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PubMed1992

Effect of the D2-autoreceptor agonist B-HT 958 on both spontaneous and ACTH-induced stretching, yawning and grooming in the rat.

The D2 autoreceptor agonist B-HT 958, intraperitoneally injected into Wistar male rats in a novel environment, significantly increased stretching and yawning (SY) while inhibiting grooming. Pretreatment with the D2 antagonist sulpiride reversed these effects, antagonizing SY and restoring grooming. Similarly, when B-HT 958 was administered to rats in their home cages, it elicited SY and abolished grooming; moreover, when administered before the i.c.v. injection of adrenocorticotropin hormone, dose-dependently enhanced SY and strongly antagonized the typical syndrome of intensified grooming induced by the peptide. The possible relationship between SY and grooming and the involvement of D2 autoreceptors are discussed.

Adrenergic alpha-Agonists↗
PubMed1985

Cardiovascular effects of tetanus toxin after systemic and intraventricular administration in rats.

A single intraperitoneal injection of tetanus toxin (50,100 and 200 minimum lethal dose per rat) produced a significant and dose-dependent increase in systemic blood pressure and heart rate in conscious rats. On the contrary, tetanus toxin, given directly into the third cerebral ventricle (20 and 40 minimum lethal dose), produced a gradual and dose-dependent decrease in blood pressure accompanied by bradycardia. In conclusion, the present findings show that tetanus toxin is able to affect cardiovascular activity and it is suggested that this may be due to an interference with central GABAergic mechanisms.

Animals↗
PubMed1982

Vagal mediation of the cholecystokinin satiety effect in rats.

Central (intracerebroventricular) and peripheral (intraperitoneal) injections of the octapeptide of cholecystokinin (CCK-8) were compared to determine the most effective route of administration to elicit satiety for food intake in the rat. Subdiaphragmatic bilateral vagotomy and spinal cordotomy (T2-T3) were also performed to investigate the importance of visceral nerves for the satiety effect. CCK-8 suppressed feeding and elicited satiety resting behavior when injected peripherally but it was less effective when injected centrally. The satiety effect of CCK-8 or CCK-33 following peripheral injections was blocked by vagotomy whereas spinal cordotomy had no effect. The results indicate that some component of the vagus is required to mediate the peripherally induced cholecystokinin satiety effect, but the splanchnic nerves are not necessary. The weak effect of CCK-8 following ventricular administration is additional evidence suggesting that cholecystokinin of intestinal origin acts in the periphery rather than directly on the brain to elicit its typically rapid satiety effect in rats.

Adrenergic Fibers↗
PubMed1993

Ginsenoside Rg1 prevents histaminergic modulation of rat adaptive behavior from elevation of ambient temperature.

Effects of ginsenoside Rg1 (Rg1) on histaminergic modulation of both adaptive behavior and thermoregulation were investigated at high ambient temperature. Continuous infusion of Rg1 using an osmotic minipump into the rat third cerebroventricle attenuated anorexia induced by elevation of ambient temperature from 21 degrees C to 31 degrees C. Intraperitoneal injection of alpha-fluoromethylhistidine (FMH), a specific suicide inhibitor of a histamine synthesizing decarboxylase enzyme, also prevented the anorexia induced by elevated temperature. The ratio of water intake to food intake, which showed no change on the first day after elevation of room temperature, was not influenced by treatment of either FMH or Rg1. Rectal temperature, which was normally maintained at a constant level even after shifting ambient temperature from 21 degrees C to 31 degrees C, elevated after FMH treatment. The Rg1 infusion, however, maintained rectal temperature normally at 31 degrees C. Hypothalamic histamine content increased in response to elevation of ambient temperature. The Rg1 infusion maintained constant histamine level against elevation of environmental temperature. Under the heated condition FMH reduced hypothalamic histamine. These findings suggest that Rg1 may modulate rat adaptive behavior by blockade of temperature-related information into the hypothalamic histamine neurons.

Acclimatization↗
PubMed1988

Study of the hypothermia induced by methionine sulfoximine in the rat.

L-Methionine sulfoximine (MSO) intraperitoneally injected at subconvulsive and convulsive doses induced a rectal hypothermia in the restrained rat maintained at an ambient temperature of 23 degrees C; this hypothermia developed during the preconvulsive period, and it was not suppressed by simultaneous injection of L-methionine which antagonized the behavioral effects of ammonia elevated contents in the central nervous system. The development of rectal hypothermia was faster when the injection of MSO was made into the lateral cerebral ventricle and particularly into the third ventricle. MSO-induced hypothermia seemed to be a poikilothermia-like state in the cold environment with retention of a normal regulation in the heat environment. Infusion of MSO into the anterior hypothalamic/preoptic (AH/PO) area induced a rapid rectal hyperthermia, but infused into the mammillary region MSO had no effect on rectal temperature. It is suggested that rectal hypothermia induced by MSO may be directly related to a depressive effect on glucose oxidative metabolism in cell structures, maybe astroglial cells, located in the vicinity of the ventricle or the capillary walls.

Animals↗
PubMed1985

Oxytocin stimulates lordosis behavior in female rats.

Oxytocin, either intraperitoneally injected (200 ng/rat) or intracerebroventricularly infused (1 ng/rat in 4 microliters saline) 60 and 15 min respectively before testing, significantly increased the lordosis response to the mounting male of ovariectomized, estrogen/progesterone treated rats. The intracerebroventricular infusion of oxytocin 0.1 ng/rat had no effect; nor did saline. These results indicate that oxytocin increases female receptivity, the site of action probably being in the central nervous system.

Animals↗
PubMed1993

Inhibition of IL-1 beta-induced peripheral inflammation by peripheral and central administration of analogs of the neuropeptide alpha-MSH.

Interleukin-1 (IL-1) is a proinflammatory cytokine, alpha-MSH(1-13) molecules inhibit inflammation induced by cytokines, other mediators of inflammation, and by peripheral irritants. D-valine substitution in the antiinflammatory/antipyretic message sequence [alpha-MSH(11-13), Lys-Pro-Val] of alpha-MSH(1-13) increases the activity of the tripeptide. Our aim was to learn if D-valine substitution also enhances the antiinflammatory activity of the entire alpha-MSH(1-13) molecule and to determine if an antipyretic D-valine-substituted alpha-MSH(8-13) molecule is also antiinflammatory. Intraperitoneal injection of alpha-MSH(1-13) and of (D-Val13)alpha-MSH(1-13) caused dose-related suppression of ear edema induced in mice by intradermal injection of IL-1 beta; the two molecules were equipotent. (D-Val13)alpha-MSH(8-13) likewise inhibited inflammation, but the potency was less than that of the larger molecules. Intracerebroventricular injections of (D-Val13)alpha-MSH(1-13) and of the unsubstituted molecule were equipotent in reducing inflammation; the (D-Val13)alpha-MSH(8-13) molecule was less effective. The results support the idea that the alpha-MSH(1-13) molecule inhibits inflammation and suggest that the L-conformation of alpha-MSH(1-13) is maximally effective with regard to its antiinflammatory activity. The results with alpha-MSH(8-13) are consistent with previous findings of lesser antihost response activity of alpha-MSH fragments that contain the COOH-terminal tripeptide Lys-Pro-Val.

Animals↗
PubMed1996

The role of cerebral noradrenergic systems in the Fos response to interleukin-1.

Peripheral administration of interleukin-1 (IL-1) has been shown to activate induction of Fos in the brain, but the mechanism is not known. Because cerebral noradrenergic systems have been implicated in Fos induction, we studied the IL-1-induced appearance of Fos in mice pretreated with 6-hydroxydopamine (6-OHDA) which depleted cerebral norepinephrine (NE) by more than 90%, but did not significantly alter dopamine. Intraperitoneally injected IL-1 beta increased Fos in several brain regions, but most obviously in the hypothalamic paraventricular nucleus (PVN). Pretreatment with 6-OHDA substantially reduced the IL-1-induced Fos increase in the PVN which was no longer statistically significant. When the 6-OHDA treatment was preceded by administration of desmethylimipramine which prevents NE depletion, IL-1 treatment increased Fos in the PVN, suggesting that the effect of 6-OHDA was indeed related to the depletion of NE. These results suggest that the noradrenergic innervation of the PVN is involved in the IL-1-induced induction of Fos in the PVN. By contrast with previous experiments is rats, the IL-1-induced increase in plasma corticosterone was not significantly altered by the 6-OHDA pretreatment in mice.

Adrenergic Uptake Inhibitors↗
PubMedDate not supplied

Effect of colchicine on micturition reflex in rats.

Intracerebral or intraspinal cord, but not intraperitoneal, injection of low doses of colchicine in rats induces specific toxic symptoms. This paper deals in particular with the effect of colchicine on micturition. After the injection of 5-25 micrograms/rat in cerebral ventricle or 2.5-20 micrograms/rat intraspinal cord, bladder content was markedly increased, due to a dramatic urine retention. Time of latency of vesical retention was related to the dose and to the route of colchicine administration. Cystometrographic analyses were performed in control and treated rats at various intervals of time after the injection: bladder tone, as expressed by the delta P/delta V ratio, monitored from 12 to 120 hr after colchicine injection, decreased more and more during time, suggesting that the observed vesical hypotonicity is an irreversible phenomenon.

Animals↗
PubMed2004

Pharmacokinetic study of acyl-protected hydroxylamine probe, 1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine, for in vivo measurements of reactive oxygen species.

1-Acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP) is a unique probe for in vivo measurements of reactive oxygen species (ROS), because it is hydrolyzed by esterase to a hydroxylamine form (CP-H), which is oxidized to an electron spin resonance-detectable nitroxyl radical (CP) by a reaction with superoxide anion radical, etc. Although a knowledge of pharmacokinetics is essential for the use of ACP in vivo, such information is limited. We investigated the pharmacokinetics of ACP in mice by examining the time course of the tissue distribution of ACP, CP-H, and CP after intravenous or intraperitoneal injection of ACP. Esterase activity for ACP in tissue homogenates was also measured. The concentration of ACP decreased in all tissues obeying a one-compartment model. ACP was hydrolyzed to CP-H in the liver and kidney predominantly, and the first-pass effect of liver on the hydrolysis of ACP was very large. A homogeneous biodistribution of CP-H was obtained 10 min after the injection of ACP regardless of the injection route, and concentrations remained stable over at least 20 min. Because of these pharmacokinetic properties, ACP should be suitable for the imaging of ROS in animals.

Animals↗
PubMedDate not supplied

Effects of gadolinium chloride (GdCl(3)) on the appearance of macrophage populations and fibrogenesis in thioacetamide-induced rat hepatic lesions.

Macrophages infiltrating injured tissue play an important part in fibrogenesis. To shed light on the functional roles of macrophages, we investigated the appearance of macrophage populations in thioacetamide (TAA)-induced rat hepatic lesions, with or without pretreatment with GdCl(3), a chemical capable of inhibiting Kupffer cell functions. In the GdCl(3)+TAA group rats received a single intraperitoneal injection of GdCl(3) (7.5mg/kg body weight) and, after 24h, a single intravenous injection of TAA (300mg/kg body weight). Rats in the TAA group received TAA only. Rats in both groups were examined on post-TAA injection (PTI) days 3, 5, and 7. In the TAA group, on PTI day 3, when TAA-induced hepatocyte injury was particularly prominent, the number of macrophages peaked, subsequently decreasing until PTI day 7. As compared with the TAA group, the GdCl(3)+TAA group showed significantly decreased numbers of ED1-immunolabelled cells (exudate macrophages) and ED2-immunolabelled cells (Kupffer cells) on PTI days 3, 5, and 7, and OX6-immunolabelled cells (antigen-presenting macrophages) on PTI days 3 and 5. Although less strikingly, the numbers of alpha-smooth muscle actin-positive myofibroblasts and fibrotic areas were decreased in the GdCl(3)+TAA group. By RT-PCR, the expression of TGF-beta1 mRNA was suppressed on PTI days 3 and 7 in the GdCl(3)+TAA group, and the suppressed expression was confirmed in vitro by treating rat macrophage-like cells (HS-P) with 1% GdCl(3). The study showed that GdCl(3) treatment decreased the numbers of macrophages appearing in hepatic lesions and inhibited TGF-beta1 mRNA expression in macrophages. Decreased numbers of macrophages may contribute to improvement of hepatic fibrosis.

Alanine Transaminase↗
PubMed2005

Immune pre-activation exacerbates hemorrhagic brain injury in immature mouse brain.

Premature infants with placental infection and adult stroke patients with fever have worse outcomes following intracerebral hemorrhage (ICH). We hypothesized that immune pre-activation would aggravate brain injury in mouse brain following ICH. The immune system of 2-day, 10-day and 7-week young adult CD1 mice was stimulated by intraperitoneal injection of concanavalin A (ConA), lipopolysaccharide (LPS) or polyinosinic-polycytidilic acid (PolyI:C) 12 h prior to intracerebral injection of blood. Two days later, brain damage and inflammation were worse in 2-day mice that had received LPS. The other agents had less consistent effects in 2-day mice. Brain damage in young adults was aggravated less after immune stimulation. These data suggest that immune pre-activation modifies hemorrhagic brain injury in immature mouse brain.

Aging↗
PubMed2002

The effects of melatonin and Ginkgo biloba extract on memory loss and choline acetyltransferase activities in the brain of rats infused intracerebroventricularly with beta-amyloid 1-40.

Intraventricular infusion of rats with beta-amyloid for 14 days resulted in memory deficit in the water maze as well as decreases in choline acetyltransferase activities and somatostatin levels in the cerebral cortex and hippocampus. These changes were not altered by daily intraperitoneal injection of 20 mg/Kg melatonin. Orally administered Ginkgo biloba extract, however, partially reversed the memory deficit and the decrease in choline actyltransferase activities in the hippocampus. The latter treatment failed to reverse the decrease in somatostatin levels. The results indicate that orally administered Ginkgo biloba extract can protect the brain against beta-amyloid from changes leading to memory deficit through its effect on the cholinergic system.

Administration, Oral↗
PubMed2003

Pharmacokinetics and feeding responses to muramyl dipeptide in rats.

N-acetyl-muramyl-L-alanine-D-isoglutamine or muramyl dipeptide (MDP) is the minimally active subunit of bacterial peptidoglycan. During a systemic infection, the involvement of MDP has been demonstrated in food intake depression by the macrophage hydrolysis of Gram-positive bacteria. Under normal conditions, mammals are constantly exposed to the release of endogenous MDP from degraded gut flora and that of exogenous MDP from the diet. However, MDP digestion and absorption in the gastrointestinal tract are not fully understood, and their physiological significance needs to be clarified. After gavage (1.5 mg/kg), very low levels of MDP were found in the systemic circulation of rats and feeding patterns were not altered. In contrast, after the intraperitoneal injection of a similar dose, a depression in food intake was observed. The rats reduced their meal frequency and constant feeding rate, showing signs of satiety. The behavioral satiety sequence (BSS) was modified by behavioral changes, similar to those which appear during sickness, such as an increase in resting and a reduction in grooming. Our data suggest that the hypophagic effect of MDP may result from satiety and sickness behavior.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2001

Morphine withdrawal-facilitated aggression is attenuated by morphine-conditioned stimuli.

There is a considerable body of evidence indicating that stimuli associated with drug administration may become conditioned and evoke drug-like effects. The purpose of this study was to evaluate the ability of morphine-paired stimuli to affect an expression of morphine withdrawal-facilitated aggression. Individually housed aggressive adult mice were subjected to the repeated subcutaneous administration of morphine (twice a day, 8 days, increasing doses 10-80 mg/kg). Morphine treatment cessation facilitated an aggressive behaviour of animals during the second day of withdrawal. Subcutaneous but not intraperitoneal injection of saline attenuated the aggressive behaviour in morphine-withdrawn mice. These results suggest that the site of drug injection may serve as a conditioned stimulus.

Aggression↗
PubMed1997

Sex differences in ibogaine antagonism of morphine-induced locomotor activity and in ibogaine brain levels and metabolism.

The present study demonstrates that the putative antiaddictive agent ibogaine produces more robust behavioral effects in female than in male rats and that these behavioral differences correlate with higher levels of ibogaine in the brain and plasma of female rats. There were no differences in basal locomotor activity between the sexes, and the response of rats to ibogaine differed between the sexes even in the absence of morphine. Five h after receiving ibogaine (40 mg/kg, i.p.). antagonism of morphine-induced locomotor activity was evident in female but not in male rats. Either 19 h after administration of ibogaine (10-60 mg/kg, i.p.), or one h after administration of noribogaine (5-40 mg/kg, i.p.), a suspected metabolite, antagonism of morphine was significantly greater in female than in male rats. Brain and plasma levels of ibogaine (1 h) and noribogaine (5 h), measured by gas chromatography-mass spectrometry, were greater in females as compared with males receiving the same dose of ibogaine. Levels of both ibogaine and noribogaine were substantially lower at 19 h than at earlier times after ibogaine administration, contrary to a previous study in humans. For both sexes, subcutaneous administration of ibogaine (40 mg/kg, i.p., 19 h) produced greater antagonism of morphine-induced locomotor activity than did a comparable intraperitoneal injection, consistent with previous studies from this laboratory demonstrating that the former route of administration produces higher levels of ibogaine in the brain. These data show that there are sex differences in the effects of ibogaine and that this may be due to decreased bioavailability of ibogaine in males as compared to females.

Animals↗
PubMed1996

Immunization against exon 1 decapeptides from the lutropin/choriogonadotropin receptor or the follitropin receptor as potential male contraceptive.

Pituitary gonadotropin hormones lutropin (LH) and follitropin (FSH) control steroidogenesis and gametogenesis in male and female gonads through interaction with G protein-coupled receptors, LHR and FSHR. In the male, LH acts on leydig cells and is mostly responsible for the acquisition of puberty and the production of androgens while FSH, together with androgens, regulates spermatogenesis within Sertoli cells. We have engineered filamentous phages displaying mouse LHR and human FSHR decapeptides chosen in hormone binding regions. Peptides from both receptors displayed on phages belong either to the receptor specific exon 1 (amino acids 18-27) or to the homologous exon 4 (amino acids 98-107). Vaccination of prepubertal BALB/c male mice with hybrid phages using sub-cutaneous or intraperitoneal injections induced immunity against receptors. Anti-receptor immunization produced agonist or antagonist effects depending only on the circulating levels of the antibodies. Both anti-LHR and anti-FSHR vaccines induced efficient as well as reversible male contraception, through different mechanisms: targeting LH receptors inhibited or hyperstimulated Leydig cell testosterone production while targeting FSH receptors did not affect testosterone levels.

Amino Acid Sequence↗
PubMed1988

Biodistribution studies of anti-Thy 1.2 IgM immunoconjugates: implications for radioimmunotherapy.

We have prepared 111In radioimmunoconjugates (RICs) of the IgM isotype with specificity for the murine T cell/neuroectodermal surface antigen, Thy 1.2. Using gamma camera immunoscintigraphy, we have analyzed the biodistribution patterns of the RICs after intravenous and intraperitoneal injection into normal Thy 1.2+ and Thy 1.2- mice. Both routes of administration show antigen-specific uptake by the splenic T lymphocyte population. A high degree of nonspecific uptake by the reticuloendothelial system is also observed. Analysis of the specific activity of various segments of spleens from RIC-injected animals shows inhomogeneous uptake of the RIC not readily apparent by immunoscintigraphy. Animals injected with the RIC and then given high dose total body irradiation showed rapid shifts in radionuclide distribution away from the target cell population and into the general reticuloendothelial system, suggesting that death of the target cell can alter RIC biodistribution. Analyses of RIC biodistribution patterns will contribute to optimization of treatment by radioimmunotherapy.

Animals↗