GabaB receptors activation in the NTS blocks the glycemic responses induced by carotid body receptor stimulation.

The carotid body receptors participate in glucose regulation sensing glucose levels in blood entering the cephalic circulation. The carotid body receptors information, is initially processed within the nucleus tractus solitarius (NTS) and elicits changes in circulating glucose and brain glucose uptake. Previous work has shown that gamma-aminobutyric acid (GABA) in NTS modulates respiratory reflexes, but the role of GABA within NTS in glucose regulation remains unknown.

Carotid chemoreceptor reflex modulation by arginine-vasopressin microinjected into the nucleus tractus solitarius in rats.

Background: In addition to their role of sensing O2, pH, CO2, osmolarity and temperature, carotid body receptors (CBR) were proposed by us and others to have a glucose-sensing role in the blood entering the brain, integrating information about blood glucose and O2 levels essential for central nervous system (CNS) metabolism. The nucleus tractus solitarius (NTS) is an important relay station in central metabolic control and receives signals from peripheral glucose-sensitive hepatoportal afferences, from central glucose-responsive neurons in the brainstem and from CBR and arginine-vasopressin (AVP)-containing axons from hypothalamic nuclei.

Methods: In normal Wistar rats anesthetized with pentobarbital, permanent cannulas were placed stereotaxically in the NTS.

Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptor stimulation with Na-cyanide.

Hypoxic stimulation of the carotid body receptors (CBR) results in a rapid hyperglycemia with an increase in brain glucose retention. Previous work indicates that neurohypophysectomy inhibits this hyperglycemic response. Here, we show that systemic arginine vasopressin (AVP) induced a transient, but significant, increase in blood glucose levels and increased brain glucose retention, a response similar to that observed after CBR stimulation.

Induction of brain glucose uptake by a factor secreted into cerebrospinal fluid.

It is well established that the carotid body receptors (CBR), at the bifurcation of the carotid artery, inform the brain of changes in the concentration of CO(2) and O(2) in arterial blood. More recent work suggests that these receptors are also extremely sensitive to blood glucose levels suggesting that they may play an important role as sensors of blood components important for brain energy metabolism. Much less is known about changes in brain glucose metabolism in response to CBR activation.

Floral transcription factor AGAMOUS interacts in vitro with a leucine-rich repeat and an acid phosphatase protein complex.

We are interested in identifying potential protein interactors of MADS domain transcription factors during Arabidopsis thaliana flower development. We based our biochemical search on a conserved motif in the MADS domain that includes putative phosphatase and phosphorylation sites that may mediate protein interactions. An affinity column with this motif and a few surrounding hypervariable amino acids derived from the AGAMOUS sequence was prepared and used to isolate potential interactors from floral crude extracts.

Arginine-vasopressin in nucleus of the tractus solitarius induces hyperglycemia and brain glucose retention.

Hypothalamic arginine-vasopressin (AVP) plays an important role both as a neurotransmitter and hormone in the regulation of blood glucose and feeding behavior. AVP-containing axons from the parvocellular subdivision of paraventricular nucleus of the hypothalamus terminate in the nucleus of the tractus solitarius (NTS), but the function of this projection is not known. Interestingly, the NTS also receives afferent information from the carotid body and other peripheral receptors involved in glucose homeostasis.

Parotid gland tissue is able partially to assume pituitary functions under the influence of hypothalamic factors: in vivo and in vitro studies.

To test whether salivary tissue can secrete pituitary hormones, female Sprague-Dawley rats were hypophysectomized (hypox) and the following were transplanted to the sella turcica: parotid gland (group 3, n=33), adrenal gland (group 4, n=30), muscle (group 5, n=24). Group 2 (n=21) had the sella turcica filled with dentist's cement. In addition a group of rats (group 1, n=22) remained intact as controls.

Pituitary and adrenals are required for hyperglycemic reflex initiated by stimulation of CBR with cyanide.

We have previously shown that stimulation of carotid body receptors (CBR) with sodium cyanide (NaCN) elicits a rapid hyperglycemic reflex. Here we explore whether the pituitary and adrenals, two glands involved in glucose homeostasis, are necessary for this reflex. Experiments were performed on anesthetized rats that were artificially ventilated.

Influence of the pituitary gland on the immune response in young rats.

The response of hypophysectomized (HYPOX) and sham-operated (S-HYPOX) female and male Wistar young rats (8 weeks old) to antigenic stimulation was compared. Humoral antigenic responses against hemocyanin were measured by ELISA. [3H]thymidine incorporation into cultured spleen cells was used to determine proliferative response to concanavalin A (ConA) or antigenic stimulation.

Changes in blood glucose concentration in the carotid body-sinus modify brain glucose retention.

To test whether blood glucose concentration in the carotid body-sinus may influence the amount of glucose retained by the brain, the isolated carotid sinus was perfused with glucose-rich blood or glucose-poor blood from a second animal. The circulation of the right carotid body-sinus was temporarily isolated in rat A, and perfused with blood coming from rat B. Blood glucose in rat B was modified by injections of glucose or insulin.

Developmental changes in blood glucose and tissue carbohydrates in the fetal rat: effects of insulin and adrenaline.

The ontogeny of glucose regulation was studied in the rat by measuring the levels of plasma glucose, tissue glucose and tissue glycogen from fetal day 15 (E15) to adulthood. Since insulin and adrenaline are important glucose regulators in the adult, we also tested the effects of these hormones on above variables. The main findings are the following: 1) Umbilical blood glucose was very low (25 mg/100 ml) from E15 to E19, increasing to 66 mg/100 ml by E21 but still below maternal levels (110 mg/100 ml).

Changes in brain glucose retention produced by the stimulation of an insulin-sensitive reflexogenic zone in rats.

Although it has been reported that insulin decreases glucose efflux from the brain causing an increase in brain glucose retention, its mechanism of action is still unknown. The present results indicate that peripheral insulin may act through the stimulation of insulin-sensitive receptors localized in the region irrigated by the coeliac trunk and innervated by the vagus nerve. Stimulation of this zone in anaesthetized, artificially ventilated rats with a bolus millidose of insulin (50 mU) caused a significant increase in brain glucose retention as a result of decreased glucose efflux from the brain.

Technical note: removal of the unfragmented pituitary gland (hypophysectomy) in the rat.

A technique to excise the pituitary gland (hypophysis) in rats is described. The basisphenoid bone is reached from the ventral neck and is perforated to expose the pituitary gland and its stalk. An aspirator allows the removal of the hypophysis and the stalk, including pars tuberalis, in one piece.

Compensation by fetal erythrocytes of plasma glucose changes in rats.

Changes in plasma glucose and glucose and glycogen content in fetal erythrocytes (FRBCs) were studied in rats between days 15 and 21 of gestation and in adult rats. Plasma and FRBC glucose concentrations increased during fetal life and were higher in erythrocytes than in plasma. Glycogen was higher in FRBCs than in adult erythrocytes and tended to decrease from day 15 to 19 of gestation and to increase again on day 21.

Erythrocytes and glucose homeostasis in rats.

The capacity of erythrocytes to modify their glycogen stores to compensate for changes in glucose concentration in plasma was studied. Experiments in vitro and in vivo demonstrated that erythrocytes absorbed and incorporated glucose into their glycogen stores when glucose concentration in the medium was high and liberated it when the concentration was low. Epinephrine administration inhibited glucose absorption by erythrocytes, and in its presence, erythrocytes liberated glucose from their glycogen stores, being unable to compensate for this rise in glucose concentration in plasma.

Carotid sinus receptors participate in glucose homeostasis.

This paper describes (a) the influence of glucose on carotid chemoreceptor activity, and (b) the participation of carotid receptors in glucose homeostasis. After eliminating the carotid body baroreceptors in anesthetized cats, the injection of glucose to the vascularly isolated carotid sinus region reduced by 20% the electrical activity of carotid body chemoreceptors and increased their threshold to hypoxia. Mannitol in the same concentration did not change the chemoreceptor activity.

Effects of intracisternal glucose or insulin injections on glucose homeostasis in cat.

The injection of glucose (100 mg) into the cisterna magna of intact anesthetized cats elicited immediate glycosuria and natriuresis without significant changes in blood glucose concentration. Immunoreactive insulin (IRI) increased 140% in plasma, and Na+ concentration decreased in cerebrospinal fluid (CSF). After kidney denervation there was a significant decrease in glucose and Na+ concentrations in urine.

Reflex hypoglycemia initiated by insulin.

The injection of a bolus of insulin (40 millimicrons) in the coeliac trunk in anesthetized rabbits elicits an immediate rapid rise of arterial IRI. Inferior vena cava and jugular glucose levels drop precipitously 2 min after insulin injection, increasing the A-V glucose difference. The same amount of insulin injected via the coeliac trunk in abdominal-vagotomized rabbits, failed to induce any significant changes in venous glucose concentration and A-V glucose, although there was a similar rise of IRI concentration in arterial plasma.

Adrenocortical function in hypophysectomized dogs with parotid gland transplants in direct contact with the basal hypothalamus.

Adrenocortical activity was studied in three groups of dogs: control-normal, hypophysectomized (hypox), and dogs with a piece of parotid gland grafted into the sella turcica immediately after removal of the whole hypophysis (hypox + graft). Cortisol plasma level (Fk) was estimated by the competitive protein binding method. The mean base-line Fk for 21 normal dogs was 0.

Histological study of the operative zone in dogs with parotid gland grafts in the sella turcica.

No remnants of adenohypophyseal tissue were found in 83% of the 70 dogs studied; in 17% of the animals remnants amounting to from 1 to 3% of normal hypophyseal tissue were found. These traces showed significant histological and cytological changes, and were most frequently found located on the floor of the sella turcica at some distance from their usual site. It is doubtful whether these residua have any functional significance, since the hypophysectomized dogs with such remnants had a survival time that corresponded to that of dogs with total hypophysectomy (6 months).