Thermoregulation in adult rats which have been treated with capsaicin as neonates

1. Subcutaneous or intrahypothalamic injections of capsaicin produce hypothermia in the neonate rat. Repeated injections with increasing doses of capsaicin result in unresponsiveness to this drug (capsaicin-desensitization).
2. Young rats aged 8–10 days which had received serial injections of capsaicin solution (a cumulative dose of 4.63 mg per animal) or of the solvent alone were subsequently tested as adults for their ability to thermoregulate.
3. On exposure to an ambient temperature of 41° C, adult rats which had been capsaicin-desensitized as neonates were unable to thermoregulate against overheating by means of autonomic responses whereas control littermates could maintain normal rectal temperature. However, autonomic thermoregulation against cold was unimpaired in the desensitized rats.
4. Skin-cooling operant behavior in heat stress was impaired in adult rats which had been capsaicin-desensitized as neonates whereas their skin-heating behavior was not different from that of control littermates.
5. These results suggest that the central and peripheral warm-receptors responsible for thermoregulation in the neonate rat are functionally mature at least inasmuch as they form a part of thermoregulatory system involved in lowering body temperature and can be desensitized by capsaicin. Moreover, such receptors, once desensitized 8–10 days after birth, apparently do not regain their function and are not regenerated or replaced during subsequent maturation of the animal.

     

Some properties of the junctional and extrajunctional receptors in the vas deferens of the guinea-pig

1. Pharmacological properties of the neuromuscular junction in the isolated hypogastric nerve-vas deferens preparation of the guinea-pig were studied using the sucrosegap technique.
2. Earlier observations concerning the ineffectiveness of α-adrenergic blocking agents on transmission were confirmed.
3. Noradrenaline exerted a dual influence on the nerve-mediated contraction, i.e. inhibitory at a low concentration (10^?8 to 10^?7 g/ml) but potentiating at a higher concentration.
4. Noradrenaline invariably reduced the size of the excitatory junction potential (EJP) without altering the resting potential. This effect was not blocked by β-adrenergic blocking agents. The inhibitory action of a low concentration of noradrenaline may be accounted for by this EJP-suppressing effect.
5. In the presence of an α-adrenergic blocking agent, noradrenaline reduced the height of nerve-induced contraction even at a high concentration. This is explained by the selective blocking of the potentiating effect without altering the EJP-depression.
6. Tyramine reduced the height of nerve-mediated contraction.
7. These experimental results can consistently be explained by assuming the presence of two different kinds of adrenergic receptors in the vas deferens, ‘junctional’ and ‘extrajunctional’. While the extrajunctional receptors are typical α-type receptors, the junctional receptors are resistant to both α- and β-blocking agents, and seem to be desensitized by noradrenaline.
8. The K⁺-contracture was also reduced in size by the combination of dibenamine and noradrenaline. The assumption that the transmitter released from depolarized nerve-endings would contribute to the height of K⁺-contracture was substantiated by experiments using reserpinized vas deferens.

     

Acute effects of food, 2-deoxy-d-glucose and noradrenaline on metabolic rate and brown adipose tissue in normal and atropinised lean and obese (fa/fa) Zucker rats

1. Intragastric feeding (40 kJ) produced a 17% rise in metabolic rate in lean Zucker rats but only an 8% increase in obese (fa/fa) rats, and both of these responses were significantly reduced by β-adrenergic blockade with propranolol (10 mg/kg, s.c.).
2. Parasympathetic blockade with atropine (0.5 mg/kg, s.c.) caused a doubling of the response to food in lean rats and a threefold increase in the obese mutants, such that all atropinised animals showed the same increase in metabolic rate after food.
3. Feeding also caused a significant rise in interscapular brown adipose tissue temperature, which was greatest in the lean animals and was enhanced by atropine in both groups.
4. Injection of noradrenaline (250 μg/kg, s.c.) caused a similar (40%) rise in metabolic rate in lean and obese animals but this response was unaffected by atropine.
5. 2-Deoxy-d-glucose injection (360 mg/kg, s.c.) depressed oxygen consumption by 25 and 8% in lean and obese rats respectively and this effect was totally abolished by atropine.
6. These results suggest that the rise in metabolic rate after a meal is partly due to sympathetic activation of brown adipose tissue. The reduced thermic response in obese Zucker rats is not due to insensitivity to noradrenaline, but may be partly due to parasympathetic inhibition of thermogenesis and partly to insensitivity to glucose availability.

     

Regional differences in electrolyte,short-chain fatty acid and water absorption in the hindgut of two species of arboreal marsupilas

1. Short-chain fatty acid, electrolyte and water absorption from the hindgut of two arboreal marsupial species, the greater glider (Petauroides volans) and the brushtail possum (Trichosurus vulpecula) were studied in vivo using a single perfusion technique.
2. Qualitative and quantitative differences in the net movement of sodium, potassium and chloride were found between the different hindgut segments and between the two species. All transport processes exhibited active characteristics. Net Na⁺ transport in all segments was concentration-dependent in the range of 45–135 mmol·l^?1 Na⁺. The proximal colon of the greater glider showed a net Na⁺, Cl^? and water secretion and K⁺ absorption, all electrolyte movements being against the electrochemical gradient.
3. Water followed passively the osmotic gradient generated mainly by the net movement of Na⁺.
4. Short-chain fatty acids were absorbed according to their chain length in a constant ratio of 1.0:1.2:1.3 for acetate, propionate and butyrate, respectively.
5. Our data indicate that absorptive and secretory processes in the hindgut of these marsupials are basically similar to those of eutherians, even in epithelia differing significantly in the direction of net solute transport.

     

Cell volume regulation in goldfish intestinal mucosa

1. Ion and water content of goldfish intestinal mucosa, stripped free from muscular layers were measured under various incubation conditions.
2. Ouabain induces an increase in cation content that is electrically compensated for by chloride. The increase in solute content is accompanied by an increase in water content.
3. When extracellular chloride is partially replaced by sulphate, ouabain does induce cell shrinkage.
4. Anoxia induces a rapid increase in cell volume that is restored by oxygenation of the incubation solution. Ouabain prevents the restoration of volume.
5. It is concluded that the classical ouabain-sensitive Na/K pump participates in the maintenance of cellular volume. We suggest that the constancy in volume after ouabain poisoning as is reported for many tissues might be due to a low chloride conductance of its membranes.
6. Anisotonic media (range: 0.6–1.2 isotonicity), made by variation in mannitol concentration, induced changes in cell water content that deviates from the simplified van 't Hoff equation by about 10%. No change in water content after the initial increase was found.
7. We conclude that goldfish enterocytes do not possess a mechanism for rapid volume readjustment.

     

Influence of noradrenaline on blood flow to brown adipose tissue in rats exhibiting diet-induced thermogenesis

1. The influence of noradrenaline on regional blood flow was determined using radioactive microspheres in rats maintained on either stock diet or a palatable cafeteria diet.
2. Cardiac output and blood flow to brain, lungs, liver and skeletal muscle were similar for rats on the two diets.
3. Blood flow to total dissectable brown adipose tissue in control and cafeteria rats represented 1 and 2% of cardiac output respectively but these values rose to 7 and 15.5% during infusion of noradrenaline.
4. Arterial oxygen content was similar for all groups but the oxygen content of venous blood draining the interscapular brown adipose tissue fell to 6 ml O₂/100 ml blood in control rats and 1 ml/100 ml in cafeteria rats after noradrenaline.
5. The total oxygen consumption of brown adipose tissue was calculated and found to account for 42% of the response to noradrenaline in control rats and 74% in cafeteria animals. The increments in the oxygen consumption of other tissues were almost identical in both groups and so all the diet-induced changes in thermogenic capacity can be attributed to increases in brown adipose tissue metabolism.
6. These findings demonstrate the quantitative importance of brown adipose tissue in diet-induced thermogenesis and confirm the similarities between diet and non-shivering thermogenesis.

     

Batrachotoxin protects sodium channels from the blocking action of oenanthotoxin

1. The blocking action of oenanthotoxin (OETX) and butanol on Na⁺ channels was studied in voltage clamp experiments on single myelinated nerve fibres treated by batrachotoxin (BTX).
2. OETX (40 μM) blocked Na⁺ currents through normal channels but did not affect significantly the BTX modified Na⁺ current.
3. BTX removed the depolarization-induced charge immobilization and slowed down significantly the OFF charge movement. However, the maximum charge displaced, as well as the kinetics of the ON charge movement during a strong membrane depolarization, remained unchanged.
4. OETX blocked the charge movement in normal Na⁺ channels but did not affect noticeably the charge movement modified by BTX.
5. BTX did not modify the K⁺ currents and did not protect them from the blocking action of OETX.
6. Butanol (0.01–0.1 M) decreased almost identically and reversibly both normal and BTX-modified Na⁺ currents.
7. It is concluded that binding of BTX to its receptor protects the Na⁺ channel from interaction with OETX but left it accessible to butanol.

     

Actions and cross-reactivity of antiallergic agents and a calcium channel antagonist on rat peritoneal mast cells. Difference in the action mechanisms and cross-reactivity among the agents

The actions of the antiallergic agents, disodium chromoglycate (DSCG), tranilast and ketotifen, and of a calcium channel antagonist, nicardipine, and cross-reactivity among the agents were examined by observing the inhibition of⁴⁵Ca uptake and histamine release in rat mast cells stimulated by antigen and compound 48/80 (comp. 48/80).

1. All agents inhibited⁴⁵Ca uptake and histamine release in mast cells stimulated by antigen. The inhibition of⁴⁵Ca uptake by the antiallergic agents paralleled the inhibition of histamine release, while nicardipine inhibition of⁴⁵Ca uptake was stronger than its inhibition of histamine release.
2. The action of DSCG on⁴⁵Ca uptake and histamine release was significantly decreased in cells stimulated with antigen and phosphatidylserine (PS), while tranilast inhibition of histamine release was not affected by the addition of PS despite a significant decrease in the inhibition of⁴⁵Ca uptake.
3. The inhibitory effect of DSCG and tranilast was significantly lower in mast cells stimulated by comp. 48/80 than in the cells stimulated by antigen.
4. Tachyphylaxis was observed in cells re-exposed to DSCG and tranilast following previous exposure to the agents.
5. Cross-reactivity was found between DSCG and tranilast.

     

Reabsorption of monocarboxylic acids in the proximal tubule of the rat kidney

1. Renal handling of pig-and rat-insulin was studied in the isolated perfused rat kidney.
2. Metabolic clearance rates of both pig- and rat-insulin excceded GFR.
3. Peritubular uptake of pig-insulin accounted for 13%, of rat-insulin for 31% of the total metabolic clearance.
4. The nonfiltering kidney does not remove insulin from the peritubular circulation.
5. Metabolic clearance rates of pig- and rat-insulin are directly related to GFR.
6. The filtration process seems to be necessary for the uptake of insulin at the peritubular site.

     

Glomerular tubular balance of renald-glucose transport during hyperglycemia

d-Glucose transport in the kidney of glucose loaded rats was investigated using clearance and micropuncture techniques. The range of plasma glucose concentration in clearance experiments was 20–140 mmol·l^?1 and in micropuncture experiments 17–94 mmol·l^?1.

1. During hyperglycemia, the glucose concentration in endproximal tubular fluid was elevated above that in arterial plasma. At plasma concentrations above 60 mmol l^?1 intratubular glucose concentration was found to be about 1.2 times higher than in plasma.
2. At endproximal puncture sites TF/P_osmol was unity throughout the investigated range of hyperglycemia.
3. Proximal tubular glucose reabsorption during hyperglycemia is close to saturation which is compatible to aK _m=10.8 mmol l^?1 as determined previously.
4. Passive glucose permeability does not change during hyperglycemia. The permeability constant of 2.03·10^?5 cm·s^?1 does not differ significantly from that during normoglycemia, 1.9·10^?5 cm·s^?1.
5. Single nephron glomerular filtration rate (SNGFR) and fluid reabsorption in the proximal convolution (C) were significantly correlated during hyperglycemia (r=0.78,P<0.001). Fractional volume reabsorption during hyperglycemia was decreased to 0.36 as compared to control, but during hyperglycemia it was not affected by the magnitude of the glucose plasma concentration.
6. During hyperglycemia, proximal tubular glucose reabsorption (T_G) was correlated to SNGFR (r=0.64,P<0.001). This relation became insignificant when the influence of volume reabsorption (C) is controlled for (r=0.17,P>0.5). However, the significance of the correlation between T_G and C persists when the influence of SNGFR is held constant.
7. Calculations indicate that when glucose reabsorption was doubled, et sodium transport was increased about fourfold.
8. In hyperglycemia, renal transport rate (T_G), when factored by renal glomerular filtration rate (GFR) seems to be linearly related to glucose plasma concentration. Up to endproximal puncture site 25.5% and by the entire kidney 68.2% of the tubular glucose load were reabsorbed. The difference may be attributed either to glucose transport systems which are localized distal to the proximal convoluted tubules and/or to an inhomogenity of the glucose transport in the different types of nephrons.

     

Molybdenum toxicity: Interactions between copper,molybdenum and sulphate

Molybdenum toxicity and the interactions between copper, molybdenum and sulphate are reviewed. The main signs of molybdenum poisoning are poor growth and anaemia (rat, chick, rabbit, cattle and sheep), anorexia (rat), diarrhoea and achromotrichia (cattle and sheep), joint and bone deformities (rat, rabbit, cattle), central nervous system degeneration and loss of crimp in wool (sheep). The following topics are discussed:

1. The effect of sulphate and sulphur compounds on molybdenum toxicity.
2. The effect of molybdenum on tissue copper levels.
3. The effect of molybdenum on the distribution of copper in plasma.
4. The effect of molybden8m on uptake and excretion of copper.
5. The possible existence of copper(II) molybdate in vivo.
6. The influence of molybdenum on sulphide production by ruminal micro-organisms.
7. Competition between molybdenum and sulphate in intestinal transport.
8. Interaction of sulphur with copper in vivo.
9. The possible involvement of molybdenum in gout and multiple sclerosis in humans.

     

Calibration and performance of a small animal gradient layer calorimeter box

Calorimetry, using the gradient layer technique, has become well established in the study of energy metabolism. The use of a commercially constructed gradient layer box within a calorimetry system designed to measure directly and indirectly the metabolic sequelae of thermal injury in rats, is described. Variations in the signal output were discovered. These were found to be dependent upon:

1. stability of the ambient temperature
2. stability of the gradient layer box water jacket temperature
3. position and size of the calibrating heat source.

Calibration with heat sources which simulate the heat emission from a rat, established that a measurement accuracy of ±2% can be achieved by controlling (a) and (b)     

Vasopressin-mediated blood pressure response to intraventricular injection of angiotensin II in the rat

1. The role of stimulation of argininevasopressin (AVP) release in the blood pressure (BP) response to intracerebroventricular (ivt) injection of angiotensin II (AII) was investigated.
2. Ivt injection of AII to normal Long-Evans (LE) rats, which were conscious and unrestrained, induced a dose-related increase of BP in close correlation with the rise of plasma AVP concentrations (r=0.93;y=34.0 log X-14.4). This regression line crossed the X-axis at plasma AVP concentrations found under control conditions.
3. In comparison with the correlation obtained after intravenous injection of AVP (r=0.99;y=35.6 log X-46.9), the correlation between BP increase and plasma AVP after ivt AII exhibited a parallel shift to the left by a factor of 7.5.
4. When 0.5 ml of a specific AVP antiserum was injected intravenously, the BP response to subsequent ivt injection of AII was completely blocked in 2 of 7 rats tested and reduced by 50% or more in the other 5 rats.
5. In Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus (DI), in which plasma AVP remained undetectable after ivt AII, BP response was reduced by 50–80% in comparison with the response in LE rats. Drinking response, however, was not altered. During spontaneous drinking, DI rats showed a BP increase of similar magnitude as that after the highest dose of ivt AII.
6. We conclude that a close relationship exists in normal LE rats between the rise of BP and of plasma AVP after ivt AII; this correlation represents a cause-effect relationship, since after the intravenous injection of AVP antiserum the BP response to ivt AII is markedly or completely blocked; and sensitization to the vasopressor effect of AVP occurs after ivt AII. The BP increase observed in unrestrained DI rats after ivt AII as well as during spontaneous drinking might be related to a general arousal reaction which would be insignificant in normal LE rats.

     

Fast bicarbonate-chloride exchange between plasma and brain extracellular fluid at maintainedP_{CO_2 }

The aim of this paper was to investigate the kinetics and mechanism of bicarbonate exchange at the blood-brain ECF barrier. The experiments were performed on anaesthetized and artificially ventilated cats in such a way that acid-base parameters of the brain extracellular fluid were continuously measured while an approximately rectangular increase in the arterial plasma bicarbonate concentration was produced at maintained \(P_{CO_2 } \) . The results from such a preparation were:

1. A rapid increase in the brain extracellular bicarbonate concentration was observed in response to an i.v. bolus injection of 3 ml molar NaHCO₃. The bolus was followed by a slow infusion of bicarbonate solution. The brain extracellular bicarbonate reached a new steady state within a minute.
2. This increase was almost simultaneously accompanied by a decrease in the extracellular chloride concentration. The HCO ₃ ^? ?Cl^? exchange ratio very closely approached one.
3. The extracellular bicarbonate concentration in the brain, after an initial increase, returned towards control in spite of elevated arterial bicarbonate at maintained \(P_{CO_2 } \) .
4. The results are discussed in terms of a 5-compartment model, where the extracellular fluid is interposed between the glial cells and the interstitial side of the endothelial cells, similar to the blood plasma being interposed between the red cells and the luminal side of the endothelial cells.
5. A non-electrogenic carrier-mediated HCO ₃ ^? ?Cl^? exchange at the interphase of the blood brain barrier is postulated.

     

Optokinetic,vestibular, and optokinetic-vestibular responses in albino and pigmented rats

Horizontal eye movements and neuronal activity in the vestibular nuclei and pretectum were recorded in albino and pigmented rats in response to optokinetic, vestibular (VS), combined visual-vestibular (VVS) sinusoidal stimulations.

1. VOR slow phase velocity in VS condition leads head velocity. This phase lead is smaller in albino than in pigmented rats.
2. Presence of vision (VVS) improves the phase angle of the VOR in both strains, especially at low frequencies. In pigmented rats the VOR is perfectly compensatory with respect to phase at all frequencies whereas in albinos the eye velocity still leads the head velocity.
3. There is no difference in the response characteristics of vestibular nuclear neurons (VN) to VS between albino and pigmented rats which could explain the difference in their VORs.
4. In the pigmented rat, there is a strong optokinetic input to VN which provokes a shift of the response peak towards peak head velocity. These visual-vestibular interactions at VN level are in agreement with the changes in the phase angle of the VOR.
5. In albino rat, there are no differences in the response characteristics of VN between VS and VVS, thus the decrease of the VOR phase lead observed in VVS compared to VS is due either to visual-vestibular interactions outside of the vestibular nuclei or to some general arousing effect of light.
6. Recording of responses of pretectal neurons to visual stimulation in albino rats has shown that they are activated in a phasic or tonic way by light on (“On cells”) or off (“Off cells”). Contrary to the pigmented rat, pretectal neurons in albino exhibited no detectable direction specific optokinetic responses.

     

Effects of Cs on acetylcholine induced current

1. 20 mM Cs⁺ ions reduce background current and decrease drastically the K⁺ depletion process, probably as a consequence of the reduction ofi _K1. The background current-voltage relationship becomes linear.
2. 20 mM Cs⁺ ions completely abolish the current induced by acetylcholine.
3. The possibility that the K⁺ current induced by acetylcholine is due to an increase ofi _K1 is discussed.

     

Pancreatic secretory response to cholecystokinin-pancreozymin and caerulein in the conscious rat

1. The effects of graded intravenous doses of cholecystokinin (CCK) and caerulein on exocrine pancreatic secretion have, been assessed in conscious rats. Bile and pancreatic juice were separately returned to the duodenum between and during tests.
2. Low doses of CCK (from 417 to 3,335 ng kg^?1 h^?1) or caerulein (from 37.5 to 150 ng kg^?1 h^?1) slightly increased flow rate but increased K⁺ and HCO ₃ ^? outputs to a greater extent, without altering Cl^? output. The sum of the anion concentrations (Cl^?+HCO ₃ ^? ) stayed constant, which explains the decrease in Cl^? concentration when the HCO ₃ ^? concentration increased.
3. High doses of CCK (6,670 and 13,335 ng kg^?1 h^?1) and of caerulein (600 ng kg^?1 h^?1 strongly inhibited volume flow and outputs of all the ions, and the sum of the concentrations of anions fell.
4. Protein concentration and output increased with the same time course in response to both CCK and caerulein, i. e. course in response to both CCK and caerulein, i. e. a sustained stimulation during infusion, without any delayed inhibitory effect afterwards. The increase followed a linear dose-response relation to both CCK and caerulein. D50 was approximately 1,000 ng kg^?1 h^?1 for CCK and 95 ng kg^?1 h^?1 for caerulein. The maximal secretory rate of protein in our experiments was obtained with 300 ng kg^?1 h^?1 caerulein (20.27 mg 30 min^?1) and was almost twice that obtained with CCK (10.6 mg 30 min^?1) which suggests that the most potent agonist is a shorter derivative of CCK. Finally, both hormones decreased protein output at supramaximal levels.
5. It is concluded that both CCK and caerulein have similar effects on pancreatic secretion in the conscious rat and in other species. However, the conscious rat differs from other species in that water, HCO ₃ ^? and K⁺ secretions are stimulated by low doses of agonists. In contrast, high doses of agonists inhibited all components of secretion.

     

Thermoregulation in the diabetic-obese (db/db) mouse

1. Thermoregulation and non-shivering thermogenesis have been studied in the genetically diabeticobese (db/db) mouse.
2. At all environmental temperatures between 33 and 10°C the body temperature of the diabetic mice was lower than that of the normal littermates, the difference varying from 1.1°C at 33°C to 4.5°C at 10°C.
3. At 4°C the diabetic mice rapidly died (3.2 h) of hypothermia while the normal mice maintained their body temperature within the normal range.
4. At 23°C the diabetic animals exhibited a diurnal rhythm in body temperature which was similar in both phase and amplitude to the controls, but at every point throughout the 24h cycle the temperature of the mutants was lower by 1–2°C.
5. The resting metabolic rate at thermoneutrality (33°C) was higherper whole animal for the diabetics than for the normals. However, at temperatures below thermoneutrality the converse was observed; between 30 and 4°C the RMR of the mutants was lower than the controls by approximately 25%.
6. The capacity for non-shivering thermogenesis in diabetic mice was only one-half that found in normal animals.
7. The diabetic mouse has abnormalities in thermoregulation and non-shivering thermogenesis which are similar to those found in the genetically obese (ob/ob) mouse.

It is concluded that the high metabolic efficiency of the diabetic mouse, like that of the ob/ob mouse, can be explained by a reduced energy expenditure on thermoregulatory thermogenesis; this may represent a primary mechanism for the operation of the “thrifty genotype” associated with obesity and diabetes.     

Effects of a chronic corticotropin treatment on brown adipose tissue of cold acclimated rats

1. This study deales with the effects of chronic corticotropin treatment (daily injection of 2U · kg^?1 i.p. for 10 days) upon the lipolytic action of norepinephrine (NE) on abdominal and interscapular brown adipose tissues (BAT) and on epididymal white fat of rats acclimated to either 28°C or 5°C and compared to controls.
2. In incubated BAT pieces from both 28°C and 5°C control animals no stimulation of lipolysis (release of glycerol and fatty acids) was induced by NE (10^?4 mol). A similar absence of effect was observed in BAT from corticotropin-treated rats. In epididymal fat, the in vitro enhancement of lipolysis by NE (300–400%) in controls was not modified in ACTH-treated rats.
3. The in vivo lipolysis in interscapular BAT was estimated by determining the arteriovenous differences in free glycerol and fatty acids levels and measuring blood flow. In control animals the blood flow stimulation by NE and the in situ utilization of the hydrolyzed fatty acids were larger in 5°C rats than in 28°C ones. In corticotropin-treated animals compared to controls, blood flow stimulation and fatty acid utilization were enhanced in 28°C group, and in opposite they were reduced in 5°C group; no significant difference was observed between the two groups.
4. It is concluded that chronic corticotropin treatment induces a “pseudo cold-acclimation” of BAT in 28°C rats and, inversely, a “loss of acclimation” in cold-acclimated ones. These opposite effects may be related to both the corticotropic and lipolytic action of the hormone.

     

Sleep, brain energy levels, and food intake

Background

The feeling of hunger and feeding, a wake–state-dependent behavior, is regulated by specific centers within the hypothalamus. While paraventricular nucleus (PVN), arcuate nucleus (ARC), and dorso- and ventromedial hypothalamus (DMH/VMH) regulate feeding, the lateral hypothalamus (LH) is associated both with feeding and wake/REM sleep regulation. In order to examine the effects of sleep and wakefulness on food intake and body weight, we also measured hypothalamic ATP concentrations, which are known to be involved in feeding behavior and sleep–wake regulation.

Methods

In rats, food intake and body weight was measured during a 24-h light–dark cycle and during 6 h of sleep deprivation (SD) performed by gentle handling. Tissue samples from the PVN, ARC/DMH/VMH, and LH were collected after 6 h of SD and from time-matched diurnal controls. ATP was measured by luciferin-luciferase bioluminescence assay.

Results

Across the 24-h light–dark period, rats consumed approximately 28.13±4.48 g of food and gained 5.22±1.65 g with a positive correlation between food intake and body weight. During SD, while food intake increased significantly +147.31±6.13%, they lost weight significantly (–93.29±13.64%) when compared to undisturbed controls. SD resulted in a significant decrease in ATP levels only in LH (–44.60±21.13%) with no change in PVN, ARC/DMH/VMH region when compared with undisturbed controls.

Conclusion

The results indicate a strong overall correlation between ATP concentrations in the LH and individual food intake and suggest a sleep–wake dependent neuronal control of food intake and body weight.