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Biomedical subjects

S Amir

Publications and source records attributed to S Amir.

At least 73 records · Page 4Linked to original sources
PubMed1991

Activation of brown adipose tissue thermogenesis by chemical stimulation of the hypothalamic supraoptic nucleus.

Glutamate microinjection (1 M, 250 nl) into the hypothalamic supraoptic nucleus (SON) stimulated heat production in brown adipose tissue (BAT) and caused a rapid and sustained increase in interscapular BAT and core temperatures in urethane-anaesthetized rats. This effect was blocked by intraperitoneal pretreatment with a sympathetic ganglionic blocker, chlorisondamine chloride (2.5 mg/kg), or a beta-adrenergic receptor blocker, propranolol (2.5 mg/kg), but not by prior hypophysectomy or intracerebroventricular pretreatment with specific receptor blockers to vasopressin (d(CH2)5[Tyr(Me)2]AVP, 5 micrograms) or oxytocin (d(CH2(5)[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT, 5 micrograms). The results demonstrate that stimulation of SON cells with glutamate elicits a non-vasopressinergic/non-oxytocinergic neural signal that can bring about a sympathetically-mediated increase in BAT thermogenesis. Heat production in BAT is an important mechanism of thermal protection during cold stimulation, and there is evidence that osmotic stimulation can influence thermoregulation. SON neurons play a major role in osmoregulation via release of the peptide hormones vasopressin and oxytocin. The present results suggest the possibility that apart from releasing peptide hormones for osmoregulation, SON neurons might be involved in mediating the effect of osmotic stimulation on thermoregulatory responses involved in thermal adaptation.

Adipose Tissue, Brown↗
PubMed1991

An inhibitor of nitric oxide production, NG-nitro-L-arginine-methyl ester, improves survival in anaphylactic shock.

Induction of anaphylactic shock in mice by i.v. antigen challenge (bovine serum albumin, 100 micrograms) or i.v. treatment with the mast cell degranulator compound 48/80 resulted in 80 and 90% mortality rate, respectively. Inhibition of nitric oxide (NO) synthesis from L-arginine by co-injection of the L-arginine analog NG-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) reduced the mortality rate by 40 and 20% in the antigen- and compound 48/80-induced shock models. Treatment with 60 mg/kg L-NAME reduced the mortality rate by 60% in these shock models. This beneficial effect was reversed by addition of L-arginine (120 mg/kg) but not D-arginine (120 mg/kg). These results suggest NO production as a possible mechanism involved in the pathophysiology of anaphylactic shock.

Anaphylaxis↗
PubMed1991

NG-monomethyl-L-arginine co-injection attenuates the thermogenic and hyperthermic effects of E2 prostaglandin microinjection into the anterior hypothalamic preoptic area in rats.

Prostaglandin E2 (PGE2) microinjection (25 ng, 250 nl) into the preoptic area of the anterior hypothalamus (POAH) stimulated heat production in brown adipose tissue (BAT) and increased core temperature in urethane-anesthetized rats. These thermogenic and hyperthermic effects were attenuated by co-injection of NG-monomethyl-L-arginine (NMMA, 25 micrograms), a competitive inhibitor of nitric oxide (NO) production from L-arginine. Inclusion of L-arginine (50 micrograms), though not D-arginine (50 micrograms) reversed the inhibitory effect of NMMA (25 micrograms) on intra-POAH PGE2-induced increases in interscapular BAT (IBAT) and core temperatures. Intra-POAH injection of NMMA (25 micrograms) or L-arginine (50 micrograms) alone had no effect on IBAT and core temperatures. The results suggest that the effect on thermoregulation induced by action of PGE2 in the POAH is modulated by a local L-arginine-dependent and NMMA-sensitive NO-generating system.

Animals↗
PubMed1990

Activation of brown adipose tissue thermogenesis by chemical stimulation of the posterior hypothalamus.

The posterior hypothalamus (PH) is involved in the generation of behavioral thermoregulatory responses, but the importance of the PH in the control of autonomic thermoregulatory responses such as heat production in brown adipose tissue (BAT) is not well defined. In the present study, selective stimulation of PH neurons by local application of the excitatory amino acid glutamate (250 nl of 1 M solution, unilaterally) caused a sharp, transient increase in interscapular BAT (IBAT) and core temperature in urethane-anesthetized rats. This effect was blocked by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride (2 mg/kg) or the beta-adrenergic receptor blocker, propranolol (2 mg/kg), implicating the involvement of the sympathetic system. The effect of intra-PH injection of glutamate on IBAT and core temperatures could be mimicked by injection of the gamma-aminobutyric acid (GABA) receptor antagonist, bicucullin methiodide (BMI, 50 ng), into the same PH site. This effect of BMI could be blocked by co-injection of the GABA(A) receptor agonist, muscimol (25 ng). Further, BMI co-injection potentiated the effect of intra-PH injection of glutamate on IBAT and core temperatures. Conversely, muscimol co-injection prevented the stimulatory effect of intra-PH injection of glutamate. Taken together, the results indicate that direct chemical stimulation of neurons in the PH can activate an autonomic mechanism controlling heat production in BAT. Further, they suggest the neural mechanism in the PH mediating this effect is tonically inhibited by GABA, as blockade of GABAergic function in the PH produces an effect similar to that observed after direct stimulation of PH neurons with glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1990

Factors regulating the expression of acetylcholinesterase-containing neurons in striatal cultures: effects of chemical depolarization.

The influence of chemical depolarization on the survival and differentiation of acetylcholinesterase (AChE)-containing neurons was examined in primary rat striatal cultures, maintained in different types of media (serum-free and serum-supplemented) and substrate (poly-ornithine and astrocyte monolayer). Chronic application of 5 microM veratridine resulted in a significant loss of neurites by AChE-positive cells, while a higher concentration (20 microM) reduced the number of stained cell bodies. These effects appeared to be selective with regard to AChE-positive cells, as indicated by morphological observations of the cells in the treated cultures and receptor binding measurements. Similarly, elevation of extracellular KCl levels (20-60 mM) produced a dose-dependent neurite loss by AChE-containing cells. Blockers of voltage-sensitive Ca2+ channels--verapamil (1 microM) and nifedipine (1 microM)--did not affect the veratridine-induced neurite loss, while tetrodotoxin (0.1 microM) had a partial effect. When cultures treated with 5 microM veratridine were allowed to recuperate for several days, the number of AChE-positive cells possessing neurites returned close to control values, thus indicating the reversibility of the effect of chemical depolarization. The possibility that chronic neuronal depolarization in the striatum might play a role in regulation of the neuronal processes outgrowth by AChE-containing cells is discussed.

Acetylcholinesterase↗
PubMed1990

Injection of prostaglandin E2 into the anterior hypothalamic preoptic area activates brown adipose tissue thermogenesis in the rat.

E series prostaglandins (PGE) are known to elicit potent hyperthermia when injected into the anterior hypothalamic preoptic area (POAH) in rats, but the effector mechanisms mediating the rise in temperature are not well defined. In the present study, microinjection of PGE2 into the POAH dose-dependently increased non-shivering thermogenesis in brown adipose tissue (BAT) in urethananesthetized rats, bringing about a marked and sustained rise in interscapular BAT (IBAT) and core temperatures. The effect of intra-POAH PGE2 injection on IBAT and core temperatures could be blocked by systemic pretreatment with the sympathetic ganglionic blocker chlorisondamine chloride or the beta-adrenergic receptor blocker propranolol, thus implicating the involvement of the sympathetic system. Furthermore, the increase in IBAT and core temperatures induced by intra-POAH PGE2 could be blocked by prior injection of the local anesthetic procaine or the GABA receptor agonist muscimol into the ipsilateral ventromedial hypothalamic nucleus (VMH). Taken together, the results suggest that PGE2 increases body temperature by acting in the POAH to stimulate heat production in BAT via a sympathetic efferent mechanism located in the VMH.

Adipose Tissue, Brown↗
PubMed1990

Insulin co-injection suppresses the thermogenic response to glutamate microinjection into the VMH in rats.

Selective stimulation of ventromedial hypothalamic nucleus (VMH) neurons by microinjection of the excitatory amino acid glutamate sharply increased interscapular brown adipose tissue (IBAT) and core temperatures in urethane-anaesthetized rats. This effect was blocked by co-injection of insulin (0.1-1 microgram) though not an inactive insulin analog, TNB3 insulin. Injection of insulin (1 microgram) into the contralateral VMH or systemic administration of insulin (1 microgram) had no effect on the thermogenic response to intra-VMH glutamate. These results complement those showing that intra-VMH insulin suppresses the basal firing rate of sympathetic nerves to IBAT and diminishes cold-induced nonshivering thermogenesis in BAT and add support to the view that insulin functions as an inhibitory signal on VMH neurons controlling thermogenesis in BAT.

Adipose Tissue, Brown↗
PubMed1990

Intra-ventromedial hypothalamic injection of glutamate stimulates brown adipose tissue thermogenesis in the rat.

The ventromedial hypothalamic nucleus (VMH) has been recognized for its role in the control of thermogenesis in brown adipose tissue (BAT) in the rat. However, the neural elements within the VMH that might be involved have not been clearly identified. In the present study, intra-VMH microinjections of the excitatory amino acid glutamate (100 mM to 1 M, in 0.25 microliters), which excites cell bodies and dendrites but not axons and nerve terminals, dose-dependently increased interscapular BAT (IBAT) temperature in urethane-anaesthetized rats. This effect of glutamate was blocked by prior treatment with the sympathetic ganglionic blocker, chlorisondamine chloride (2.5 mg/kg, i.p.) or the beta-adrenergic receptor antagonist, propranolol (2.5 mg/kg, i.p.), implicating the involvement of sympathetic norepinephrine. These results are consistent with the view that cells in the VMH are implicated in the transmission of thermogenic signals to BAT.

Adipose Tissue, Brown↗
PubMed1990

Stimulation of the paraventricular nucleus with glutamate activates interscapular brown adipose tissue thermogenesis in rats.

The paraventricular nucleus (PVN) of the hypothalamus is involved in the control of energy balance in rodents through its influences on feeding, pituitary hormone secretion and the autonomic nervous system. In the present study, selective stimulation of PVN neurons by means of local microinjection of the excitatory amino acid glutamate (100 mM, 500 mM or 100 nl) led to a concentration-dependent increase in interscapular brown adipose tissue (IBAT) temperature in urethane-anaesthetized rats. This effect could be prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride, or the beta-adrenergic receptor antagonist, propranolol, but not by hypophysectomy, implicating the involvement of the sympathetic outflow. Thermogenesis in brown adipose tissue (BAT) is an important accompaniment of overfeeding in small mammals, and previous studies have shown that signals generated in response to feeding gain access to the PVN. The present finding that direct activation of PVN neurons stimulates thermogenesis in BAT, taken together with data that the PVN receives dietary signals from the gut, support the view that PVN neurons may function in monitoring the balance between energy intake and its expenditure.

Adipose Tissue, Brown↗
PubMed1990

Cognitive and behavioral determinants of compliance in diabetics.

The interaction between patient and medical team is especially stressful in cases of diabetes, because of the high potential for critical behaviors by the team and for avoidance or aggressive behaviors by the patient. This study examined some cognitive and behavioral correlates of compliance behaviors in 70 insulin-dependent diabetics. A special scale was developed to evaluate specific cognitions, behaviors, and anxiety during confrontations with the physician, dietitian, nurse, and secretary. Another special scale was developed to evaluate compliance with self-care behaviors in diabetes. Cognitive and behavioral coping skills specific to patient-medical team encounters were found to be significant correlates of various compliance variables in the following order: maintenance of positive self-esteem and efficacy during criticism, positive acceptance of criticism, avoidance of conflict by offering compromise solutions, and assertive request for follow-up with a specific doctor. Each was found to be a significant predictor of compliance behaviors. The findings indicate the importance of positive cognitive and assertive coping skills in specific stressful situations involving the patient and medical team.

Adaptation, Psychological↗
PubMed1989

Retinohypothalamic tract stimulation activates thermogenesis in brown adipose tissue in the rat.

We have shown that injecting glutamate into the hypothalamic suprachiasmatic nucleus (SCN) stimulates interscapular brown adipose tissue (IBAT) thermogenesis in rats. In the present study, electrical stimulation of the retinohypothalamic tract (RHT), a projection of retinal ganglion cell axons that course via the optic tract and terminate in the SCN, mimicked the effect of intra-SCN glutamate injection on IBAT thermogenesis. This effect could be blocked by prior injection of the local anesthetic procaine or the excitatory amino acid blockers kynurenic acid and delta-D-glutamylaminomethyl-phosphonic acid into the contralateral SCN, implicating the involvement of SCN glutamate receptors. The primary function of the RHT is to communicate photic information to the SCN, and it has been shown that glutamate might be involved in mediating this effect. On the basis of these observations and our finding of thermogenic responses to RHT stimulation or intra-SCN glutamate, we conclude that photic signals transmitted to the SCN via release of glutamate from the RHT might be capable of acutely modulating thermogenesis in IBAT.

Adipose Tissue, Brown↗
PubMed1989

Glutamate injection into the suprachiasmatic nucleus stimulates brown fat thermogenesis in the rat.

Injection of glutamate (100 mM to 1 M, in 0.25 micrograms saline) into the hypothalamic suprachiasmatic nucleus (SCN) dose-dependently increased interscapular brown adipose tissue (IBAT) and core temperatures in the urethane-anaesthetized rat. This effect was more pronounced in rats tested during the light-off period than in animals tested during the light-on period. Prior injection of the local anaesthetic, procaine (5% in 0.5 microliter saline), into the ipsilateral ventromedial hypothalamic nucleus (VMH) attenuated the increases in IBAT and core temperatures induced by intra-SCN glutamate. The VMH has previously been implicated in the central regulation of BAT thermogenesis; the present results suggest the pathway arising in the SCN exerts an excitatory influence on VMH neurons involved in the control of BAT function.

Adipose Tissue, Brown↗
PubMed1989

Intra-ventromedial hypothalamic injection of insulin suppresses brown fat thermogenesis in the anaesthetized rat.

Insulin can affect metabolic functions such as glucose production and fat mobilization through action in the ventromedial nucleus of the hypothalamus (VMH), and the VMH has been implicated in the regulation of heat generation in brown adipose tissue (BAT) in the rat. To study the role of insulin in modulating VMH mechanisms concerned with BAT thermogenic activity we evaluated the effect of intra-VMH microinjection of insulin on BAT (T(bat)) and core (T(core)) temperatures and BAT thermogenic activity (T(bat)-T(core)) in anaesthetized rats. Intra-VMH insulin (10 ng, 100 ng and 1 microgram) enhanced the decreases in T(bat) and T(core) resulting from exposure of the anaesthetized rats to mild cold, as well as diminished BAT thermogenic activity in a dose-dependent manner. This effect could be partially reversed by systemic treatment with norepinephrine (400 micrograms/kg). Intra-VMH injection of insulin analogs having reduced binding affinity to insulin receptors and diminished biological activity--i.e., acetyl3 insulin, succinyl3 insulin and TNB3 insulin--was much less effective at enhancing the decrease in T(bat) and T(core) or at inhibiting BAT thermogenic activity. These results demonstrate that insulin can modulate BAT thermogenesis in a specific manner through action in the VMH.

Adipose Tissue, Brown↗
PubMed1989

Intra-hypothalamic injection of thyrotropin-releasing hormone suppresses brown fat thermogenesis in the anaesthetized rat.

Thyrotropin-releasing hormone (TRH) has diverse effects on body temperature in rodents, but the effector mechanisms that mediate its thermoregulatory actions are not well defined. In the present study, microinjection of 10 ng to 5 micrograms of TRH into the anterior hypothalamus (AHy) dose-dependently suppressed heat production in interscapular brown adipose tissue (BAT) in chloral hydrate-anaesthetized rats tested at a room temperature of 23 +/- 2 degrees C. This effect of TRH was mimicked by the structurally related peptides acid-TRH and luteinizing hormone releasing hormone (LH-RH), and by the TRH analog CG 3509, but not by the TRH fragments pGlu-His and His-Pro. The AHy plays a role in the regulation of BAT thermogenic activity, and the present results suggest that some of the effects of TRH on body temperature involve an AHy-mediated inhibitory action on BAT thermogenesis.

Adipose Tissue, Brown↗
PubMed1989

Vanadate stimulates in vivo glucose uptake in brain and arrests food intake and body weight gain in rats.

Vanadate, administered via drinking fluid (0.2-0.8 mg/ml in 80 mM NaCl), attenuated food intake and strongly suppressed body weight gain in normally-fed or 20-hour food-deprived rats. At 0.8 mg/ml for 4 days, oral vanadate significantly stimulated the rate of hexose uptake by brain tissue. When microinjected into the lateral cerebral ventricle at a dose of 82 nmol, vanadate strongly and specifically suppressed food intake and body weight gain in 20-hour food deprived rats previously maintained on tap water. This inhibitory effect was reversed by coadministration of 3-O-methyl glucose. Collectively, the results suggest that vanadate is capable of blocking food intake by a specific effect in the central nervous system that involves stimulation of local glucose uptake.

3-O-Methylglucose↗
PubMed1988

Immunological blockade of endogenous thyrotropin-releasing hormone impairs recovery from hyperglycemia in mice.

Administration of antiserum to thyrotropin-releasing hormone (TRH) into the lateral cerebral ventricle of mice significantly attenuated recovery from hyperglycemia induced by treatment with 2-deoxyglucose but had no effect on the plasma glucose of saline-treated mice. TRH, injected centrally together with the anti-TRH antibody, reversed the effect of the antiserum and blocked the development of hyperglycemia. These findings suggest that activation of TRH neurons in the central nervous system may be a physiological event influencing recovery from hyperglycemia.

Animals↗