Hypothalamic knife-cut hyperphagia and obesity in weanling rats

In previous reports weanling female rats fed a high-fat diet had a delayed response to hypothalamic knife cuts. In the present report similar cuts in similar rats fed a standard low fat diet became overweight without delay, suggesting that dietary fat is a critical variable in juvenile onset obesity. Adult rats given knife-cuts comparable to those in the weanlings gained weight far more rapidly and achieved higher weights than did those cut as weanlings, suggesting that appetite modulating axons can develop after weaning. Finally, group vs single housing did not influence the age of onset or the magnitude of knife-cut obesity.     

Hyperdipsia produced by severing ventral septal fiber systems.

The septum of male hooded rats (N = 59) was completely isolated from the rest of the brain (ISS) or was partially isolated by severing dorsal (DP), ventral (VP), anterior (AP), or posterior (PP) fiber tracts using a knife-cut technique. Daily water intakes and intakes following hypertonic NaCl and polyethylene glycol (PG) injections were measured. The septum totally degenerated for the ISS group and these rats had normal or hypodipsic daily intakes, likewise for intakes following NaCl and PG. Rats of the VP group sustained little septal damage, yet these cuts yielded the highest percentage (55 percent) of hyperdipsic daily drinkers of any group. The daily hyperdipsic rats drank normally in response to NaCl and PG, demonstrating a dissociation between daily drinking and drinking in response to specific thirst stimuli. The results indicate the importance of ventral fiber systems in the production of Septal Hyperdipsia, and support the notion that the septum has multiple effects upon water regulation.     

Impaired diet-induced thermogenesis in brown adipose tissue from rats made obese with parasagittal hypothalamic knife-cuts

Two experiments were performed to determine if bilateral parasagittal hypothalamic knife-cuts (KCs), which produce long-term overeating and obesity, after biochemical indices of brown adipose tissue (BAT) reactivity to thermogenic stimuli. In the first study, responses to environmental cold were tested. Four weeks after surgery, KC rats had gained 4-5 times more weight than controls and were obese (increased Lee Obesity Index and weight of gonadal white fat). Before being sacrificed, groups of KC and control rats were exposed to 4 degrees C for 21 hr or remained at 28 degrees C. Interscapular BAT weighed 300% more in KC rats, due largely to increased white fat content. Functional indices of BAT thermogenic capacity (protein content, DNA content, cytochrome oxidase activity and mitochondrial guanosine diphosphate (GDP) binding) were normal at 28 degrees C. Exposure to 4 degrees C produced greatly enhanced responses but these were equivalent for both groups. This suggested an intact capacity for non-shivering thermogenesis in obese KC rats. In the second study, the same BAT responses were examined in other rats fed a palatable "cafeteria" diet (CAFE). One week after surgery, KC and control rats were subdivided into groups that received chow alone or chow plus four different palatable foods daily. Before sacrificing 4-5 weeks later, KC rats had gained 3-4 times more weight than controls and were obese. Interscapular BAT weighed 200-300% more in KC rats. CAFE feeding produced larger increments in all variables for KC vs. control rats. Most importantly, GDP binding was reduced in both KC groups, and significantly more so after CAFE feeding.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neophobia and conditioned taste aversion deficits in the rat produced by undercutting temporal cortex

Adult male hooded rats with parasagittal knife-cuts between the amygdala and temporal cortex (n = 8), with electrolytic basolateral amygdala lesions (n = 8), and sham-operated controls (n = 8), were tested for neophobia and LiCl-induced aversion to a 0.1% saccharin solution in a one-bottle forced choice paradigm. Both types of lesion produced equal deficits in neophobia and conditioned aversion. It was concluded that severing the connections between the amygdala and the temporal cortex produces the same deficits as basolateral amygdala damage. Possible anatomical substrates for these effects are discussed.