Donald V. Coscina

Body awareness in anorexia nervosa: disturbances in "body image" and "satiety".

&NA; Patients with anorexia nervosa have been shown previously to display distortions in body image perception. Bruch has postulated that these disturbances as well as disturbances in interoception are meaningfully related to the development of the syndrome. We hypothesized that disturbances in body image, as measured by a distorting photograph technique, and interoception, as measured by a satiety‐aversion to sucrose test, should be demonstrable in anorexic patients vs. normal controls. Furthermore, these disturbances should be modifiable by external cues (looking at ones image in a mirror and ingesting isocaloric “high” and “low” calorie connotation meals). We also hypothesized that body image and interoceptive disturbances would be interrelated in the same individuals. Results indicated that patients with anorexia nervosa (N = 26) differed from normal controls (N = 16) in overestimating their body sizes (p = 0.06) and in failing to develop an aversion to the sucrose tastes (p < 0.001). However, neither viewing ones image in a mirror nor ingesting both “high and “low” calorie connotation meals altered body size perception. Intrasubject body size estimates were very stable from week to week for the anorexic subjects (r = +0.75, p < 0.001) but less for the controls (r = +0.45, p < 0.05). The data revealed that overestimation of body size was closely related to the failure to develop an aversion to sucrose tastes in anorexic patients.

Dissociated feeding and hypothermic effects of neuropeptide Y in the paraventricular and perifornical hypothalamus

The present study investigated the effects of neuropeptide Y (NPY) on food intake and body temperature (Tbo) in free-feeding unrestrained rats following injection into the medial hypothalamic paraventricular nucleus (PVN) or the lateral perifornical hypothalamus (PFH). NPY (78-235 pmol) or saline was infused unilaterally into the PVN or PFH in a volume of 0.4 microliter and simultaneous measures of food intake and Tbo were taken every 30 min for 3 h. Results indicated that NPY evoked changes in eating behavior and Tbo that were dependent upon the site of hypothalamic injection. Although PVN and PFH administration of NPY both increased food intake dose dependently within 30 min of treatment, PFH NPY-injected rats (n = 9) showed a stronger behavioral response compared to rats (n = 9) receiving NPY injections into the PVN. In PVN-treated rats, however, the increased eating was associated with a significant decline in Tbo evident within the first 30-min test interval. A mean maximal decline of 0.92 +/- 0.26 degree C occurred within 90 min of PVN treatment of the highest dose, which produced a reduction in Tbo that was maintained for 2.5 h. In contrast, NPY infusion into the PFH failed to reliably alter Tbo at any of the doses tested. These findings are consistent with evidence that NPY in the PVN and PFH may have distinct functions and suggest that although PFH NPY acts to stimulate a robust and relatively specific ingestive response, PVN NPY may participate in the complex integrative mechanisms responsible for the simultaneous regulation of feeding, thermoregulatory, and metabolic processes.

Effects of dietary fat on pain threshold, thermoregulation and motor activity in rats.

Groups of young male Sprague-Dawley (albino) or Long-Evans (hooded) rats were fed the same semi-purified diets containing 20% (w/w) fat in the form of soybean oil vs. lard, or a reference diet of standard Purina Chow (4.5% mixed fats) for 21 days. Behavioral testing after this time revealed that albino rats fed the diet containing soybean oil had increased paw-lick latencies on a 58 degrees C hot plate compared to chow-fed rats. In addition, both strains fed the diet containing soybean oil were protected from hypothermia induced by placing animals in a 4 degrees C cold room for 60 min following systemic injection of 10-15 mg/kg d-amphetamine. Rats of both strains fed the lard diet displayed paw-lick latencies similar to those shown by rats fed chow and hypothermic changes intermediary to those shown by rats fed soybean oil vs. chow diets. Horizontal crossings as well as rearings in a 15 min test of open field activity were the same for all diet groups within strains. No substantial differences were observed in the number of calories consumed, amount of body weight gained or basal colonic temperatures across diet conditions. The results suggest that a soybean oil-based diet can alter physiological mechanisms which mediate these indices of pain perception and thermoregulation. More generally, they indicate that qualitative changes in dietary fat content may be capable of altering certain behavioral states.

Learning is improved by a soybean oil diet in rats

A semi-synthetic diet containing 20% polyunsaturated fat (soybean) oil was fed to young male hooded rats for 21 days. These animals exhibited improved performance on an environmentally-cued testing paradigm which is thought to reflect cognitive learning skills (i.e., Place Navigation Water Task). Other rats fed the same base diet but containing 20% saturated fat (lard) showed no such improvement compared to chow-fed (4.5% mixed fat) controls. The animals fed soybean oil also exhibited a transient resistance to extinguish this learning. This improved learning could not be explained by changes in general motor activity, basal body temperature, energy consumption, body weight, or in the brain activity of choline acetyltransferase, the marker enzyme for cholinergic neurons. These findings constitute the first evidence that short-term variations in the quality of dietary fat can enhance mammalian learning.

Induction of rage in rats by central injection of 6-hydroxydopamine.

Abstract Intracisternal injection of 300 μg of 6-hydroxydopamine in male rats elicited a syndrome of hyperreactivity or hyperemotionality, i.e., rage, similar to that previously reported after septal or ventromedial hypothalamic (VMH) lesions. Specifically, rats showed increased resistance to capture as well as increased number and magnitude of startle responses compared to vehicle injected or normal controls. As with septal but not VMH lesions, this rage subsided with repeated testings (handling). These findings are discussed with regard to the possible importance of brain neurotransmitters in the expression of behaviors.

The rewarding properties of neuropeptide Y in perifornical hypothalamus vs. nucleus accumbens.

There is a high coexistence of substance abuse in humans with eating disorders. One theory offered to account for this fact is that a common biochemical substrate may exist that mediates both processes. Brain neuropeptide Y (NPY) is one neurochemical system that might contribute to these separate, yet related, problems. To clarify the role of NPY in mediating reward processes and the possible interaction between reward and feeding, the present study examined the effects of injecting NPY bilaterally into the perifornical hypothalamus (PFH) vs. the nucleus accumbens (NAC) on intake of preferred vs. non-preferred food types, as well as on conditioned place preference (CPP) learning. NPY (24, 78, 156 and 235 pmol/side) stimulated intake of both regular powdered chow and sucrose when injected into the PFH, but not the NAC. A CPP that was negatively correlated with food intake occurred with the low (24 pmol/side) dose of NPY in the PFH, while a CPP that was not correlated with food intake was produced with the same dose in the NAC. The extent of the CPPs produced by NPY injection in both brain sites mirrored that produced by peripheral injection of amphetamine (2.5 mg/kg). These results indicate that NPY elicits reward-related behavior, but not feeding, from the NAC, and both behaviors from the PFH. However, the feeding effect derived from the PFH appears to overshadow a rewarding effect derived from this site. Considered together, these findings suggest that altered NPY functioning in both brain regions may contribute to some of the pathophysiological processes observed in eating disordered patients who have additional proclivities for substance abuse.

Selective decrease in protein intake following brain serotonin depletion

Abstract The effect of reduced brain serotonin concentration achieved with drugs or raphe lesions on the control of protein intake and energy intake by young rats was examined. All rats were provided an oppurtunity to select from 15% and 55% casein diets provided simultaneously in two food cups. Systemic parachlorphenylalanine, central 5, 7-dihydroxytryptamine or mid-brain raphe lesions reduced by 20–30% the amount of protein consumed from these two diets over a two week study period. Across these same groups total energy intake was not different from the control groups. This decrease in the proportion of dietary energy selected as protein by the treated self-selecting rats was associated with the reduction observed in brain serotonin and its major metabolite, 5-hydroxyindole acetic acid at the completion of the feeding period. These findings support previous work implicating brain serotonin metabolism in the selective control of protein intake.

Different diurnal rhythms of protein and non-protein energy intake by rats☆

Abstract Rats allowed to self-select dietary constitutents control their intake of protein and energy (calories) independently. Although absolute protein consumption per meal remains almost constant, meal size increases progressively from the mid-light period through the dark period by selective increases in the non-protein content. Hence the composition of selected meals follows a daily rhythm with protein concentration decreasing from light to dark meals. The consistency of these feeding rhythms indicates separate short-term regulation of protein and energy intakes.

Injecting 5-HT into the PVN does not prevent feeding induced by injecting 8-OH-DPAT into the raphe

The selective 5-hydroxytryptamine1A (5-HT1A) agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) activates raphe somatodendritic autoreceptors, leading to an inhibition of 5-HT neuronal activity and reduced synthesis and release of 5-HT in forebrain terminal areas. One behavioural consequence of this is increased feeding in satiated rats. Because injections of 5-HT agonists into the medial hypothalamus suppress feeding, it has been proposed that 8-OH-DPAT-induced feeding may involve a reduction of 5-HT release within this area. This hypothesis was tested by examining the ability of 5-HT injected into the medial hypothalamus to reverse the feeding-stimulant action of 8-OH-DPAT following injection into the dorsal raphe or median raphe. Two groups of rats, maintained with free access to food at all times, were used. Each was prepared with two cannulae, one aimed at the paraventricular nucleus (PVN) of the medial hypothalamus and the other at either the dorsal raphe nucleus or median raphe nucleus. Food intake over the next hour was increased following dorsal raphe or median raphe injections of 8-OH-DPAT (1 and 0.5 microgram, respectively). These effects were not blocked by injections of 7.5 or 15 micrograms 5-HT into the PVN. However, 15 micrograms 5-HT did attenuate the feeding-stimulant action of 10 micrograms norepinephrine injected into the PVN. These results do not support the hypothesis that a reduction in 5-HT release within the medial hypothalamus is responsible for the feeding-stimulant action of 8-OH-DPAT.

Differential binding of 3H-imipramine and 3H-mianserin in rat cerebral cortex

Abstract Drug competition profiles, effect of raphe lesion, and sodium dependency of the binding of two antidepressant drugs 3 H-imipramine and 3 H-mianserin to rat cerebral cortex homogenate were compared to examine whether the drugs bound to a common “antidepressant receptor.” Of the neurotransmitters tested, only serotonin displaced binding of both 3 H-imipramine and 3 H-mianserin. 3 H-mianserin binding was potently displaced by serotonin S 2 antagonists and exhibited a profile similar to that of 3 H-spiperone binding. In the presence of the serotonin S 2 antagonist spiperone, antihistamines (H 1 ) potently displaced 3 H-mianserin binding. 3 H-Imipramine binding was displaced potently by serotonin uptake inhibitors. The order of potency of serotonergic drugs in displacing 3 H-imipramine binding was not similar to their order in displacing 3 H-spiperone or 3 H-serotonin binding. Prior midbrain raphe lesions greatly decreased the binding of 3 H-imipramine but did not alter binding of 3 H-mianserin. Binding of 3 H-imipramine but not 3 H-mianserin was sodium dependent. These results show that 3 H-imipramine and 3 H-mianserin bind to different receptors. 3 H-Imipramine binds to a presynaptic serotonin receptor which is probably related to a serotonin uptake recognition site, the binding of which is sodium dependent. 3 H-Mianserin binds to postsynaptic receptors, possibly both serotonin S 2 and histamine H 1 receptors, the binding of which is sodium independent.