibitors for temporomandibular joint inflammation are presented.