scholarly journals μ-Opioid modulation in the rostral solitary nucleus and reticular formation alters taste reactivity: evidence for a suppressive effect on consummatory behavior

2011 ◽  
Vol 301 (3) ◽  
pp. R690-R700 ◽  
Author(s):  
Nicole R. Kinzeler ◽  
Susan P. Travers
Keyword(s):  
Reticular Formation ◽  
Neural Control ◽  
Suppressive Effect ◽  
Neutral Stimulus ◽  
Endogenous Opioids ◽  
Facilitatory Effect ◽  
Consummatory Behavior ◽  
Taste Reactivity ◽  
Before And After ◽  
Ventral Border

The neural control of feeding involves many neuromodulators, including the endogenous opioids that bind μ-opioid receptors (MORs). Injections of the MOR agonist, Damgo, into limbic and hypothalamic forebrain sites increase intake, particularly of palatable foods. Indeed, forebrain Damgo injections increase sucrose-elicited licking but reduce aversive responding (gaping) to quinine, suggesting that MOR activation may enhance taste palatability. A μ-opioid influence on taste reactivity has not been assessed in the brain stem. However, MORs are present in the first-order taste relay, the rostral nucleus of the solitary tract (rNST), and in the immediately subjacent reticular formation (RF), a region known to be essential for consummatory responses. Thus, to evaluate the consequences of rNST/dorsal RF Damgo in this region, we implanted rats with intraoral cannulas, electromyographic electrodes, and brain cannulas aimed at the ventral border of the rNST. Licking and gaping elicited with sucrose, water, and quinine were assessed before and after intramedullary Damgo and saline infusions. Damgo slowed the rate, increased the amplitude, and decreased the size of fluid-induced lick and gape bouts. In addition, the neutral stimulus water, which typically elicits licks, began to evoke gapes. Thus, the current results demonstrate that μ-opioid activation in the rNST/dorsal RF exerts complex effects on oromotor responding that contrast with forebrain effects and are more indicative of a suppressive, rather than a facilitatory effect on ingestion.

Effects of Depressed Mood Induction on Reasoning Performance

1988 ◽  
Vol 66 (3) ◽  
pp. 855-860 ◽  
Author(s):  
Russell A. Radenhausen ◽  
James M. Anker
Keyword(s):  
Depressed Mood ◽  
Mood Induction ◽  
Neutral Stimulus ◽  
Induction Procedure ◽  
Before And After ◽  
Perceptual Performance ◽  
Performance Results ◽  
The Relationship ◽  
Perceptual Measure ◽  
Mood Induction Procedure

The relationship between depressed mood, reasoning and perceptual performance was examined with 57 undergraduate volunteers. To intensify its effect, Velten's 1968 mood induction procedure was modified by having subjects hear a prerecording of each mood statement prior to saying it themselves. Also, midway through the experiment subjects completed an abbreviated mood induction to ensure continuation of the appropriate mood. Ratings of subjects' mood on a 13-point Likert scale before and after mood induction indicated the mood induction was effective. Subjects completed the reasoning measure of 48 syllogisms, and the perceptual measure involving identification of positive, negative, or neutral stimulus words presented tachistoscopically. “Depressed” individuals showed poorer reasoning performance of marginal significance than “elated” subjects. Mood induction did not appear to affect perceptual performance. Results are discussed in terms of the research on reasoning deficits in depression.

Suppression of renin release by antagonism of endogenous opiates in the dog

1986 ◽  
Vol 250 (4) ◽  
pp. R633-R637
Author(s):  
J. E. Szilagyi ◽  
J. Chelly ◽  
M. F. Doursout
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Endogenous Opioids ◽  
Renin Activity ◽  
Renin Release ◽  
Endogenous Opioid ◽  
Endogenous Opiates ◽  
Arterial Blood ◽  
Before And After ◽  
Arterial Constriction

The influence of blockade of endogenous opioids on the release of renin due to partial renal arterial constriction was determined acutely and chronically in unilaterally nephrectomized dogs. In acute preparations changes in plasma renin activity, arterial blood pressure, and heart rate were determined after 15 min of 60% renal arterial constriction before and after administration of either a saline vehicle, the opiate antagonist naloxone (0.05 mg/kg), or morphine (2 mg/kg). Acute antagonism of endogenous opiates abolished the increase in plasma renin activity and mean arterial pressure associated with renal arterial constriction. Repeated renal arterial constrictions in saline- or morphine-treated animals did not alter the humoral or hemodynamic responses. In chronic preparations long-term naloxone infusion attenuated the development of renovascular hypertension and diminished the increase in plasma renin activity. These data suggest that endogenous opioid peptides are modulators in the control of renin release and may be important participants in the pathogenesis of hypertension.

Endogenous opioids are differentially involved in appetitive and consummatory aspects of sexual behavior of male rats

1994 ◽  
Vol 266 (2) ◽  
pp. R606-R613 ◽  
Author(s):  
W. R. Van Furth ◽  
I. G. Wolterink-Donselaar ◽  
J. M. van Ree
Keyword(s):  
Sexual Behavior ◽  
Neural Control ◽  
Test Chamber ◽  
Endogenous Opioids ◽  
Male Rats ◽  
Opioid Antagonist ◽  
Sexual Performance ◽  
Repeated Testing ◽  
Ejaculation Latency ◽  
Male Wistar Rats

The sexual activity of 40 male Wistar rats was tested weekly in a bilevel test chamber to evaluate the involvement of endogenous opioids in the appetitive and consummatory aspects of sexual behavior. It has been suggested that the increase of the anticipatory level-changing behavior over repeated testing, displayed before the introduction of a receptive female, is sexually motivated. Two doses of the opioid antagonist naloxone, 1 and 10 mg/kg, prevented the increase of the anticipatory level-changing over four repeated tests of sexually experienced rats without prior experience in the bilevel test chamber and decreased the number of level changes of rats displaying a high number of level changes. Analysis of the pattern of inhibition suggested that the lower dose of naloxone may reduce sexual reward and that, in addition, the higher dose may block the expression of motivation. In contrast, naloxone treatment facilitated the efficiency of the sexual performance, with less mounts and intromissions preceding ejaculation and a shorter ejaculation latency, implying an inhibitory role of endogenous opioids in the neural control of some aspects of sexual performance (e.g., ejaculatory threshold). These results suggest that endogenous opioids may increase sexual appetite and diminish sexual performance.

Nitric oxide as a regulator of adrenal blood flow

1993 ◽  
Vol 264 (2) ◽  
pp. H464-H469 ◽  
Author(s):  
M. J. Breslow ◽  
J. R. Tobin ◽  
D. S. Bredt ◽  
C. D. Ferris ◽  
S. H. Snyder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Neural Control ◽  
Splanchnic Nerve ◽  
No Synthase ◽  
Catecholamine Secretion ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Synthase Inhibitor ◽  
Splanchnic Nerve Stimulation

To determine whether nitric oxide (NO) is involved in adrenal medullary vasodilation during splanchnic nerve stimulation (NS)-induced catecholamine secretion, blood flow (Q) and secretory responses were measured in pentobarbital-anesthetized dogs before and after administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). L-NAME (40 mg/kg iv over 5 min, followed by 40 mg.kg-1.h-1) reduced NO synthase activity of medullary and cortical homogenates from 5.2 +/- 0.3 to 0.7 +/- 0.1 pmol.min-1.mg protein-1 and from 1.2 +/- 0.2 pmol.min-1.mg protein-1 to undetectable levels, respectively. L-NAME reduced resting medullary and cortical Q by 42 and 60%, respectively. NS before L-NAME increased medullary Q from 181 +/- 16 to 937 +/- 159 ml.min-1.100 g-1 and epinephrine secretion from 1.9 +/- 0.8 to 781 +/- 331 ng/min. NS after L-NAME had no effect on medullary Q (103 +/- 14 vs. 188 +/- 34 ml.min-1.100 g-1), while epinephrine secretion increased to the same extent as in control animals (1.9 +/- 0.7 vs. 576 +/- 250 ng/min). L-NAME also unmasked NS-induced cortical vasoconstriction; cortical Q decreased from 96 +/- 8 to 50 +/- 5 ml.min-1.100 g-1. Administration of hexamethonium (30 mg/kg iv), a nicotinic receptor antagonist, reduced NS-induced epinephrine secretion by 90%. These data suggest independent neural control of medullary Q and catecholamine secretion, the former by NO and the latter by acetylcholine.

scholarly journals Endogenous opioids in the nucleus accumbens promote approach to high-fat food in the absence of caloric need

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Kevin Caref ◽  
Saleem M Nicola
Keyword(s):  
Nucleus Accumbens ◽  
Receptor Antagonist ◽  
Neural Control ◽  
Neural Mechanism ◽  
Endogenous Opioids ◽  
Neuronal Firing ◽  
Palatable Food ◽  
Sugar Consumption ◽  
High Fat ◽  
The Brain

When relatively sated, people (and rodents) are still easily tempted to consume calorie-dense foods, particularly those containing fat and sugar. Consumption of such foods while calorically replete likely contributes to obesity. The nucleus accumbens (NAc) opioid system has long been viewed as a critical substrate for this behavior, mainly via contributions to the neural control of consumption and palatability. Here, we test the hypothesis that endogenous NAc opioids also promote appetitive approach to calorie-dense food in states of relatively high satiety. We simultaneously recorded NAc neuronal firing and infused a µ-opioid receptor antagonist into the NAc while rats performed a cued approach task in which appetitive and consummatory phases were well separated. The results reveal elements of a neural mechanism by which NAc opioids promote approach to high-fat food despite the lack of caloric need, demonstrating a potential means by which the brain is biased towards overconsumption of palatable food.

Characterization of coronary vasoconstrictor site in medullary reticular formation

1989 ◽  
Vol 256 (4) ◽  
pp. H1218-H1227
Author(s):  
D. D. Gutterman ◽  
A. C. Bonham ◽  
J. M. Arthur ◽  
G. F. Gebhart ◽  
M. L. Marcus ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Flow Velocity ◽  
Reticular Formation ◽  
Vascular Resistance ◽  
Neural Control ◽  
Resistance Index ◽  
Adrenergic Blockade ◽  
Medullary Reticular Formation ◽  
The Right ◽  
Feline Model

The importance of sympathetic neural influences in regulating coronary blood flow has been well established. However, central nervous system pathways responsible for these effects are largely unknown. In a feline model, we have identified a site in medullary reticular formation that may play a role in neural control of the coronary circulation. Changes in heart rate (HR), mean arterial pressure (AP), Doppler coronary flow velocity (CBFV), and femoral flow velocity (FBFV) were measured in 67 anesthetized cats. Electrical stimulation in a specific region of the right medullary lateral reticular formation produced elevations in HR (12 +/- 2% from 156 beats/min), AP (41 +/- 6% from 83 mmHg), CBFV (33 +/- 7%), and femoral vascular resistance index (136 +/- 27%). After beta-adrenergic blockade (propranolol), a transient (5-15 s) stimulus-induced decrease in CBFV was observed in 67% of animals, with a 55 +/- 6% increase in coronary vascular resistance index, not the result of autoregulation. Ipsilateral stellate ganglionectomy or systemic alpha 1-adrenergic blockade abolished the CBFV decrement. Microinjection of L-glutamate into this medullary region failed to elicit either pressor or coronary vasomotor responses. It is concluded that electrical stimulation in a specific site within medullary reticular formation produces neurogenic coronary vasoconstriction as part of a more generalized activation of central sympathetic fibers. This brain stem site may play an important role in reflex or behaviorally mediated coronary responses.

Naloxone administration does not affect gonadotrophin secretion in male patients with isolated hypogonadotrophic hypogonadism

1985 ◽  
Vol 109 (2) ◽  
pp. 153-157 ◽  
Author(s):  
Mario Maggi ◽  
Maria Laura De Feo ◽  
Massimo Mannelli ◽  
Giuseppe Delitala ◽  
Gianni Forti
Keyword(s):  
Endogenous Opioids ◽  
Inhibitory Influence ◽  
Naloxone Administration ◽  
Hypogonadotrophic Hypogonadism ◽  
Gonadotrophin Secretion ◽  
Before And After ◽  
Male Patients ◽  
Age Range

Abstract. We evaluated the gonadotrophin response to acute naloxone administration (10 mg iv) in 4 male patients with isolated hypogonadotrophic hypogonadism (age range 18.5–26 years) before and after pituitary priming with daily infusions of GnRH (25 μg/h for 4 h) for 4 days. A blunted gonadotrophin response to acute GnRH administration (100 μg iv) and a lack of response to naloxone was observed before pituitary priming. After repeated infusions of GnRH, pituitary gonadotrophin responsiveness to GnRH was restored, whilst naloxone still did not affect gonadotrophin levels. Our data suggest that in male isolated hypogonadotrophic hypogonadism 1) the lack of pituitary response to naloxone is not due to pituitary hyporesponsiveness to GnRH; 2) endogenous opioids do not exert any inhibitory influence on GnRH secreting neurons and thus are not involved in the pathogenesis of this disease.

Role of the paraventricular nucleus in controlling the frequency of milk ejection and the facilitatory effect of centrally administered oxytocin in the suckled rat

1990 ◽  
Vol 125 (3) ◽  
pp. 467-NP ◽  
Author(s):  
J. B. Wakerley ◽  
T. S. Juss ◽  
R. Farrington ◽  
C. D. Ingram
Keyword(s):  
Paraventricular Nucleus ◽  
Medial Septum ◽  
Facilitatory Effect ◽  
Milk Ejection ◽  
Before And After ◽  
Radiofrequency Lesions ◽  
Group 3 ◽  
Series Of Experiments ◽  
Milk Ejection Reflex ◽  
Facilitatory Action

ABSTRACT The milk-ejection reflex was studied in anaesthetized, lactating Wistar rats in order to evaluate the contribution of the paraventricular nucleus (PVN) to the patterning of milk ejection and the facilitatory action of centrally administered oxytocin. In the first series of experiments, radiofrequency lesions were performed and centred: (1) antero-dorsal to the PVN, damaging parts of the medial septum and anterior hypothalamus; (2) in the PVN, such that much of the parvocellular division was destroyed, but parts of the magnocellular division remained intact; or (3) in the PVN, destroying both parvocellular and magnocellular divisions. Suckling tests performed before and after lesioning showed that the milk-ejection interval was significantly increased (decreased frequency) after lesioning in groups 2 and 3, but that milk-ejection amplitude was significantly decreased only in group 3. These results suggest that damage to the parvocellular division of the PVN affects milk-ejection frequency, but that damage to the magnocellular PVN only affects amplitude. Subsequent tests on rats injected into the PVN with the neurotoxin N-methyl-d,l-aspartate revealed a fall in the amplitude and frequency of milk ejection, similar to that after complete radiofrequency lesions of the PVN. In the second series of experiments, the facilitatory action of centrally administered oxytocin (1 mU, 2.2 ng) was examined in animals bearing either sham or complete PVN lesions. In both groups, intracerebroventricular injection of oxytocin was able to increase the frequency of milk ejections, although the incidence of milk ejection was lower in the pre- and post-injection period in the PVN-lesioned animals. In conclusion, the parvocellular component of the PVN may be an important site for regulating milk-ejection frequency, possibly mediated by its centrally projecting oxytocin neurones. However, the PVN does not appear to be the principle target site by which central oxytocin exerts its facilitatory effect on the frequency of milk ejection. Journal of Endocrinology (1990) 125, 467–475

The interrelationship of beta endorphin, ACTH and cortisol in depressive illness: a controlled study

1987 ◽  
Vol 17 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Rosemary Ball ◽  
Trevor Howlett ◽  
Trevor Silverstone ◽  
Lesley Rees
Keyword(s):  
Plasma Levels ◽  
Depressive Illness ◽  
Endogenous Opioids ◽  
Controlled Study ◽  
Beta Endorphin ◽  
Depressed Patients ◽  
Before And After ◽  
Relationship Of ◽  
The Relationship ◽  
Pituitary Adrenal Axis

SynopsisPlasma cortisol, ACTH and beta endorphin were measured before and after dexamethasone in 8 severely depressed patients and 8 age- and sex-matched controls to examine the relationship of ACTH and endogenous opioids to cortisol in depression. Despite having significantly higher plasma levels of cortisol than the controls, the depressed patients did not have correspondingly elevated plasma levels of ACTH. Beta-endorphin levels were also similar in the two groups. All three hormones suppressed to some degree after dexamethasone, but cortisol suppressed less in patients than controls. Our findings suggest that in severe depressive illness abnormalities exist in the hypothalamic–pituitary–adrenal axis peripherally as well as centrally.

scholarly journals Brain oscillator(s) underlying rhythmic cerebral and buccal motor output in the mollusc, Pleurobranchaea californica

1984 ◽  
Vol 110 (1) ◽  
pp. 1-15
Author(s):  
W. J. Davis ◽  
M. P. Kovac ◽  
R. P. Croll ◽  
E. M. Matera
Keyword(s):  
Neural Control ◽  
Brain Activity ◽  
Neural Oscillator ◽  
Neural Oscillation ◽  
Buccal Ganglion ◽  
Pleurobranchaea Californica ◽  
Long Latency ◽  
Before And After ◽  
The Central Nervous System ◽  
The Brain

Tonic (d.c.) intracellular depolarization of the previously identified phasic paracerebral feeding command interneurones (PCps) in the brain of the carnivorous gastropod Pleurobranchaea causes oscillatory neural activity in the brain, both before and after transecting the cerebrobuccal connectives. Therefore, cycle-by-cycle ascending input from the buccal ganglion is not essential to cyclic brain activity. Instead the brain contains an independent neural oscillator(s), in addition to the oscillator(s) demonstrated previously in the buccal ganglion (Davis et al. 1973). Transection of the cerebrobuccal connectives immediately reduces the previously demonstrated (Kovac, Davis, Matera & Croll, 1983) long-latency polysynaptic excitation of the PCps by the polysynaptic excitors (PSEs) of the PCps. Therefore polysynaptic excitation of the PCps by the PSEs is mediated by an ascending neurone(s) from the buccal ganglion. The capacity of feeding command interneurones to induce neural oscillation in the isolated brain declines to near zero within 1 h after transection of the cerebrobuccal connectives, suggesting that this capacity is normally maintained by ascending information from the buccal ganglion. The results show that this motor system conforms to a widely applicable general model of the neural control of rhythmic behaviour, by which independent neural oscillators distributed widely in the central nervous system are coupled together to produce coordinated movement.

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