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PubMed2006

Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis.

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.

Energy Metabolism↗

PubMed1984

In vivo stimulation of pancreatic hormone secretion by norepinephrine infusion in the dog.

Norepinephrine is generally regarded as an inhibitor of insulin release. It has been shown, however, that under hyperglycemic circumstances, norepinephrine infused at a high dose may also stimulate insulin secretion. The goals of this study were, under normoglycemic conditions, to confirm this stimulatory effect and to determine whether a beta-adrenergic mechanism or central neural pathways were involved. Secretion of pancreatic somatostatin and glucagon were also studied. Fasted, anesthetized dogs had norepinephrine (2 micrograms X kg-1 X min-1) infused into a peripheral vein for 60 min; blood was sampled from the pancreaticoduodenal vein. Norepinephrine stimulated insulin, somatostatin, and glucagon secretion without significant changes in either blood glucose concentration or pancreaticoduodenal venous blood flow. The stimulatory effect of norepinephrine on the three hormones was abolished by propranolol pretreatment, thus implicating a beta-adrenergic mechanism. Because bilateral cervical vagotomy prevented stimulation of insulin secretion by norepinephrine, central neural pathways must have been involved in the stimulatory process. However, norepinephrine-induced glucagon secretion was not decreased by vagotomy, showing that the stimulation was due to either a direct action on the pancreatic A cell or of a central pathway not mediated via the vagus nerve. Norepinephrine-induced somatostatin secretion was partly reduced by vagotomy, indicating that several mechanisms could be implicated.

Animals↗

PubMed2003

Opposed effects of lithium on the MEK-ERK pathway in neural cells: inhibition in astrocytes and stimulation in neurons by GSK3 independent mechanisms.

Lithium is widely used in the treatment of bipolar disorder, but despite its proven therapeutic efficacy, the molecular mechanisms of action are not fully understood. The present study was undertaken to explore lithium effects of the MEK/ERK cascade of protein kinases in astrocytes and neurons. In asynchronously proliferating rat cortical astrocytes, lithium decreased time- and dose-dependently the phosphorylation of MEK and ERK, with 1 mM concentrations achieving 60 and 50% inhibition of ERK and MEK, respectively, after a 7-day exposure. Lithium also inhibited [3H]thymidine incorporation into DNA and induced a G2/M cell cycle arrest. In serum-deprived, quiescent astrocytes, pre-exposure to lithium resulted in the inhibition of cell cycle re-entry as stimulated by the mitogen endothelin-1: under this experimental setting, lithium did not affect the rapid, peak phosphorylation of MEK taking place after 3-5 min, but was effective in inhibiting the long-term, sustained phosphorylation of MEK. Lithium inhibition of the astrocyte MEK/ERK pathway was independent of inositol depletion. Further, compound SB216763 inhibited Tau phosphorylation at Ser396 and stabilized cytosolic beta-catenin, consistent with the inhibition of glycogen synthase kinase-3 beta (GSK-3 beta), but failed to reproduce lithium effects on MEK and ERK phosphorylation and cell cycle arrest. In cerebellar granule neurons, millimolar concentrations of lithium enhanced MEK and ERK phosphorylation in a concentration-dependent manner, again through an inositol and GSK-3 beta independent mechanism. These opposing effects in astrocytes and neurons make lithium treatment a promising strategy to favour neural repair and reduce reactive gliosis after traumatic injury.

Animals↗

PubMed1989

Ascending enteric reflex: multiple neurotransmitter systems and interactions.

Isolated segments of the guinea pig small intestine were used to examine the transmitter circuitry of the neural pathways subserving the ascending enteric reflex (AER) contraction of the circular muscle. Inflation of an intraluminal balloon provided the distension stimulus for the AER. The ascending contraction was reduced to 5% of its original amplitude by atropine and to 10% by hexamethonium, which indicates that cholinergic interneurons and cholinergic motor neurons constitute the main AER pathway. However, in the continued presence of atropine or hexamethonium for 60 min, the AER recovered to approximately 30% of its original amplitude. The atropine-resistant AER was blocked by hexamethonium and the tachykinin antagonist spantide [( D-Arg1,D-Trp7,9, Leu11]-substance P) suggesting that it involved cholinergic interneurons and tachykinin-utilizing motor neurons. The hexamethonium-resistant AER was abolished by atropine but left unaffected by spantide, suggesting the participation of as yet unidentified interneurons and cholinergic motor neurons. These findings demonstrate that the AER is mediated by multiple neural pathways with different transmitters and that adaptive interactions between these pathways take place after blockade of one of its neurotransmitters systems.

Analgesics↗

PubMed1999

Nitric oxide synthase is increased following small intestinal transplantation in the rat.

Transplantation of the small intestine is a neural model that could include extrinsic denervation, loss of intrinsic enteric neurons, or loss of intrinsic neural pathways. Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity was measured in normal rat ileum, ileum 3 months after resection of the jejunum, and ileum 3 months after isotransplantation of the ileum. The distribution of NADPH diaphorase activity and immunoreactive neuronal nitric oxide synthase were examined. Nicotinamide adenine dinucleotide phosphate diaphorase activity was increased in transplanted ileum (16.5+/-3.5 mU/mg protein) compared to normal controls (6.6+/-0.7) and resection controls (6.8+/-0.6) (P < 0.05, ANOVA). Histologically, NADPH diaphorase activity and immunoreactive nitric oxide synthase appeared increased within nerve cell bodies following transplantation. These findings may represent an adaptive response of the enteric nervous system to extrinsic denervation. Loss of intrinsic neural pathways was not supported as a mechanism.

Analysis of Variance↗

PubMed2001

Systemic pharmacomodulation of transient lower esophageal sphincter relaxations.

Transient lower esophageal sphincter relaxations (TLESRs) are the major mechanism of reflux in patients with gastroesophageal reflux disease. They are therefore attractive targets for pharmacotherapy. During the past 5 years, there has been a burgeoning interest in the neural pathways that control these events and in the pharmacologic receptors involved in these pathways. Several agents have been shown to reduce the rate of TLESRs, including cholecystokinin-A antagonists, anticholinergic agents, nitric oxide synthase inhibitors, morphine, somatostatin, serotonin type 3-receptor antagonists, and gamma-aminobutyric acid-B (GABA(B)) agonists. Their predominant site of action appears to be on either the afferent pathways and/or the central integrative mechanisms within the dorsal vagal complex in the brainstem. Most of the agents tested are unsuitable for clinical use either because of side effects or because of the lack of an orally effective formulation. The most promising agents identified to date are the GABA(B) agonists. Baclofen, the prototype GABA(B) agonist, inhibits the rate of TLESRs by more than 50%. Control of TLESRs is a major new approach to the treatment of reflux disease. It is likely to be applicable to the majority of patients, particularly those without macroscopic mucosal lesions or only mild erosive disease. Further development of more effective agents will depend both on a better understanding of the neural pathways and receptors involved in the control of TLESRs, as well as on investigation of other novel agents. At present, inhibition of TLESRs is at the threshold of transition from concept to practical use. Whether it makes the final leap into the mainstream of therapy will depend on the development of new, novel, and well-targeted pharmacologic agents.

Cholecystokinin↗

PubMed1992

Effect of intraduodenal HCl and soybean extract on pancreatic juice secretion during atropinization and cold vagal blockade in calves.

In order to elucidate the mechanisms by which intraduodenal hydrochloric acid (HCl) and soybean extract influence exocrine pancreatic secretion in the young ruminant, we conducted experiments repeatedly on six conscious calves with and without blockade of the extrinsic and intrinsic neural pathways. In the absence of blockade, each of the two stimuli increased the juice volume, the HCl effect being far stronger than that of soybean extract. Intrinsic cholinergic blockade by atropinization blocked the stimulatory work of soybean extract on pancreatic secretion and on HCl-stimulated protein but had a weak effect on the amount of juice evoked by HCl. Temporary vagal blockade by chilling virtually abolished the excitatory effects of both soybean extract and HCl. With or without blockade, duodenal HCl resulted in a noteworthy increase in plasmal secretin and a slight increase in cholecystokinin (CCK). With alimentary proteins, acidification of the duodenum was responsible for both the composition and secretion of pancreatic juice in young calves, generally via neural pathways. Atropine-sensitive nerves of the pancreas totally regulate the intestinal phase of pancreatic juice secretion allied with intraduodenal protein, whereas HCl-dependent excitation of the exocrine pancreas takes place partly via atropine-resistant nerves. However, as hardly any pancreatic juice was secreted independently of the vagi, the vagi are deemed to govern all the postprandial regulatory mechanisms of the exocrine pancreas in the young calf.

Animals↗

PubMed2002

Photic resetting of the human circadian pacemaker in the absence of conscious vision.

Ocular light exposure patterns are the primary stimuli for entraining the human circadian system to the local 24-h day. Many totally blind persons cannot use these stimuli and, therefore, have circadian rhythms that are not entrained. However, a few otherwise totally blind persons retain the ability to suppress plasma melatonin concentrations after ocular light exposure, probably using a neural pathway that includes the site of the human circadian pacemaker, suggesting that light information is reaching this site. To test definitively whether ocular light exposure could affect the circadian pacemaker of some blind persons and whether melatonin suppression in response to bright light correlates with light-induced phase shifts of thecircadian system, the authorsperformed experiments with 5 totally blind volunteers using a protocol known to induce phase shifts of the circadian pacemaker in sighted individuals. In the 2 blind individuals who maintained light-induced melatonin suppression, the circadian system was shifted by appropriately timed bright-light stimuli. These data demonstrate that light can affect the circadian pacemaker of some totally blind individuals--either by altering the phase of the circadian pacemaker or by affecting its amplitude. They are consistent with data from animal studies demonstrating that there are different neural pathways and retinal cells that relay photic information to the brain: one for conscious light perception and the other for non-image-forming functions.

Adult↗

PubMed1984

Fluid regulation, body weight and drinking responses following hypothalamic knife cuts.

Electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) alters fluid and electrolyte regulation. In addition, these lesions produce neural degeneration in the supraoptic nucleus (SON) and neural lobe, which suggests a neural pathway from the AV3V region to the SON. To determine if pathways in this brain area may mediate some of the effects which follow AV3V periventricular ablation, food and water ingestion, urine volume, and body weight, as well as drinking responses to a number of dipsogenic challenges were determined following placement of small knife cuts between the level of the organum vasculosum lamina terminalis (OVLT) and the SON. Metabolism measurements were taken daily for 7 days following either knife cuts or control operations, and again 4 weeks after surgery. Drinking responses following subcutaneous injections of angiotensin II, water deprivation, and cellular dehydration were determined at least 2 weeks after surgery. Rats with knife cuts exhibited an increase in water ingestion and urine volume, an enhanced water consumption following water deprivation and acute cellular dehydration, and did not gain weight at the same rate as control operated rats. The hyperdipsia following cellular dehydration was abolished by bilateral nephrectomy. These data indicate that a neural pathway coursing through this brain region is critical for fluid regulation and maintenance of body weight.

Angiotensin II↗

PubMed1991

Total denervation of the pancreas does not alter the pancreatic polypeptide-induced inhibition of pancreatic exocrine secretion in dogs.

Pancreatic polypeptide (PP) is a potent inhibitor of pancreatic exocrine secretion in vivo. The mechanism of pancreatic inhibition by PP is unknown, but the absence of PP receptors on pancreatic exocrine cells makes a direct effect of this hormone on the gland unlikely. In this study, we investigated the hypothesis that PP exerts its inhibitory effect via extrinsic neural pathways. Ten dogs with gastric and pancreatic fistulas were given an intravenous infusion of 250 ng/kg-1 h-1 secretin and 50 ng/kg-1 h-1 caerulein over 3 h. One hour after starting the infusion, 400 pmol kg-1 h-1 porcine PP were administered over 1 h. Pancreatic bicarbonate and protein secretions were measured. Later, the pancreas was extrinsically denervated. PP infusion decreased bicarbonate secretion in the intact gland by 47% and in the denervated pancreas by 57%. Protein secretion was diminished by exogenous PP by 31% in the intact and by 44% in the denervated pancreas. Despite pancreatic denervation, PP still exerted a significant inhibitory effect. Atropine infusion completely blocked the inhibitory effect of PP on caerulein-stimulated pancreatic protein secretion both in the intact and denervated pancreas and of secretion-evoked bicarbonate output in the denervated gland. We conclude that the inhibitory action of the hormone is not mediated via extrinsic neural pathways of the pancreas, but PP may exert its effect via intrinsic atropine-sensitive mechanisms.

Animals↗

PubMed2001

Sensory exploitation of prey: manipulation of the initial direction of prey escapes by a conspicuous "rare enemy".

The painted redstart (Myioborus pictus) represents a group of non-cryptic predators, the flush pursuers, who visually trigger prey escapes by spreading and pivoting their conspicuously patterned tails and wings. The prey are then chased in aerial pursuits. Such an exploitation of prey may be possible because the predation risk from redstarts is smaller than that from the predatory guild of insectivores and their neural pathways are adapted to helping prey avoid common predators rather than "rare enemies". I propose that the pivoting movements of flush pursuers direct insect escapes across the central field of vision of a predator, where it is easier to track and intercept the prey. Eighty per cent of chases by wild redstarts were in a direction suggesting that prey were entering the birds' area of stereoscopic vision. The redstart's fanned and raised tail creates a stronger visual stimulus than a redstart's head. Flies escaped away from the section of the fly's field of vision in which the model's tail was located and towards the area where the predator's stereoscopic vision is likely to be located, in front of a bird's forehead. The experiments suggested that redstarts may not only exploit the sensitivity of typical neural escape pathways, which are non-directionally sensitive, but that they may also exploit the sensitivity of some directionally sensitive neural pathways in prey.

Animals↗

PubMed2002

Long-lasting changes in central nervous system responsivity to colonic distention after stress in rats.

BACKGROUND & AIMS: The highly prevalent functional gastrointestinal disorders involve visceral pain and disturbed bowel habit and are associated with preceding stressful experiences, although causality and biological mechanisms remain unclear. The aim of the present study was to establish whether stress can directly and lastingly alter central nervous system responsivity to colonic distention in the rat as well as which neural pathways are likely to be involved. METHODS: Rats were treated with a brief session of stressful foot shocks known to induce long-term behavioral and autonomic sensitization. Two weeks later, after induction of inhalation anesthesia, a balloon catheter was inserted in the distal colon and repeatedly inflated with brief, constant-pressure air pulses. RESULTS: Reflex decreases in blood pressure and heart rate indicative of visceral afferent activation were greater in previously shocked rats than in controls. Colonic distention increased the expression of Fos, a marker of neuronal activation, in the sacral spinal cord and caudal brain stem. In the central amygdala and several cortical areas (prelimbic, infralimbic, agranular insular, cingulate), previously shocked rats showed reduced Fos expression following colonic distention compared with relevant controls. CONCLUSIONS: The results indicate that a brief but intense stressful experience causes long-lasting alterations in higher-order central nervous system responsivity to colonic distention even in the absence of conscious affective responses, pointing to basic alterations in the neural pathways involved.

Animals↗

PubMed1999

Caverno-pudendal nervous communicating branches in the penile hilum.

Classically, the peripheral neural pathways for erection are proerectile, issuing from the parasympathetic sacral fibres, and antierectile from the thoracolumbar sympathetic trunk. The cavernous nerves as terminal branches of the pelvic plexus convey the parasympathetic fibres to the penis. The pudendal nerve conveys sensory fibres from the penis and somatic fibres to the bulbos-pongiosus and ischiocavernosus striated mm. In animals, it has been demonstrated that the dorsal nerve of the penis contains sympathetic fibres. These findings suggest that communicating branches exist between the cavernous nerves and the dorsal nerve. Our aim in this study was to demonstrate the presence of such connections in man. We dissected 20 fresh male cadavers. The pelvic plexus and pudendal nerves were dissected to identify their terminal branches and connections. Histologic study was performed. Our results showed evidence of communicating nervous branches between the cavernous nerves and the dorsal nerve of the penis. Several variants existed concerning the number and type of connections. The presence of such communicating branches proves that the supralevator and infralevator neural pathways communicate and suggest the possibility of a kind of plasticity of the nervous supply of penile erection. Further studies are needed to identify the nature of these communicating branches.

Adult↗

PubMed1994

Glucagon-like peptide-1 7-36 amide and peptide YY from the L-cell of the ileal mucosa are potent inhibitors of vagally induced gastric acid secretion in man.

BACKGROUND: Glucagon-like peptide (GLP-1) 7-36 amide and peptide YY (PYY) from the L-cell of the ileal mucosa are potent inhibitors of gastric acid secretion in man. It is not clear, however, by which mechanism(s) they inhibit acid secretion. In dogs the inhibitory effect of PYY on acid secretion may be mediated mainly through neural pathways. The mechanism of action of GLP-1 might be similar. The aim of the present study was to examine the effects of GLP-1 might be similar. The aim of the present study was to examine the effects of GLP-1 and PYY on the vagally induced gastric acid secretion in man. METHODS: A modified sham feeding technique, chew and spit, was used. Six healthy volunteers were randomly assigned to receive intravenous infusion of saline, GLP-1 (41 pmol/kg/h), or peptide YY (50 pmol/kg/h). RESULTS: The infusion of GLP-1 and PYY resulted in plasma concentrations of 60 +/- 9 pmol/l and 84 +/- 11 pmol/l, respectively. GLP-1 and PYY both significantly inhibited the intergrated acid output by 67 +/- 6% and 68 +/- 9%, respectively, compared with the integrated outputs in a control experiment with saline infusion. Serum gastrin and plasma somatostatin concentrations remained unchanged during saline, GLP-1, and PYY infusions. CONCLUSIONS: GLP-1 and PYY are both potent inhibitors of the cephalic phase of acid secretion, indicating that at least part of the inhibitory effect of GLP-1 and PYY in man is mediated through neural pathways. Furthermore, the inhibitory effect seems to be independent of circulating concentrations of gastrin and somatostatin.

Adult↗

PubMed1987

High dorsal column cordotomy plus subdiaphragmatic vagotomy prevents acute ionizing radiation sickness in cats.

Our purpose was to determine the effects on acute radiation sickness of interrupting afferent neural pathways that converge upon the medullary vomiting center but which bypass the emetic chemoreceptor trigger zone in the area postrema. A comparison was made of the vomiting response and other signs of sickness in three groups of chronic cats surgically prepared as follows: high spinal cord section of the dorsal columns, subdiaphragmatic vagotomy, and the combination of procedures. Every cat was exposed over the whole body to 45 Gy 60Co gamma-radiation which was effective in evoking emesis in 11 of 12 normal cats. Neither cordotomy alone (8 cats) nor vagotomy alone (2 cats) reliably blocked the vomiting response but they separately delayed its onset. On the other hand, the cordotomy prevented the loss of appetite and behavioral malaise that was invariably caused by the irradiation in normal cats. Finally, the combination of cordotomy and vagotomy protected all of 3 cats against the entire radiation syndrome. These cats then vomited appropriately in response to the injection of deslanoside which induces emesis through an action on the area postrema. Histological examination of the lower medulla revealed no damage of the area postrema resulting from the cordotomies. We conclude that acute radiation sickness in the cat is signaled through afferent neural pathways originating in the abdomen and that the area postrema does not participate in the causation of this syndrome.

Animals↗

PubMed1996

Expression of mRNA for vasoactive intestinal peptide in rat small intestine.

Transplantation of small intestine is a neural model that permits studies of expression of the neuropeptide, vasoactive intestinal peptide, following extrinsic denervation, transection of intrinsic neural pathways, and an ischemic interval. Tissue levels of vasoactive intestinal peptide were examined at 3 months in ileum from a sham operation, in ileum after resection of proximal small intestine, in ileum after resection of proximal small intestine and extrinsic denervation, in ileum after resection of proximal small intestine and 30 min of ischemia, and in ileum obtained 3 months after ileal isografting in Lewis-to-Lewis combinations. Vasoactive intestinal peptide levels were increased in transplanted rat ileum, resection controls, denervation controls, and ischemic controls compared to sham-operated ileum (pANOVA < 0.01). The increased levels of this peptide were highest in denervation controls and lowest in ischemic controls. Northern blot analysis using rat vasoactive intestinal peptide cDNA identified a single 1.7-kb transcript in normal and transplanted rat ileum. The density of vasoactive intestinal peptide transcripts was increased in transplanted ileum (8450 +/- 540) compared to normal ileum (5790 +/- 620) (P < 0.01), and the ratio of this transcript to glyceraldehyde-3-phosphate dehydrogenase density units was also increased in transplanted ileum (0.81 +/- 0.08) compared to normal ileum (0.40 +/- 0.07; P < 0.01). Enhanced transcriptional regulation was the likely mechanism for increased tissue vasoactive intestinal peptide. The increased tissue levels appeared to be a response to extrinsic denervation and transection of intrinsic neural pathways, while an ischemic interval appeared to decrease tissue levels of the peptide.

Animals↗

PubMed1983

Hypothalamic knife cuts alter fluid regulation, vasopressin secretion, and natriuresis during water deprivation.

To investigate central neural pathways involved in release of vasopressin and in fluid electrolyte regulation, a retractable wire knife was used to make coronal knife cuts posterior to the organum vasculosum lamina terminalis (OVLT). 4 days following cuts or control surgery, animals were housed in metabolism cages and: (1) deprived of food and water for 48 h; (2) deprived of water only for 48 h; or (3) allowed continuous access to food and water. Water ingestion, food ingestion, urine volume, sodium excretion and urine osmolality were recorded daily. Trunk blood was then collected following decapitation for determination of plasma vasopressin, sodium, and protein concentrations, and osmolality. Animals with knife cuts and ad libitum access to food and water had significantly higher plasma osmolality (310 +/- 2 mosm/kg), and plasma vasopressin concentration (2.02 +/- 0.5 microunits/ml) than controls (306 +/- 1 mosm/kg and 0.60 +/- 0.04 microunits/ml, respectively). When rats were deprived of both food and water, there were no significant differences between the two groups in plasma vasopressin concentration, although plasma osmolality wa higher in animals with cuts. However, rats with knife cuts deprived of water only had significantly higher plasma osmolality (358 +/- 8 mosm/kg), sodium (164 +/- 19 mEq/l) and vasopressin (17.7 +/- 4 microunits/ml), than similarly treated control animals (317 +/- 1 mosm/kg, 145.5 +/- 1.0 mEq/1, 5.5 +/- 3 microunits/ml, respectively). These data indicate that a neural pathway in this brain region is critical for normal fluid and electrolyte balance during ad libitum access to food and water, and during water deprivation.

Animals↗

PubMed1989

Effects of intrahypothalamic injections of GABA, muscimol, pentobarbital, and L-glutamic acid on feed intake of satiated sheep.

Five wethers were surgically prepared with cranial implants to study the role of gabaminergic neural pathways on the hypothalamic control of feeding behaviour in ruminants. In the first experiment, the animals were injected (1 microL) with a physiological Tyrode (0.95%) solution, muscimol (0.5 and 1.0 nmol), GABA (0.5 and 1.0 nmol), and L-glutamic acid (0.5 and 1.0 nmol). Feed intake following injections of muscimol (1.0 nmol) and L-glutamic acid (0.5 and 1.0 nmol) was twice as large as that following the Tyrode solution, at 60-min postinjections. These results, however, were not statistically significant (p = 0.12-0.15). In the second experiment, the animals were injected (1 microL) with saline, muscimol (0.8 nmol), L-glutamic acid (0.8 nmol), and pentobarbital (0.26 mumol). Fifteen minutes after the injections, pentobarbital had induced a significant feeding response when compared with control values (p less than 0.01), whereas the effect of L-glutamic acid was not significant. However, 30 min after the injections, feed intake of sheep having received L-glutamic acid was higher than that obtained with the control injections (p less than 0.01). The response to pentobarbital was stronger than that to either muscimol or L-glutamic acid. Histological analyses of brain tissue indicated that injections were performed in the ventromedial hypothalamus of four sheep and in the dorsomedial hypothalamus of the other. The data indicate that L-glutamic acid stimulates feed intake by acting either as a precursor of GABA or by a direct stimulation of glutaminergic neural pathways involved in the control of feed intake.

Animals↗