Dorsomedial Hypothalamic Nuclei Lesions Research Articles

Failure to demonstrate alterations in gluconeogenesis in growth‐retarded weanling rats with dorsomedial hypothalamic lesions

Bilateral electrolytic lesions were placed in the dorsomedial hypothalamic nuclei (DMN) of weanling male Sprague-Dawley rats. Sham-operated rats served as controls. After 22 days on lab chow and tap water ad libitum, the animals were injected with U-14 C-alanine 0.167 muC/mu moles intraperitoneally (5 muC and 30 mu moles/100 gm body weight) and sacrificed 2 hr later. There was no significant difference, in the incorporation of the label into total lipid, free fatty acids, glycogen, or tissue protein of both liver and diaphragm, between the DMN-lesioned and the sham-operated rats. Similarly, there was no significant difference in the incorporation into plasma glucose or protein. It is concluded that in spite of profound alterations in both ponderal and linear growth and food intake, there is no disruption of normal gluconeogenesis in the weanling rat with DMN lesions.

Feeding studies in weanling rats with dorsomedial hypothalamic lesions: Maintenance of competence to compensate for additional calories

Weanling rats received bilateral electrolytic lesions in the dorsomedial hypothalamus primarily destroying the dorsomedial hypothalamic nuclei (DMN). Sham-operated rats served as controls. After a 14 day postoperative period during which food intake (lab chow) and body weight were recorded, each of the above groups were subdivided into 2 groups. One DMN group and one sham-operated control group were continued on lab chow alone throughout the remainder of the study. The other DMN group and the second control group were given additional calories in the form of a liquid diet by stomach tube during 2 separate periods of 10 and 14 days, respectively, to increase their caloric intake beyond that taken in spontaneously. Both tube-fed groups reduced their ad lib caloric intake from chow considerably and to the same extent. Body weight gains were similar in tube-fed versus non-tube-fed rats, whether with or without DMN lesions. After the second, 14-day-long tube feeding period, however, DMN rats regulated their body weight somewhat less precisely than the controls. This may be related to their reduced food intake during that time period. The data indicate that weanling rats with DMN lesions, despite their basic hypophagia, do not show a deficit in caloric metering and gross body weight regulation.

The Dorsomedial Hypothalamic Nucleus In Autonomic And Neuroendocrine Homeostasis

Median eminence and ventromedial hypothalamus have in the past been the principal foci of research in neuroendocrine and neurovisceral control mechanisms. The present report provides an overview of work involving the dorsomedial hypothalamic nucleus (DMV). This structure is located dorsal to the ventromedial hypothalamic nucleus (VMN) to the plane of the dorsal premammillary nucleus. Fibers from the DMN pass with the periventricular system and the dorsal longitudinal fasciculus of Schütz and have been traced to the midbrain tegmentum and reticular formation. Intrahypothalamic connections involve intensive networks between DMN, lateral hypothalamic nucleus (LHN) and VMN. Regarding neurotransmitters, recent studies indicate that the DMN receives noradrenergic innervation along two pathways, a dorsal and a ventral one. Monoamine-containing systems approach the DMN From the lateral hypothalamus and the bulk of these fibers are carried in the medium forebrain bundle from their cells of origin in the brain stem. Studies of the vascular supply indicate that both VMN and DMN receive their blood supply from the internal carotid artery...

Effect of dorsomedial hypothalamic lesions before and after placement of obesity-producing ventromedial hypothalamic lesions in the weanling male rat

Bilateral electrolytic lesions in the ventromedial hypothalamic nuclei (VMN) were produced in two groups of weanling male rats. Two groups of rats received lesions in the dorsomedial hypothalamic nuclei (DMN). Six days later, one of the VMN groups received DMN lesions (VMN and DMN), while VMN lesions were produced in one of the DMN groups (DMN and VMN). Sham-operated animals served as controls. The animals were maintained for 18 days during which time food intake was measured. On the 19th day they were decapitated and the following parameters determined: carcass fat, plasma insulin, glucose, triglyceride and cholesterol, and body weight and length. DMN lesions failed to attenuate the ‘principal’ parameters of the weanling rat ventromedial syndrome: hyperinsulinemia, hyperlipidemia and increased carcass fat. This was irrespective of the sequence of the two hypothalamic operations. Food intake, body weight and length proved amenable to DMN lesions only when DMN were produced prior to VMN lesions, but it is noteworthy that in these animals plasma insulin and lipid levels remained elevated despite a reduced food intake. Neither of the groups with double lesions had glucose values which were significantly different from those of the controls. The data point to a profound autonomy of the ventromedial hypothalamic nuclei and their related circuits in the development of the weanling rat VMN syndrome.

BODY SIZE AND METABOLIC RATE

BODY SIZE AND METABOLIC RATE