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Biomedical subjects

D Richard

Publications and source records attributed to D Richard.

At least 91 records · Page 5Linked to original sources
PubMed1996

Effect of dexfenfluramine on the transcriptional activation of CRF and its type 1 receptor within the paraventricular nucleus of the rat hypothalamus.

1. The present study investigated the effect of intraperitoneal (i.p.) administration of the indirect 5-hydroxytryptamine (5-HT) receptor agonist, dexfenfluramine, on the transcriptional activity of corticotropin-releasing factor (CRF) and its type 1 receptor in the brains of conscious male Sprague-Dawley rats via in situ hybridization histochemistry (ISHH) using both intronic and exonic probe technology. 2. The immediate early gene (IEG) c-fos mRNA was also used as index of cellular activity, whereas localization between CRF-immunoreactive (ir) perikarya and the IEG was accomplished to determine the site of CRF neuronal activation in the brain of dexfenfluramine-treated rats. 3. Thirty minutes, 1, 3, and 6 h after a single injection of either dexfenfluramine (10 mg kg-1) or the vehicle solution, adult male rats (230-260 g) were deeply anaesthetized and rapidly perfused with a 4% paraformaldehyde-borax solution (PF). The brains were removed from the skull, postfixed, and placed in a solution of 4% PF-10% sucrose overnight at 4 degrees C. Frozen brains were mounted on a microtome and cut from the olfactory bulb to the medulla in 30-microns coronal sections. 4. Dexfenfluramine induced a general neuronal activation as indicated by the strong signal of c-fos mRNA in several structures of the brain, including the parietal cortex, caudate putamen, circumventricular organs, medial preoptic area, bed nucleus of the stria terminalis, choroid plexus, choroidal fissure, supraoptic nucleus, paraventricular nucleus of the hypothalamus (PVN), paraventricular nucleus of the thalamus, central nucleus of the amygdala, dorsomedial nucleus of the hypothalamus, laterodorsal tegmental nucleus, locus coeruleus, and several subdivisions of the dorsal vagal complex. In most of these structures, the signal was maximal at 30 min, still strong and positive at 60 min, largely decreased at 3 h, and had completely disappeared 6 h after injection. 5. In the parvocellular division of the PVN, the large majority of CRF-ir perikarya displayed a positive signal for the mRNA encoding c-fos, indicating a profound CRFergic activation within this neuroendocrine nucleus after dexfenfluramine administration. 6. Colocalization between CRF-ir neurones and c-fos positive cells was not detected in any other regions. This selective activation of PVN CRF neurones was also confirmed by the presence of CRF primary transcript; 30 min after i.p. injection of the indirect 5-HT agonist, a positive signal for CRF hnRNA was observed, specifically in the parvocellular PVN. 7. Transcription of the gene encoding the type 1 receptor for CRF was highly stimulated in the PVN following 5-HT activation. Although this hypothalamic nucleus exhibited a barely detectable signal under basal conditions, dexfenfluramine induced a strong signal of CRF1 receptor mRNA in the parvocellular PVN. Interestingly, CRF-ir neurones displayed a positive signal for the mRNA encoding the CRF1 receptor, 3 and 6 h after systemic treatment with dexfenfluramine. 8. These results indicate that although dexfenfluramine can generate a wide neuronal activation throughout the brain, this 5-HT agonist triggers the activity of CRF neurones selectively in the parvocellular division of the PVN, a mechanism possibly related to the activity of hypothalamic-pituitary-adrenal axis. Induction of CRF1 receptor mRNA in CRF cells of the PVN indicates that neuroendocrine CRF neurones can be targeted by CNS CRF under 5-HT stimulation.

Animals↗
PubMed1996

Involvement of type I corticosteroid receptor in the effects of ovariectomy on energy balance.

The effects of the glucocorticoid receptor antagonist, RU-38486 (RU-486), and the mineralocorticoid receptor (MR) antagonist, RU-28318, on energy balance were investigated in a 2 [surgery: ovariectomy (OVX) and sham operation] x 3 (corticosteroid antagonist: placebo, RU-28318, RU-486) experimental design. Rats were treated for 28 days. Food intake and body weight were monitored throughout the treatment period. At the end of the treatment, rats were killed and their carcasses were analyzed for energy and nitrogen contents. Energy content was determined by adiabatic bomb calorimetry, whereas nitrogen was determined in 250-to 300-mg samples of dehydrated carcasses, with the use of the Kjeldahl procedure. The energy as protein was subtracted from total carcass energy to determine energy as fat. The gains in energy, fat, and protein were calculated by subtracting the values obtained at the end of the treatment period from initial values estimated from the body weights measured at the beginning of the experiment. A significant interaction effect of surgery and corticosteroid antagonist was observed on body energy gain, energetic efficiency, and fat gain. Whereas body energy gain, energetic efficiency, and fat gain were larger in OVX rats than in sham-operated animals treated with either placebo or RU-486, they were comparable in OVX and sham-operated rats treated with RU-28318. Surgery, but not corticosteroid antagonist, had a significant effect on digestible energy intake, energy expenditure, and protein gain. All these variables were higher in OVX rats than in sham-operated animals. Surgery also affected corticosterone levels and adrenal weight. Both of these variables were lower in OVX rats than in sham-operated animals. By demonstrating the ability of RU-28318 to attenuate the effects of OVX on energy balance, the present study provides evidence that MR occupation by corticosteroids facilitates the OVX-induced changes in energy balance.

Animals↗
PubMed1996

Role of CRH in the effects of 5-HT-receptor agonists on food intake and metabolic rate.

Two series of experiments were conducted to investigate the role of corticotropin-releasing hormone (CRH) in the effects of 5-hydroxytryptamine (5-HT) on energy intake and energy expenditure. The first set of experiments was carried out to confirm the influence of 5-HT1A-, 5-HT1B-, 5-HT2A/2C-receptor agonists on the activation of the hypothalamic-pituitary-adrenal axis. Plasma corticosterone levels were measured, and a double-immunolabeling procedure was used to determine whether the neuronal activity marker, c-Fos protein (Fos), could be found within brain neurons containing CRH after treatments with 5-HT1A-, 5-HT1B-, 5-HT2A/2C-receptor agonists. The second series of experiments was conducted to assess the involvement of CRH in the effects of 5-HT on food intake and metabolic rate (VO2). The effects of the 5-HT1A-, 5-HT1B-, 5-HT2A/2C-receptor agonists on food intake and VO2 were measured in rats treated with the CRH antagonist, alpha-helical CRH-(9-41). In both experiments rats were intraperitoneally injected with either a vehicle (NaCl 0.9%), the 5-HT1A-receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT), the 5-HT1B-receptor agonist 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridinyl)-1H-indole succinate (RU-24969), or the 5-HT2A/2C-receptor agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). Fos immunoreactivity was detectable within the CRH-containing neurons of the paraventricular nucleus of the hypothalamus (PVH) after injection of each of the 5-HT-receptor agonists used. The CRH antagonist alpha-helical CRH-(9-41) attenuated the increases in metabolic rate induced by DOI and 8-OH-DPAT. alpha-Helical CRH did not, however, prevent the effects of RU-24969 and DOI on either nocturnal metabolic rate or food intake. The present results provide further evidence for a role of CRH in 5-HT-mediated thermogenic effect, which likely involves the 5-HT2A/2C receptor during the day and the 5-HT1A receptor during the night. Moreover, these results do not support a role for CRH in 5-HT anorectic effects, which likely involves 5-HT1B and 5-HT2A/2C receptors. Finally, the results of this study indicate that the stimulation of CRH-containing neurons located in the PVH does not necessarily predict changes in food intake and energy expenditure.

Animals↗
PubMed1996

Expression of corticotropin-releasing factor and its receptors in the brain of lean and obese Zucker rats.

Expression of CRF messenger RNA (mRNA) and heteronuclear RNA (hnRNA) as well as the mRNAs encoding the CRF receptors of type 1 (CRF1R) and type 2 alpha (CFR2R) in the brain has been investigated in lean (Fa/?) and obese (fa/fa) Zucker rats. Exonic and intronic in situ hybridization histochemistry was employed to measure the mRNA and hnRNA levels in rats killed before (resting state), during, and 120 min after a treadmill running session. The resting expression of CRF hnRNA in the hypothalamic paraventricular nucleus (PVN) of obese rats was minimal and comparable to that of lean rats. However, during treadmill running, this expression was higher in obese than in lean rats. In obese rats, the transcription of the CRF1R mRNA in the PVN was high under resting conditions, dropped considerably during running, and rose again to elevated levels 120 min after the treadmill session. In lean rats, CRF1R mRNA in the PVN was minimal before and during running, but rose to a value similar to that in obese rats 120 min after running. In the PVN of obese rats, expression of the CRF1R gene measured during resting conditions was comparable to the level seen after running and proved to be dependent upon the feeding state of the rats. Expression of the CRF2R transcript was reduced in the ventromedial nucleus of the hypothalamus (VMH) of the obese rat. Plasma ACTH concentrations during treadmill running were lower in obese than in lean animals. Basal and postrunning levels of circulating corticosterone were higher in fa/fa than in Fa/? rats. However, there was no difference in corticosterone levels between lean and obese animals during running. The present results provide evidence for differences between lean and obese rats in the expression of CRF and its receptor within selective hypothalamic nuclei. Given the anorectic and thermogenic properties of CRF and the roles of PVN and VMH in the regulation of energy balance, it can be argued that the observed alterations in the biosynthesis of CRF and its receptors within the PVN and VMH might be related to the development of obesity.

Adrenocorticotropic Hormone↗
PubMed1995

Synaptic control of rat supraoptic neurones during osmotic stimulation of the organum vasculosum lamina terminalis in vitro.

1. The effects of osmotic or electrical stimulation of the organum vasculosum lamina terminalis (OVLT) were examined during intracellular recordings (32 degrees C) obtained from ninety-five supraoptic nucleus magnocellular neurosecretory cells (MNCs) in superfused explants of rat hypothalamus. 2. Brief (10-20 s) applications of hypertonic and hypotonic solutions to the area of the OVLT caused prolonged (> 1 min) increases and decreases, respectively, in electrical activity in seventy of seventy-four trials performed on neurones with membrane potentials near spike threshold (approximately -55 mV). Changes in firing frequency were related to changes in external osmolality in a dose-dependent manner between 275 and 355 mosmol kg-1. 3. When 30 s periods recorded immediately before, and 30 s following, the application of an osmotic stimulus were examined, the frequency of spontaneous EPSPs (sEPSPs) was related in a dose-dependent manner to the osmolality of the solution superfusing the OVLT region. The increased EPSP frequency was maintained and did not adapt if the osmolality of the medium was raised for periods of > 10 min. In contrast, the frequency of spontaneous IPSPs (sIPSPs) was virtually unaffected by changes in external osmotic pressure. 4. Osmotically evoked changes in MNC firing were strongly correlated with accompanying changes in the frequency of sEPSPs (slope, 0.9; correlation coefficient (r) = 0.7), but not sIPSPs (r = 0.2), suggesting that changes in firing rate following osmotic stimulation of the OVLT are selectively mediated by changes in synaptic excitation. 5. In the presence of bicuculline (5-10 microM), electrical stimulation of the OVLT evoked fast EPSPs in forty-seven of forty-eight MNCs tested. These responses were reversibly reduced by application of 20-40 microM kynurenic acid (n = 3) or 20-40 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; n = 11). Similarly, bath application of CNQX (n = 3) or kynurenic acid (n = 4) reversibly abolished the excitatory response of supraoptic neurones following hypertonic stimulation of the OVLT. 6. Brief (10-15 s) applications of gamma-aminobutyric acid (GABA) over the OVLT reversibly abolished increases in sEPSP frequency and action potential firing rate evoked by hyperosmotic stimulation of the OVLT. In the presence of GABA, the rates of sEPSP and sIPSP frequency were reduced to 37 +/- 10 and 44 +/- 13% (means +/- S.E.M.), respectively, of those observed under isotonic conditions (295 mosmol kg-1). 7. These results suggest that inhibitory and excitatory pathways originating from neurones located within the OVLT are tonically active under resting osmotic conditions in rat hypothalamic explants. Osmotically evoked changes in MNC firing, however, are selectively mediated through increases or decreases in the intensity of the excitatory component of OVLT-derived inputs.

Animals↗
PubMed1995

Expression of a multidrug resistance gene in human rheumatoid synovium.

The objective of this study was to assess the expression of a multidrug resistance (MDR) phenotype, implicated in the cellular resistance of tumor to chemotherapy, in rheumatoid synovial membrane. Synovial membrane from 16 rheumatoid (RA) patients was studied. Six patients with osteoarthritis constituted the control group. The cell membrane expression of the glycoprotein Pgp 170, encoded by the MDR 1 gene, was determined by an immunoperoxidase technique using two different monoclonal antibodies (JSB 1, C 219). The polymerase chain reaction (PCR) methods were used in parallel to detect the presence of the MDR 1 gene mRNA in the synovial cells. Pgp 170 was expressed on the cell membrane of five RA patients and MDR 1 cellular transcription was detected in one other RA patient. We did not observe any association between synovial glycoprotein expression and age, disease activity, and a specific treatment with a long-acting drug. However, MDR protein expression was associated with the successive treatment with more than three disease-modifying antirheumatic drugs (DMARDs). We concluded that the synovial membrane expresses a glycoprotein recognized by the antibodies JSB 1 and C 219. The absence of concomitant MDR 1 transcription suggests the expression of an atypical MDR phenotype in the synovial membrane, distinct from the Pgp 170 encoded by the MDR 1 gene. The implications of the MDR phenotype and the resistance of RA to DMARDs is further discussed.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Acute intraventricular CRF lowers the hoarding threshold in male rats.

The influence of intracerebroventricular rat-CRF on the food-hoarding behavior of rats has been studied in relation to the animals' body weights. A group of six male rats was trained to feed every day from 1000 to 1200 h. Then their threshold for the onset of food hoarding was measured from the intercept of regression line of food hoarded during meal time vs. body weight with the x-axis. Thirty minutes before the hoarding session, the rats received 4 micrograms CRF, or saline control, in the lateral ventricle. The mean threshold for food hoarding was significantly lowered to 299 +/- 61 g after CRF, from control 418 +/- 68 g. Mean food intake during the hoarding sessions was also diminished to 6.0 +/- 0.6 g after CRF, from control 14.5 +/- 0.5 g. These results suggest that the set-point for body weight regulation is acutely lowered by intracerebral CRF.

Animals↗
PubMed1995

Metabolic and hormone-related responses to caffeine in rats.

The time course of effects of caffeine on plasma glucose and non-esterified fatty acids (NEFA) were measured and related to various hormonal responses associated with substrate mobilization and utilization. Participation of the sympatho-adrenal system (SAS) in the metabolic and hormonal actions of caffeine was also investigated by the use of ganglionic blockade. Following 50 mg kg-1 i.p. injections of caffeine in rats, plasma glucose increased 25% and NEFA 40%, and these actions were parallelled by an elevation of plasma insulin, ACTH and corticosterone, without changes in glucagon. It is suggested that the insulin response is related to the plasma glucose increase and possibly also to an action of cAMP. When caffeine was injected in rats previously treated with the ganglionic blocker, hexamethonium, none of the responses mentioned above were modified. These results show that the glucose and NEFA responses are independent of glucagon secretion and are due not only to SAS activation but also to other mechanisms such as the increased ACTH and corticosterone secretion. It is also suggested that the mobilization of substrates by caffeine is mediated, through these various mechanisms, by the activation of cAMP and by phosphodiesterase inhibition.

Adrenocorticotropic Hormone↗
PubMed1995

Functional assessment of the 5-HT 1A-, 1B-, 2A/2C-, and 3-receptor subtypes on food intake and metabolic rate in rats.

The 5-hydroxytryptamine (5-HT) agonists (+/-)-8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT), RU-24969, (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI), and 1-phenylbiguanide were administered to male Wistar rats to assess the respective involvement of the 5-HT 1A-, 1B-, 2A/2C-, and 3-receptor subtypes in the control of food intake and metabolic rate (VO2). Four series of experiments were carried out, each series addressing the effects of four doses (including saline or dose 0) of each of the agonists selected. The drugs were intraperitoneally injected in spontaneously fed animals. Injections were performed during the first 15 min of either the diurnal or the nocturnal phases of the light-dark daily cycle. Food intake and VO2 measurements were carried out over the 12-h periods ensuing after the agonist injections. The two highest doses of the 5-HT1A-receptor agonist 8-OH-DPAT led to a quickly appearing but transient elevation of diurnal VO2. During the night, VO2 was higher when the rats were treated with 8-OH-DPAT than when they were treated with saline. There was no significant effect of 8-OH-DPAT on either diurnal or noctural food intake. The highest dose of RU-24969 induced a significant increase in diurnal VO2, whereas all doses of RU-24969 blunted the nocturnal rise in metabolic rate characteristically observed in rats kept under a daily light-dark cycle. Importantly, RU-24969 induced marked diurnal and nocturnal hypophagia.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Lesion of central nucleus of amygdala promotes fat gain without preventing effect of exercise on energy balance.

Male Wistar rats with intact or lesioned central nucleus of amygdala (CeA) were kept at rest or subjected to a treadmill running program for 21 consecutive days. Food intake and body weight were monitored throughout the exercise training program. At the end of the program, rats were killed and their carcasses processed for analysis of the contents in energy, fat, and protein. Exercise and CeA lesions induced opposite effects on energy balance; exercise delayed gains in body energy and fat, whereas CeA lesions promoted them. Total energy intake was lower in exercised rats than in sedentary ones over the 12 and 24 h that followed exercise. Food intake was higher in lesioned rats than in intact animals over the second half of the 12-h period that followed exercise. There was no interaction effect of exercise and CeA lesions on energy balance and intake and on body composition. Plasma levels of adrenocorticotropin hormone and corticosterone were higher in exercised rats than in sedentary ones, but there was no difference between lesioned and intact rats. This study, as well as confirming the effect of exercise on energy balance, indicates that CeA lesions may promote energy deposition in rats. Above all the present results provide evidence that CeA does not represent a necessary neuroanatomic structure in the effect of exercise on energy balance.

Adipose Tissue↗
PubMed1995

Prolonged episodes of hypoxemia in preterm infants undetectable by cardiorespiratory monitors.

OBJECTIVE: To determine whether episodes of prolonged hypoxemia occur without prolonged apneic pauses (> or = 20 seconds) and without bradycardia (pulse rate, < or = 100 beats per minute) in apparently well preterm infants. METHODS: Long-term recordings of arterial oxygen saturation as measured by pulse oximetry (SpO2), photoplethysmographic (pulse) waveforms from the oximeter, and breathing movements were performed in 96 preterm infants (median gestational age at birth, 34 weeks; range, 28 to 36 weeks) who were breathing room air. Recordings started at a median age of 4 days (range, 1 to 60 days). RESULTS: During a median duration of recording of 25 hours, 88 episodes in which SpO2 fell to 80% or less and remained there for 20 seconds or longer were identified in 15 infants. The median duration of these prolonged desaturations was 27 seconds (range, 20 to 81 seconds). In 73 episodes (83%), SpO2 continued to fall to 60% or less. Twenty-three desaturations were associated with prolonged apneic pauses and 54 with bradycardia; 19 of these were associated with both apnea and bradycardia. Thirty desaturations (34%; 10 infants) occurred without bradycardia and without prolonged apnea. CONCLUSIONS: These results indicate that a proportion of apparently well preterm infants exhibit episodes of severe prolonged hypoxemia unaccompanied by prolonged apneic pauses or bradycardia. Such episodes, therefore, would be difficult to detect if only breathing movements and heart rate are monitored. Indications for the use of oxygenation monitors in preterm infants should be reconsidered.

Apnea↗
PubMed1995

Exercise and the neurobiological control of food intake and energy expenditure.

Knowledge of the effects of exercise in the regulation of energy balance is imperative for the assessment of the value (or limit) of exercise as a therapeutic adjunct in the treatment of obesity. This short review addresses the effects of exercise on the neurobiological control of food intake and energy expenditure. It has been proposed that exercise may affect the regulation of energy balance through the stimulation of corticotropin-releasing hormone (CRH) and neuropeptide Y (NPY). It is likely that the CRH and NPY neuropeptidergic systems exert some degree of control on food intake and energy expenditure. The increase in the CRHergic activity induced by moderately intense exercise would potentiate the effects of muscular activity in reducing energy stores by decreasing energy intake and increasing thermogenesis. Reduced food intake and increased thermogenesis are two of the more recognized biological actions of CRH. Exercise would also contribute to the stimulation of brain NPY neurons by reducing energy stores and plasma insulin levels. By producing orexigenic effects and reducing thermogenesis, activation of the NPY system would tend to oppose the physiological effects of CRH and therefore cancel out the effects of exercise on energy loss.

Body Temperature Regulation↗
PubMed1994

Effects of intracranial injections of scopolamine on olfactory conditioning retrieval in the honeybee.

The role of the cholinergic system on learning abilities and memory performance has been investigated in the honeybee. The behavioural experiment was the olfactory conditioning of the proboscis extension reflex, elicited by an antennal sucrose stimulation. Intracranial scopolamine (0.5 mg/kg) or saline injections (0.25 microliter) were given at different times before or after a one trial learning session in order to interfere with acquisition of information, storage or recall processes. Neither scopolamine injections, ranging from 20 min to 5 min prior to the acquisition task, nor post-trial drug injections given in the same time-window, impaired the retention performance measured one hour after conditioning. Scopolamine injected 20 min after a learning session induced a time-dependent decrease of information retrieval, as was seen in retention testing performed from 5 min to one hour after injection. Then, the amnestic effect of intracranial scopolamine injection seems to be related to a specific and temporary inhibition of recall processes. We can conclude that, in the present task, muscarinic-like receptors are involved in information retrieval but not in acquisition or consolidation processes.

Animals↗
PubMed1994

[Psycho-behavioral disorders in geriatric institution].

Residents in geriatric institutions are progressively older, and they increasingly present psycho-behavioural disorders that affect the function of these institutions. Only after failure of classical medical investigation based on the observed symptoms and seeking a well-defined syndrome and treatment are these disorders attributed to progressive intellectual deterioration which escapes all classical "technical" medical efforts. Drug treatment thus becomes accessory and the disorders must be viewed as complex interactions between the subject and his institutional and familial circles. These interactions are highly pathogenic and feed the symptomatology, aggravating the disorders and producing new symptoms. For this reason, management must be adaptative, aiming at the best possible equilibrium of the subject in the institution. It should also be fully encompassing, engaging the whole of the actors within the institution. The objective can only be attained by a team equipped with gereologic knowledge, used to interdisciplinary work and constantly seeking an explicit institutional aim, taking into account all the required medical, psychological, social, familial, judicial and ethic factors.

Aged↗
PubMed1994

Osmoreceptors, osmoreception, and osmoregulation.

Mammals have evolved sophisticated behavioral and physiological responses to oppose changes in the osmolality of their extracellular fluid. The behavioral approach consists of regulating the intake of salt and water through changes in sodium appetite and thirst. The physiological approach comprises adjustments of renal excretion of water and sodium which are achieved through changes in the release of antidiuretic and natriuretic hormones. Individually, these osmoregulatory responses are controlled by "osmoreceptors": groups of specialized nerve cells capable of transducing changes in external osmotic pressure into meaningful electrical signals. Some of these sensors are located in the region of the hepatic portal vein, a strategic site allowing early detection of the osmotic impact of ingested foods and fluids. Changes in systemic osmolality, however, are detected centrally, within regions that include the medial preoptic area, the median preoptic nucleus, the organum vasculosum lamina terminalis (OVLT), the subfornical organ, and the supraoptic nucleus (SON). While studies have indicated that these central and peripheral osmoreceptors participate in the control of osmoregulatory responses, little is known of the mechanisms by which this is achieved. One notable exception, however, consists of the osmotic control of electrical activity in SON neurons which, in the rat, contributes to the regulation of natriuresis and diuresis through effects on the secretion of oxytocin and vasopressin. Previous studies have shown that these cells are respectively excited and inhibited by hypertonic and hypotonic conditions. Experiments in vitro indicate that these responses result from both the endogenous osmosensitivity of these cells and changes in synaptic drive. Patch-clamp analysis has revealed that SON neurons are respectively depolarized and hyperpolarized by increases and decreases in external osmolality and that these intrinsic responses result from changes in the activity of mechanosensitive cationic channels. Moreover, intracellular recordings in hypothalamic explants have shown that changes in electrical activity are associated with proportional changes in the frequency of glutamatergic excitatory postsynaptic potentials derived from osmosensitive OVLT neurons. Both of these mechanisms, therefore, may participate in the osmotic regulation of neurohypophysial hormone release in situ.

Animals↗
PubMed1994

The effect of caffeine on food intake in rats: involvement of corticotropin-releasing factor and the sympatho-adrenal system.

The involvement of CRH and the sympatho-adrenal system in the effects of caffeine on food intake and body weight gain has been investigated in rats. Food intake and body weight gain were measured in male rats after the treatment with caffeine in combination with either an injection of the CRH antagonist alpha-helical CRH(9-41), a surgical adrenal demedullation (medullectomy), or a ganglionic blockade. Alpha-helical CRH(9-41) was injected in the lateral ventricle of the brain and hexamethonium was used to chemically block the ganglionic transmission. From 4 to 24 h following a caffeine injection, spontaneous food intake, which was cumulated from the time caffeine was injected, was significantly (p < 0.01) lower in caffeine- than in saline-treated rats. In food-deprived rats, the anorectic effect of caffeine was biphasic, being significant at 0.5 and 1 h after the caffeine administration, then vanishing for 3 h, and becoming significant again 6 h after the caffeine administration. In both the spontaneously fed and food-deprived rats, caffeine reduced the rate of weight gain, which was measured at the end of a 12- or a 24-h period following the caffeine injection. A significant (p < 0.05) interaction effect of caffeine and alpha-helical-CRH(9-41) was found on the cumulative food intake at 1, 6, and 8 h, and on the amount of food eaten between the 4-6-h interval following the injection of caffeine; the effects of caffeine on food intake and body weight gain seem largely prevented by the use of a CRH antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1994

Lesions of hypothalamic paraventricular nuclei do not prevent the effect of estradiol on energy and fat balance.

The chronic effects of estradiol (E2) on energy balance have been investigated in ovariectomized rats with hypothalamic paraventricular nuclei (PVH) lesions. Body weight and food intake were monitored throughout the E2 treatment, which lasted 26 days. At the end of this treatment, rats were decapitated, and their carcasses were processed to determine the body contents in energy, fat, and protein. Plasma adrenocorticotropic hormone (ACTH) and corticosterone were determined by radioimmunoassay and protein-binding assay at the end of the study. Regardless of whether they were sham- or PVH-lesioned, E2-treated rats ate, expended, and gained significantly less energy than untreated animals. In addition, E2-treated rats deposited less fat and protein than the rats not receiving E2. In contrast to the E2 treatment, PVH lesions accelerated the gains in energy and fat regardless of whether the rats were treated with E2 or with a placebo. There were no interaction effects of PVH lesions and the E2 treatment on energy or fat gains. Plasma levels of corticosterone and ACTH were higher in E2-treated rats than in animals receiving the placebo treatment. The present results provide evidence that the hypothalamic PVH is not an essential neuroanatomical structure in the effects of E2 on energy and fat balances.

Adipose Tissue↗