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PubMed1994

Effects of dizocilpine in withdrawal seizure-prone (WSP) and withdrawal seizure-resistant (WSR) mice.

Mice selectively bred to be Withdrawal Seizure-Prone (WSP) or Seizure-Resistant (WSR) after chronic ethanol administration have been reported to be differentially sensitive to the anticonvulsant and proconvulsant effects on alcohol withdrawal of drugs interacting with glutamate receptors. Several behavioral effects of the noncompetitive glutamate receptor antagonist, dizocilpine, were determined in WSP and WSR mice to see whether their differential sensitivity generalized to effects unrelated to seizures, and to see whether it was only apparent during ethanol withdrawal. Dizocilpine potentiated the loss of righting reflex induced by ethanol, and dose-dependently stimulated habituated and nonhabituated open field activity. WSP and WSR mice were equally sensitive to these effects of dizocilpine. Pretreatment with dizocilpine increased the transcorneal amperage necessary to produce maximal electroshock seizures: WSR mice were more sensitive than WSP to this effect. Ethanol withdrawal (i.e., testing 6 h after a 24-h exposure to ethanol vapor) and dizocilpine had several effects on mice tested in the hole-in-wall apparatus. Several differences between WSP and WSR mice were also found, but in no case did dizocilpine differentially affect ethanol-withdrawing WSP and WSR mice. Across these experiments, differences between WSP and WSR mice in response to dizocilpine were rather specific. For some responses, WSP and WSR mice were equally sensitive, but only in the seizure-related measure assessed were naive WSR mice more sensitive than WSP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Genetic influences on locomotor activating effects of ethanol and sodium pentobarbital.

The paradoxical capability of sedative-hypnotics to produce behavioral disinhibition varies among genotypes. In DBA/2 mice ethanol (ETOH) produced strong locomotor stimulation with the peak of the biphasic curve at 1.5 g/kg IP. C57BL/6 mice showed no activation, and F1S were intermediate. These characterizations held for a variety of behavioral indices derived from 15 min tests, such as distance, speed, and rest time, at doses in the 0-2.0 g/kg range. Analogous studies with sodium pentobarbital (0-40 mg/kg) yielded a similar pattern of strain differences in locomotor stimulation. In contrast, loss of righting reflex durations (60 mg/kg PENTO, IP) were similar in the two strains, indicating dissociation of activating and sedative effects. In complementary studies, long- and short-sleep mice, which were bred for differences in soporific effects of ETOH, showed similar activation profiles at ETOH doses up to 1.5 g/kg and PENTO doses up to 30 mg/kg. These studies provide support for an hypothesis of common genetic control of the activation effect for ETOH and PENTO.

Animals↗

PubMedDate not supplied

Structure-activity relationships of BDB and its monomethyl and dimethyl derivatives.

The purpose of the present study was to evaluate the behavioral effects of 3,4-methylenedioxyphenyl-2-butanamine (BDB), N-methyl BDB (MBDB), and N,N-dimethyl BDB (MMBDB) in the newly hatched chicken. The primary amine, BDB, produced effects that are commonly seen in the chicken after administration of both hallucinogens and psychomotor stimulants (i.e., distress vocalization, tremor, and wing extension). It also produced abnormal body posture and bursting forward locomotion, effects elicited only by hallucinogens. Loss of righting reflex also occurred at the highest (16 mg/kg) dose of BDB, and this effect is typical of d-amphetamine but has not been reported for hallucinogens. The monomethylated derivative of BDB, MBDB, was less potent than BDB, and the N,N-dimethyl analogue of BDB, MMBDB, had no effect on behavior at the doses tested.

Animals↗

PubMedDate not supplied

A behavioral comparison of Nexus, cathinone, BDB, and MDA.

The effects of 4-bromo-2,5-dimethoxyphenethylamine (Nexus), 3,4-methylenedioxyamphetamine (MDA), 3,4-methylenedioxyphenyl-2-butanamine (BDB), and cathinone were studied in the newly hatched chicken and compared to the effects of d-amphetamine and three hallucinogens in the same species. Cathinone, a psychomotor stimulant in man (6), produced effects that were qualitatively similar to effects seen after administration of d-amphetamine (i.e., distress vocalization, wing extension, inability to stand, and loss of righting reflex). BDB, a compound with unknown activity in man, and two known hallucinogens, Nexus (5) and MDA (1), produced effects in the chicken that are common to both stimulants and hallucinogens in this species. For example, both MDA and BDB produced abnormal body posture that was identical to that reported after administration of hallucinogens such as lysergic acid diethylamide (LSD) and harmine (11). Nexus, on the other hand, produced rigid penguin-like posture, an effect seen in the chicken after administration of another hallucinogen, mescaline (12). BDB also produced bursting forward movements, an effect commonly observed after LSD and harmine. Our findings suggest that the young chicken can be used as an alternative, nonmammalian, model for predicting classification of new compounds.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗

PubMed1996

Genetic differences in tolerance and sensitization to the sedative/hypnotic effects of alcohol.

Initial sensitivity to alcohol and the development of alcohol tolerance were examined in rats of the selectively bred alcohol-preferring (P) and -nonpreferring (NP) lines. All rats received two alcohol injections (3.0 g/kg b.wt., IP) separated by either 1 or 2 days. P rats were less sensitive to the behaviorally impairing effects of alcohol than were NP rats, as evidenced by a longer latency to lose righting reflex (RR) and a shorter time to recover RR following an initial alcohol injection. When 1 day separated the two alcohol injections, P rats recovered the RR more rapidly following a second injection compared to the first, indicating that the P rats developed tolerance to the sedative/hypnotic effects of alcohol. In contrast, the NP rats recovered the RR more slowly following the second injection compared to the first, indicating that the NP rats developed sensitization to alcohol. Tolerance in the P line and sensitization in the NP line disappeared when 2 days separated the two alcohol injections. Line differences in initial sensitivity and tolerance/sensitization to the behaviorally impairing effects of alcohol may contribute to the differences in alcohol consumption observed in the P and NP lines.

Alcohol Drinking↗

PubMed1996

Neurochemical and neurobehavioral effects of repeated gestational exposure to chlorpyrifos in maternal and developing rats.

Acute exposure to the organophosphate pesticide chlorpyrifos (CPF) on gestation day 12 (GD12, 200 mg/kg/ml, SC) causes extensive neurochemical changes in maternal brain but lesser changes in fetal brain. In the present study, we examined the relative neurotoxicity of repeated, lower-level CPF exposures during gestation in rats. Pregnant Sprague-Dawley rats were exposed to CPF (6.25, 12.5, or 25 mg/kg per day, SC) from GD12-19 and sampled at either GD16, GD20, or postnatal day 3 (PND3) for measurement of various maternal and developmental neurochemical markers. In contrast to the high acute dose exposure, no maternal toxicity was noted with repeated lower-level dosing. Extensive acetylcholinesterase (AChE) inhibition (83-90%) was noted in maternal brain at all three time points following repeated exposures (25 mg/kg). Higher AChE inhibition (58%) was noted in fetal brain at GD20 compared to 19-25% on PND3 in treated pups cross-fostered to control dams and in control pups cross-fostered to treated dams following repeated exposures (25 mg/kg per day). Whereas similar reductions in brain muscarinic receptor binding were noted at GD20 and PND3 in dams and developing brain between acute and repeated dosing regimens, greater changes in [3H]CD and [3H]cytisine binding were evident following repeated exposures. Righting reflex and cliff avoidance tests were markedly altered following repeated exposures. The results suggest that lower-level repeated exposures to CPF cause extensive neurochemical and neurobehavioral changes in developing rats in the absence of maternal toxicity.

Acetylcholinesterase↗

PubMed1990

Effect of endothelin-1, endothelin-3 and C-terminal hexapeptide, endothelin (16-21) on motor activity in rats.

Intracerebroventricular administration of ET-1 (12.5 and 25 pmol/rat) and ET-3 (25 and 50 pmol/rat) induced the loss of the righting reflex and barrel-rolling behaviour in rats. The C-terminal hexapeptide ET(16-21) did not produce these effects. The automated recording of motor activity revealed that, unlike ET (16-21), both ET-1 and ET-3 evoke a dose-regulated increase of the immobility time. Pretreatment with peptidase inhibitors did not modify the activity of subthreshold doses of peptides. Since ET (16-21) display full agonist properties at ETB but does not interact with ETA receptors, the present data suggest that the behavioural syndrome induced by centrally administered ET-1 and ET-3 may be mediated by stimulation of ETA receptors.

Animals↗

PubMed1993

Spatial learning in an enclosed eight-arm radial maze in rats with sodium arsanilate-induced labyrinthectomies.

Bilateral vestibular dysfunction was induced in Long-Evans male rats (n = 7) by intratympanic injections of sodium arsanilate (30 mg/side). Control rats (n = 6) received isotonic saline. Animals were tested for labyrinthine integrity by measuring air-righting and contact-righting reflexes. Rats were reduced to 85% of free-feeding body weight and tested in an enclosed 8-arm radial maze (1 trial/day over 10 days). Labyrinthectomized animals made significantly more errors (p < .001) and, unlike the controls, showed no significant improvement on this measure over acquisition training. These rats also made significantly more (p = 0.018) sequential same arm reentries and fewer sequential adjacent arm entries (p < .01). These findings demonstrate that information obtained from the vestibular system is very important in spatial learning in the rat.

Animals↗

PubMed1995

Coloboma hyperactive mutant exhibits delayed neurobehavioral developmental milestones.

The coloboma mutation (Cm) is a neutron-irradiation induced gene deletion located on the distal portion of mouse chromosome 2. This deletion region includes a gene encoding the synaptic vesicle docking fusion protein, synaptosomal-associated protein of 25 kDa (SNAP-25). The resulting mutation is semi-dominant with heterozygote mice exhibiting a triad of phenotypic abnormalities that comprise profound spontaneous hyperactivity, head bobbing and a prominent eye dysmorphology. Because the expression pattern of two SNAP-25 isoforms begins to change during the first postnatal week, neurobehavioral developmental milestones were examined in order to determine if the expression of the coloboma behavioral phenotype could be detected during this period of postnatal development. The early classification of coloboma mutant offspring may help to further describe the penetrance of this mutation as well as the contribution of developmental changes to the adult behavioral phenotype. The coloboma mutation resulted in delays in some tests of complex motor skills including righting reflex and bar holding. In addition, coloboma mutants were characterized by body weight differences (first appearance day 7) and hyperreactivity to touch (day 11) and head bobbing (day 14). These data demonstrate disruptions in the time course of attaining developmental milestones in coloboma mutants and provide further evidence supporting the hypotheses that alterations in Snap gene expression are associated with functional behavioral consequences in developing offspring.

Aging↗

PubMed1987

Persistence of habituation deficits after neurological recovery from severe thiamine deprivation.

Rats were fed a thiamine-deficient diet for 4 weeks and injected daily with pyrithiamine during the last two weeks of the diet. This regime induced severe neurological anomalies such as ataxia, loss of righting reflex and visual place reflex, and finally full tonic-clonic seizures. These symptoms are reminiscent of the clinical Wernicke-Korsakoff syndrome. Injection of thiamine dramatically reversed these symptoms within one or two hours as seen in Wernicke patients. Six weeks later these rats showed a marked deficit in habituation of exploratory behavior and of the auditory orienting response. To what extent this chronic deficit in habituation contributes to the cognitive dysfunctions seen in Wernicke-Korsakoff patients is discussed. Histological examination of the brains of 6 of the rats revealed a heterogeneous pattern of damage to the brainstem, including mamillary bodies and several thalamic nuclei, reminiscent of that seen in Korsakoff patients. In addition there were many dark abnormal cells in limited fields of hippocampus neocortex and thalamus in almost all animals.

Animals↗

PubMed1992

Effects of thyrotropin releasing hormone and its analogues on unconsciousness following head injury in mice.

We examined the effects of thyrotropin releasing hormone (TRH) and its analogues (DN-1417: gamma-butyrolactone-gamma-carbonyl-histidyl-prolinamide citrate; MK-771: L-pyro-2-aminoadipyl-histidyl-thiazolidine-4-carboxamide; TSII-37: H-Lys-Gln-His-Pro-Gly-Ser-OH) on arousal in head injured mice, an animal model of unconsciousness. TRH, DN-1417, MK-771 and TSII-37 were injected 10 min before the head injury. TRH, DN-1417 and MK-771 caused dose-dependent decreases in the time required for recovery of the righting reflex time and in the time from the head injury to the onset of spontaneous movement. TSII-37 had no effect, when compared with the control group. In terms of the minimum effective dose, TRH and DN-1417 were of similar potency, but MK-771 was about 30-fold stronger than TRH. Measurement of the cross-reactivities of these TRH analogues by radiolabeled receptor assay suggest that the structure-binding relationship is proportional to the structure-activity relationship.

Animals↗

PubMed1984

Nephrotoxic and ototoxic effects of hydroxygentamicin in cats.

Hydroxygentamicin, an aminoglycoside antibiotic, was administered subcutaneously to cats in doses up to 160 mg base/kg daily for 10 to 13 weeks. Gentamicin and a vehicle solution were tested as positive and negative control, respectively; in one test netilmicin was also included for comparative purposes. Several parameters, including serum urea nitrogen, serum creatinine, organ/body weight ratios, serum and tissue concentrations of the antibiotics, and renal pathology, were determined to ascertain the nephrotoxic potential of the three aminoglycosides. In addition, observations for the onset of ataxia and impairment of righting reflex were made during the course of the studies to compare the vestibular ototoxic effects of the three antibiotics. Although serum urea nitrogen and serum creatinine values increased markedly in those cats which eventually died or were sacrificed moribund, these parameters in survivors were slightly but not significantly higher than controls. Serum concentrations of the drugs were proportional to the doses administered, but renal concentrations were approximately two and five times as high for netilmicin and gentamicin, respectively, as they were for equivalent doses of hydroxygentamicin. The morphological changes observed in the kidney of cats given 60 mg base/kg of hydroxygentamicin were slightly less than those seen in cats administered 10 mg base/kg of gentamicin; similarly, kidney changes in cats given netilmicin were observed approximately twice as frequently as they were in those receiving equivalent doses of hydroxygentamicin. The nephrotoxic effects of aminoglycoside antibiotics were directly related to renal drug concentration and not to serum concentration, which was a function of dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoglycosides↗

PubMed1988

Fetal alcohol effects: evidence of developmental impairment in the absence of immunotoxicity.

Pregnant CD-1 mice were intubated from Days 5-17 of gestation with an isocaloric solution of ethanol and/or maltose dextrins in 10% Bio-Serv liquid diet, at doses of 0, 6, and 9 g/kg/day. The control females were food-restricted so that their food consumption matched that of the high-dose females. At delivery, the pups were assigned surrogate mothers and litters were culled to a uniform litter size, when possible. Immediately following birth some pups were examined using a battery of behavioral/developmental tests to monitor postnatal development. At 6-8 weeks of age, other pups were evaluated for changes in immune function. Another group of pups was terminated at 12 weeks of age for hematology and clinical chemistry determinations and histological examination of selected organs. Postnatal developmental delays were seen in pinna detachment, surface righting reflex, eye opening, and incisor eruption. There was no characteristic pattern to immune alterations of the plaque forming cell response to a T-dependent antigen sheep red blood cells, delayed hypersensitivity, and T- and B-lymphocyte blastogenesis. Possible kidney pathology was indicated by a reduction in blood urea nitrogen in the offspring of females treated with 9 g/kg/day. No treatment-related effects were noted in those tissues which were examined histologically.

Animals↗

PubMed1989

Absence of developmental effects in CF-1 mice exposed to aspartame in utero.

Aspartame (L-aspartyl-L-phenylalanine methyl ester) is a widely used high potency dipeptide sweetener. Developmental toxicology studies have been performed in several species documenting no effects of high doses of aspartame. Recently, a study by Mahalik and Gautieri [1984) Res. Commun. Psychol. Psychiatry Behav. 9, 385-403) reported a delay in the achievement age for the visual placing response in mice pups after maternal administration of high dosages of aspartame during late gestation. In the present study developmental parameters were determined in offspring of CF-1 mice after maternal administration of aspartame at 500, 1000, 2000, and 4000 mg/kg body wt by oral gavage. Aspartame was administered on Days 15 through 18 of gestation. Maternal body weight, food consumption, gestation length, reproductive indices, and litter size were not affected by aspartame treatment. In the pups, body weights, negative geotaxis, and surface and midair righting reflexes were not altered by treatment. There was no delay in the development of the visual placing response regardless of the method employed for assessment (grid or rope) or the manner by which the data were analyzed. There were also no changes in time of eye opening, reflex pupil closure, and ophthalmoscopic examination in the offspring. Thus, neither physical nor functional development was altered in mice after in utero exposure to extremely large dosages of aspartame. More specifically, in utero exposure to aspartame did not affect the development of the visual system in mice.

Animals↗

PubMed1989

Systemic effect of ipecac on acute toxicity of phenobarbital and theophylline in rats.

The emetic agent ipecac is widely used for the initial treatment of acute oral drug overdose. Its emetic and gastric evacuative efficacies have been studied extensively but its potential for pharmacologic interactions with various drugs and other possible poisons has not been explored. The purpose of this investigation was to determine if ipecac can alter the acute toxicity of two widely used drugs that act on the central nervous system, phenobarbital and theophylline. Ipecac syrup, 5 ml/kg, was administered by gavage to male Lewis rats either 1 hr before or 15 or 30 min after the start of an iv infusion of phenobarbital or theophylline. Control animals received the syrup vehicle only. Ipecac elicited vomiting-like behavior (frequent, wide opening of the mouth) for more than 1 hr. The drug infusion was stopped immediately after onset of the loss of righting reflex (phenobarbital) or maximal seizures (theophylline). Samples of cerebrospinal fluid, blood (for serum), and the brain were obtained at that time for analysis of drug concentrations. There were no significant differences between control and ipecac-treated animals with respect to the dose requirements and drug concentrations in cerebrospinal fluid, serum, and brain at the respective pharmacologic endpoint. It is concluded that ipecac has no apparent effect on the acute toxicity of phenobarbital and theophylline in rats.

Animals↗

PubMed1983

Pharmacology of beta-phenylethylamine-induced seizures in mice.

The endogenous trace amine beta-phenylethylamine (PE) produced tonic-clonic seizures in male Swiss mice when administered in doses of 125-200 mg/kg. The number of mice exhibiting PE-induced seizures, the latency to onset of first seizure and the latency to loss of the righting reflex were dose dependent. Pretreatment with the benzodiazepines diazepam, chlordiazepoxide, midazolam and clonazepam significantly reduced the incidence of PE-induced seizures. Similarly, increasing brain gamma-aminobutyric acid (GABA) levels by injection of the GABA-transaminase inhibitors aminooxyacetic acid or gabaculine afforded significant protection against PEA's convulsant effects. The data suggest that PE when administered at high doses may interfere either directly or indirectly with GABAergic neurotransmission in the central nervous system. In addition, since PE induces an epileptiform spiking pattern and produces seizures in rodents it appears possible that the amine may play a role in some forms of human epilepsy.

Animals↗

PubMed1990

Phaclofen antagonizes the antinociceptive but not the sedative effects of (-)-baclofen.

1. Intraperitoneal (ip) injection of (-)-baclofen induced long-lasting antinociceptive and sedative effects in rats. 2. Phaclofen, the phosphonic derivative of baclofen, fully antagonized the antinociceptive effect of (-)-baclofen. When injected intracerebroventricularly (icv), but not ip, phaclofen antagonized in a dose-dependent fashion (50-200 micrograms) the delays in behavioral response induced by (-)-baclofen (2.5-10 mg/kg ip) in both hot plate and tail flick tests. 3. In addition phaclofen (100 micrograms icv) counteracted the loss of the righting reflex induced by (-)-baclofen (7.5-15 mg/kg ip). 4. In contrast, phaclofen (100-200 micrograms icv) counteracted only in part the sedative effect of (-)-baclofen. In rats pretreated with the antagonist (200 micrograms icv), the electrocorticographic hypersynchrony due to (-)-baclofen (5 mg/kg ip) is replaced by a synchronized pattern associated with behavioral sedation. 5. These data are consistent with the reported antagonism by phaclofen on the effects of (-)-baclofen. They also seem to indicate that in rats phaclofen-sensitive GABA-B receptors play an important role in the analgesic effects of baclofen, but only a minor role in the sedative effects of this drug.

Analgesics↗

PubMed1993

Has iprindole an alpha adrenergic activity?

1. Acute administration of iprindole potentiated the toxicity of 1-norepinephrine and increased the intensity of oxotremorine-induced tremors. 2. On the forced swimming test combination iprindole with imipramine reduced the duration of immobility. 3. The action of yohimbine on the locomotor activity was antagonized by a pre-injection of iprindole. 4. Iprindole increased and prolonged exophthalmia and loss of righting reflex induced by xylazine. 5 All these results seems indicate that iprindole has an indirect alpha 1 and alpha 2 adrenergic activity.

Adrenergic alpha-Agonists↗