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PubMed1996

Alterations in serotonin1B (5HT1B) receptor subtypes in the brain of ethanol-treated rats.

The effects of acute or chronic ethanol treatment and of withdrawal (24 h) after chronic ethanol treatment on 5HT1B receptor subtypes in different regions of the rat brain were investigated. Male Sprague-Dawley rats were fed the ethanol (9% v/v)-containing Lieber-DeCarli liquid diet or the control liquid diet for 1 day in the acute study and for 15 days in the chronic study. The ethanol-withdrawn group received the Lieber-DeCarli control liquid diet instead of the ethanol diet on the 15th night. Ethanol-withdrawn rats after 15 days of ethanol treatment were rated for withdrawal symptoms (e.g. hyperactivity, piloerection, squealing, and enhanced startle reflex) and were found to exhibit such symptoms after 24 h of ethanol withdrawal. The rats were decapitated, and cortices, cerebelli, striata, and hippocampi were separated for measurement of 5HT1B receptors by receptor binding techniques using 125I-cyanopindolol (CYP) as the ligand. It was observed that acute ethanol treatment had no significant effect on the maximum number of binding sites (Bmax) or the apparent dissociation constant (KD) of 5HT1B receptor binding sites in the various brain regions. On the other hand, chronic ethanol treatment produced a significant increase in Bmax of 125I-CYP binding to 5HT1B receptors in the rat cortex and hippocampus, which remained increased after 24 h of ethanol withdrawal. In contrast, in the striatum and the cerebellum of chronic ethanol-treated and withdrawn rats, the 5HT1B binding parameters (Bmax and KD) were unchanged. These results suggest the possible involvement of cortical and hippocampal 5HT1B receptors in ethanol dependence.

Animals↗
PubMedDate not supplied

Neuropsychopharmacologic properties of a Schumanniophyton problematicum root extract.

Schumanniophyton problematicum is a plant popular among Nigerian native healers for the treatment of psychotic patients (madness). An extract obtained by ethanol extraction of the roots caused reductions in respiratory rate, body and limb tone, startle response and spontaneous locomotor activity after i.p. injection in mice, and was capable of inhibiting amphetamine-induced hyperactivity and stereotypic behaviour. It also induced passivity, piloerection, hypothermia and prolonged pentobarbital sleeping time. The i.p. LD50 of the extract in mice was 2.37 g/kg. The effects of the extract appear to be due to depression of central and autonomic system.

Amphetamine↗
PubMed1991

Reduction in insulitis following administration of IFN-gamma and TNF-alpha in the NOD mouse.

In insulin dependent diabetes mellitis (IDDM) beta cell destruction is associated with infiltration of the pancreatic islets by T lymphocytes and macrophages. Cytokine products from the infiltrating immunocytes not only have powerful immunoregulatory actions but also are capable of impairing islet cell functions and have thus been postulated to assume a central role in mediating anti-beta cell immunity and beta cell destruction. In an effort to explore further the role of cytokines in the pathogenesis of IDDM, we examined clinical, metabolic and pathological features of NOD/Wehi mice injected intraperitoneally with multiple doses of IFN-gamma and/or TNF-alpha. Blood glucose profiles were not significantly altered by injection of cytokines alone or in combination. Except for a hypoglycaemic rebound in mice injected with TNF-alpha, arginine stimulation tests revealed no disturbances in islet secretory function in cytokine injected mice. Compared with vehicle and cytokines alone, injection of IFN-gamma + TNF-alpha was associated with a variety of clinical and pathological changes including abdominal distention, piloerection, ascites, oedema, thymic atrophy, splenic enlargement and pancreatic distention. Histological examination of the pancreas in these mice revealed moderate to severe pancreatitis which included focal haemorrhagic necrosis, oedema and polymorphonuclear and mononuclear cell infiltration. The islets in these mice appeared normal morphologically and when stained for insulin. The injection of IFN-gamma + TNF-alpha, and to a lesser extent TNF-alpha alone, was associated with a significant reduction in the severity of insulitis. Examination of pancreatic MHC-class I and class II molecule expression revealed in mice given IFN-gamma + TNF-alpha, as compared with controls, significant and uniform induction of both these molecules on ductal and acinar cells; low level MHC-class II expression was also detectable on beta cells in these mice. MHC-class I molecules which were expressed at high levels by beta cells in control mice did not appear to change following administration of the cytokines alone or in combination. We conclude that despite their immunostimulatory actions in vitro and in other models in vivo, systemic administration of the cytokines IFN-gamma and/or TNF-alpha to NOD/Wehi mice does not activate or enhance, and may actually suppress, anti-beta cell immunity in this model.

Animals↗
PubMed2006

Investigating the hedonic effects of interferon-alpha on female rats using brain-stimulation reward.

Interferon-alpha (IFN-alpha) is used as a front-line treatment for cancer and other diseases. Reports of depression as a consequence of IFN-alpha therapy scatter the literature, generating interest in the CNS disruptions elicited by this cytokine. In the present work, we investigated the short- and long-term effects of a single systemic injection of vehicle, 10, or 1000 units of IFN-alpha on temperature, body weight, food intake, sickness behaviours, locomotor activity, and brain stimulation reward (BSR) thresholds elicited from the ventral tegmental area in female Long-Evans rats. Pioneered for studying motivational processes, BSR has been exploited as a tool for tracking hedonic status in animal models of depression. In this study, the main findings were that IFN-alpha did not induce anhedonia as defined by no increase in frequency thresholds. However, the analyses of sickness behaviours unveiled a significant increase in piloerection in all sham control animals that received an IFN-alpha injection while the BSR animal scores remained relatively unchanged between pre- and post-injection days. This pattern was also evident in the overall total sickness behaviour scores. Our data suggest that a single exposure to IFN-alpha treatment in female rats elicits long-term somatic effects, without altering hedonic status.

Animals↗
PubMed2004

Pregnancy outcomes following pre- and post-implantation exposure of Sprague-Dawley rats to benzyl isothiocyanate.

The present investigation examines the outcomes of rats' pregnancy following pre- and post-implantation maternal exposure (orally) to benzyl isothiocyanate (BITC; 12.5, 25 and 50 mg/kg body weight). Three maternal deaths were recorded in the group of rats treated with 50 mg/kg BITC. Obvious signs of toxicity characterized by hypo-activity, perinasal staining, piloerection, hunched posture and decrease in body weights were observed in BITC-treated rats during the treatment periods. Dose-dependent increase in early fetal resorptions was seen in rats treated with BITC prior to implantation, but was not statistically significant. There were no significant differences in the number of implantation sites in treatment groups compared with the control. Similarly, there were no significant differences in the number of fetal resorptions, relative weights of maternal liver, kidney and spleen of rats in post-implantation treatment groups compared with the control. The differences in the number of viable fetuses in treatment groups compared with the control were also not significant. However, fetal weights in rats treated with 25 and 50 mg/kg BITC and placental weights in all the treatment groups were significantly lower than the control. In conclusion, at 12.5-50 mg/kg, BITC did not cause significant pre- and post-implantation fetal loss in pregnant rats. BITC-induced low fetal and placental weights could be of obstetrical importance, but at levels/doses that would provoke maternal toxicity.

Administration, Oral↗
PubMed2005

Neurobehavioral effects of tetramisole in mice.

Acute toxicity and neurobehavioral effects of the veterinary anthelmintic tetramisole were examined in male albino mice. The 24-h median lethal doses of tetramisole were determined by the up-and-down method in mice after oral, subcutaneous and intraperitoneal administrations, and they were 110, 57 and 34 mg/kg, respectively. The intoxicated mice manifested nervousness, crouching, piloerection and tremor. Subcutaneous injection of tetramisole at 0.5 and 1mg/kg did not significantly affect general locomotor activity of the mice in 5-min open-field activity test or negative geotaxis performance and landing foot splay. However, the 1mg/kg dose of tetramisole significantly increased the stereotyped behavior (grooming, sniffing, biting and licking and head bobbing) of the mice when compared to the control group. Daily treatment of mice with tetramisole at 0.5 and 1mg/kg for six consecutive days did not significantly affect their general locomotor activity in the open-field activity test. Both doses of tetramisole significantly increased stereotyped behavior of the mice on days 3, 5 and 8 in comparison with respective control values. Repeated tetramisole treatments (0.5 and 1mg/kg) also significantly decreased the time needed to complete the negative geotaxis task and reduced landing foot splay. All tetramisole-treated mice showed crouching behavior and were nervous and difficult to handle. The results suggest nervous involvement in the acute toxicity of tetramisole. Stereotyped behavior and changes in the negative geotaxis and landing foot splay are reported for the first time in mice treated with tetramisole.

Administration, Oral↗
PubMed2006

Peptidergic sensory and parasympathetic fiber sprouting in the mucosa of the rat urinary bladder in a chronic model of cyclophosphamide-induced cystitis.

In this study, we used a well-established animal model to investigate changes in the peptidergic and parasympathetic innervation of the bladder following chronic bladder inflammation. Adult female Sprague-Dawley rats were injected with either 70 mg/kg cyclophosphamide diluted in saline, i.p., once every 3 days or saline. After 10 days, all animals were tested for urinary frequency and number of low volume voids, as well as symptoms of spontaneous pain. At the end of 12 days, all animals were perfused with histological fixatives and the urinary bladders processed for immunofluorescence using antibodies against calcitonin gene-related peptide and the vesicular acetylcholine transporter as markers, respectively, of peptidergic primary afferent fibers and parasympathetic efferent fibers. We show that animals treated with cyclophosphamide had inflamed bladders and displayed high urinary frequency as well as some indicators of spontaneous pain, such as piloerection and a rounded-back posture. Furthermore, they had a significant increase in the density of both parasympathetic and peptidergic sensory fibers in the bladder mucosa and an increase in peptidergic sensory fibers in the detrusor muscle. Based on these results, we suggest that peripheral sprouting of parasympathetic and peptidergic fibers could be a mechanism responsible for sensitization of the bladder, leading to urinary symptoms. Since we observed that the parasympathetic and peptidergic fibers often wrapped around one another and that their varicosities were very close, these two fiber populations may be interacting with each other to lead to and maintain sensitization. Future studies are required to establish the role of this fiber sprouting in bladder symptoms.

Afferent Pathways↗
PubMed2006

Peptidergic sensory and parasympathetic fiber sprouting in the mucosa of the rat urinary bladder in a chronic model of cyclophosphamide-induced cystitis.

In this study, we used a well-established animal model to investigate changes in the peptidergic and parasympathetic innervation of the bladder following chronic bladder inflammation. Adult female Sprague-Dawley rats were injected with either 70 mg/kg cyclophosphamide diluted in saline, i.p., once every 3 days or saline. After 10 days, all animals were tested for urinary frequency and number of low volume voids, as well as symptoms of spontaneous pain. At the end of 12 days, all animals were perfused with histological fixatives and the urinary bladders processed for immunofluorescence using antibodies against calcitonin gene-related peptide and the vesicular acetylcholine transporter as markers, respectively, of peptidergic primary afferent fibers and parasympathetic efferent fibers. We show that animals treated with cyclophosphamide had inflamed bladders and displayed high urinary frequency as well as some indicators of spontaneous pain, such as piloerection and a rounded-back posture. Furthermore, they had a significant increase in the density of both parasympathetic and peptidergic sensory fibers in the bladder mucosa and an increase in peptidergic sensory fibers in the detrusor muscle. Based on these results, we suggest that peripheral sprouting of parasympathetic and peptidergic fibers could be a mechanism responsible for sensitization of the bladder, leading to urinary symptoms. Since we observed that the parasympathetic and peptidergic fibers often wrapped around one another and that their varicosities were very close, these two fiber populations may be interacting with each other to lead to and maintain sensitization. Future studies are required to establish the role of this fiber sprouting in bladder symptoms.

Afferent Pathways↗
PubMed2005

Primary neurologic screening and motor coordination of Dstdt-J mutant mice (dystonia musculorum) with spinocerebellar atrophy.

The autosomal recessive dystonia musculorum (Dst(dt-J)) mutation causes degenerative lesions of peripheral and central sensory pathways. A test battery of motor, sensory, postural, and autonomic functions was used to compare young control and homozygous Dst(dt-J) mice. The Dst(dt-J) mutants were severely impaired for muscle strength, limb coordination, and postural reflexes. As a result of a loss in motor control, the mutants were hypoactive in the open-field and fell quickly from the stationary beam. In sensory tests, the acoustic startle response was impaired, but not tactile reflexes and contact righting, attesting to preserved labyrinthine function and non-lemniscal pathways. Dst(dt-J) mutants were also distinguishable from controls on the basis of tremor, a paler skin, piloerection, and half-open eyes, as well as low body weight and fecal boli. Grooming episodes were less frequent in the mutants but without any reduction in grooming time. The neurologic screening battery delineated the functional integrity of some sensorimotor pathways in a spinocerebellar mutant whose severe phenotype prevents a more elaborate evaluation.

Analysis of Variance↗
PubMed2005

Serotonin (1A) receptor involvement in acute 3,4-methylenedioxymethamphetamine (MDMA) facilitation of social interaction in the rat.

The current study assessed whether various co-administered serotonin (5-HT) receptor antagonists could prevent some of the acute behavioral effects of 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") in rats. In the social interaction test, MDMA (5 mg/kg) significantly increased the duration of total social interaction between two conspecifics meeting for the first time. Microanalysis showed that MDMA increased adjacent lying and approach behaviours while reducing anogenital sniffing. MDMA (5 mg/kg) also caused elements of the serotonin syndrome including low body posture and piloerection. In the emergence test, MDMA significantly increased hide time and emergence latency indicating increased anxiety-like behavior. Pretreatment with the 5HT 1A receptor antagonist, WAY 100635 (1 mg/kg), prevented MDMA-induced increases in social interaction and markers of the serotonin syndrome while the 5-HT 1B receptor antagonist GR 55562 (1 mg/kg) and 5-HT 2A receptor antagonist ketanserin (1 mg/kg) were ineffective. The 5-HT 2B/2C receptor antagonist, SB 206553 (2 mg/kg), prevented MDMA-induced prosocial effects but caused pronounced thigmotaxis (hyperactivity at the periphery of the testing chamber). The anxiogenic effect of MDMA on the emergence test was not prevented by pretreatment with any of the 5-HT receptor antagonists tested. These results indicate that prosocial effect of MDMA may involve 5-HT 1A and possibly 5-HT 2B/2C receptors. In contrast, MDMA-induced generalised anxiety, as measured by the emergence test, seems unlikely to involve the 5-HT 1A, 5-HT 1B or 5-HT 2A, 5-HT 2B or 5-HT 2C receptors.

Animals↗
PubMed1999

Behavioral and neurochemical consequences of lipopolysaccharide in mice: anxiogenic-like effects.

Systemic administration of lipopolysaccharide (LPS) induces sickness behaviors, as well as alterations of hypothalamic-pituitary-adrenal functioning commonly associated with stressors. In the present investigation, it was demonstrated that systemic LPS treatment induced a sickness-like behavioral profile (reduced active behaviors, soporific effects, piloerection, ptosis), which appeared to be dependent upon the novelty of the environmental context in which animals were tested. As well, LPS induced anxiogenic-like responses, including decreased time spent in the illuminated portion of a light-dark box, reduced open-arm entries in a plus-maze test, and decreased contact with a novel stimulus object in an open-field situation. The behavioral changes were accompanied by increased plasma ACTH and corticosterone levels. As well, LPS induced increased turnover of norepinephrine (NE), dopamine (DA) and serotonin (5-HT) in the paraventricular nucleus (PVN), median eminence plus arcuate nucleus, hippocampus, as well as NE turnover within the locus coeruleus and DA turnover within the nucleus accumbens. Although these neurochemical variations were reminiscent of those elicited by stressors, LPS was not particularly effective in modifying DA activity within the prefrontal cortex or NE within the amygdala, variations readily induced by stressors. Whether the LPS-induced anxiogenic-like responses were secondary to the illness engendered by the endotoxin remains to be determined. Nevertheless, it ought to be considered that bacterial endotoxin challenge, and the ensuing cytokine changes, may contribute to emotionality and perhaps even anxiety-related behavioral disturbances.

Adrenocorticotropic Hormone↗
PubMed1986

Acute toxicity of Microcystis aeruginosa and its cardiovascular effects.

The acute toxicity of a water extract from unialgal-cultured blue-green alga Microcystis aeruginosa M228 on mice and rats was studied. The mice intraperitoneally injected with the extract became lethargic and piloerection was seen. Terminally their ears, tails, limbs, and eyes became chalky white. The LD50 value of the extract for mice was estimated at 14.4 mg dry wt of cells/kg and that of rats was 67.4 mg/kg. Tachycardia was shown in the mice injected with the extract. A value of LD50 of coadministration of the extract and phenoxybenzamine in mice was significantly larger than that of the extract alone and survival time of mice injected with the extract and phenoxybenzamine was prolonged. These results suggest that the extract of the alga may take the acute toxic effects via the sympathetic nervous system.

Animals↗
PubMed2001

Attenuation of morphine dependence and withdrawal in rats by venlafaxine, a serotonin and noradrenaline reuptake inhibitor.

The effects of venlafaxine, a novel serotonin and adrenaline reuptake inhibitor, on the morphine withdrawal and activation of morphine conditioned place preference (CPP), were investigated in rats. Our results showed that the most morphine withdrawal signs, including jumping, writhing, shakes, exploring, lacrimation, piloerection, irritability, and diarrhea, were attenuated by pretreatment with 10 or 20 mg/kg venlafaxine. To investigate the effects of venlafaxine on relapse to opiate dependence, the morphine CPP was used and a dopamine D2 antagonist sulpiride was selected as a control drug. The morphine CPP disappeared following a 28-day drug-free period and appeared again after given a single injection of 1 mg/kg morphine. Acute treatment with sulpiride (25 or 50 mg/kg, i.p.) 30 min prior to 1 mg/kg morphine injection significantly blocked the reacquisition of CPP, while venlafaxine (10 or 20 mg/kg, i.p.) did not show significant effect. However, chronic treatment with venlafaxine (5 or 10 mg/kg, i.p. twice, daily, for seven consecutive days) significantly attenuated the reacquisition of morphine CPP, whereas chronic treatment with sulpiride (10 or 20 mg/kg, i.p.) have no significant effect. Our results demonstrated for the first time that venlafaxine strongly attenuates morphine withdrawal and morphine-induced reaquisition of

Adrenergic Uptake Inhibitors↗
PubMed1998

The selective cholecystokininB receptor antagonist L-365,260 diminishes the expression of naloxone-induced morphine withdrawal symptoms in normal and neuropathic rats.

The ability of a pretreatment with the cholecystokininB-receptor (CCK[B]) antagonist L-365,260 to prevent the development of morphine dependence was studied in normal and neuropathic (unilateral peripheral neuropathy) rats. A 4-day pretreatment regimen with two daily s.c. injections of either saline+saline, saline+morphine (3.0 mg/kg) or L-365,260 (0.2 mg/kg)+morphine was used, and withdrawal was precipitated by an injection of naloxone (1.0 or 2.0 mg/kg i.v.) at 24 h after the last pretreatment injection. After pretreatment with morphine alone, physical dependence developed in both normal and neuropathic rats. However, the incidence of teeth chattering and ptosis was higher in neuropathic rats. Pretreatment with the combination of L-365,260 and morphine prevented the expression of teeth chattering, ptosis, diarrhea, writhing and piloerection, but was devoid of effects on the exploratory activity among both groups of rats. These results suggest that endogenous CCK acting on CCK(B)-receptors may be involved in the development of morphine dependence both in normal and neuropathic rats.

Animals↗
PubMed1984

Both dopaminergic and adrenergic receptors in the brain are involved in the behavioural excitation induced by dibutyryl 3',5'-adenosine monophosphate and aminophylline in the rat.

Following administration of dibutyryl cyclic-AMP or aminophylline, but not vehicle solution, into the lateral cerebral ventricle of rats produced locomotor stimulation, head and body rearing, circling, (as indicated by an enhancement of gross movement), increased grooming, head swaying and scratching (as indicated by an enhancement of fine movement), tail elevation, piloerection and convulsion. The behavioural excitation produced by either dibutyryl cyclic-AMP or aminophylline was antagonized by pretreatment with intraventricular injection of either two alpha-adrenergic antagonists (phentolamine and yohimbine) or a dopaminergic antagonist (haloperidol), but not with either a beta-adrenergic antagonist (propranolol) or a narcotic antagonist (naloxone). In addition, direct administration of dibutyryl cyclic-AMP into either the anterior hypothalamus, the nucleus accumbens or the caudate-putamen complex of rats produced the same behavioural responses as those produced by the intraventricular injection. Again, the behavioural responses induced by intracerebral injection of dibutyryl cyclic-AMP was antagonized by pretreatment with either alpha-adrenergic antagonists or a dopaminergic antagonist. The present data indicate that both the dopaminergic and the adrenergic receptors in the brain are involved in the behavioural excitation induced by dibutyryl cyclic-AMP and aminophylline in the rat.

Aminophylline↗
PubMed1984

Clinical and experimental evidence of an opiate-like activity of lefetamine.

A case of lefetamine abuse (0.9-1.8 g/day in 15-30 i.m. divided doses) is reported. In this patient, the administration of naloxone precipitated a mild opiate-like withdrawal syndrome, characterized by mydriasis, piloerection, yawning and a slight increase of blood pressure. The complete withdrawal of lefetamine, substituted by a placebo regimen, aggravated these symptoms. Furthermore, experimental results showed that lefetamine induced a naloxone-reversible inhibition of the guinea-pig ileum contractile response to electric field stimulation, and that naloxone pretreatment of mice prevented lefetamine antinociceptive activity in the hot-plate test. The clinical and experimental findings suggest that lefetamine has an opiate-like activity.

Animals↗
PubMed2002

Early deprivation and behavioral and physiological responses to social separation/novelty in the marmoset.

Long-term effects of adverse early environment on neurobehavioral development have been reported for rodents and primates. The present study used daily early deprivation (ED), a paradigm developed for rats, for the first time in a nonhuman primate, the common marmoset, and investigated its effects on the behavioral and physiological responses to social separation/novelty (SSN) challenge tests in juveniles. On postnatal days (PNDs) 2-28, infants (n=5 twin pairs) were removed from the parents and placed alone in an isolation chamber for 30-120 min (9 h/week). Parents and control subjects (n=5 twin pairs) were briefly restrained (CON). At Weeks 18-20, behavioral responses of ED and CON juveniles to six 60-min SSN tests in an isolated cage, comprising 45 min alone and 15 min reunion with the father, were measured. Baseline and post-test urine samples were collected for measurement of cortisol. ED subjects exhibited significantly lower basal SSN urinary cortisol than CON, whilst SSN response cortisol values were similar in ED and CON. When alone, ED subjects were significantly less mobile and emitted significantly less contact calls than CON. Following reunion, ED subjects were significantly less in contact with or being carried by the father than CON and demonstrated significantly more tail piloerection. Although they require validation by additional parameters (e.g. cardiovascular), these data strongly suggest that early-life stress alters endocrine and behavioral responsiveness to psychosocial challenge in this primate and in a direction that could model important changes in disorders of human affective state.

Animals↗
PubMed1981

6-hydroxydopamine and aggression in cats.

The effect of 6-hydroxydopamine (6-OHDA) injected into the cerebral ventricles on behaviour of singly- and group-housed cats was investigated. 6-OHDA in doses of 0.5, 1 and 2 mg was administered every morning for 5 to 8 days. In small doses 6-OHDA in singly- and group-housed cats evoked motor phenomena such as tremor, ataxia, rigidity, weakness and sometimes clonic-tonic convulsions. Occasionally restlessness, irritability and rage were observed. Large doses of 6-OHDA in group-housed cats, after a short latent period (2-3 days) produced aggression which intensified on subsequent injections, and thereafter, on repeated administrations, no longer occurred. The aggression consisted of restlessness, irritability, anger, rage, apprehension, threat, attack, fighting, flight and crying. Of autonomic phenomena mydriasis, dyspnea and sometimes piloerection were observed. The aggression was initiated by the most restless cat, or by disturbing the animals, such as by moving the cage. When 6-OHDA no longer produced aggressive behaviour, motor changes such as tremor, ataxia, rigidity, walking on broad base, weakness with adynamia and clonic-tonic convulsions developed. These latter symptoms were produced by large doses of 6-OHDA in singly-housed cats. In these animals spontaneous signs of aggressive behaviour usually were not observed, although if handled they showed rage, snarling and hissing. When singly-housed cats were kept in the same cage with group-housed animals, the singly-housed cats usually became aggressive. It appears that hyperactivity induced aggression in 6-OHDA-treated cats.

Aggression↗