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PubMed1995

Excitatory amino acid antagonists and pentylenetetrazol-induced seizures during ontogenesis: III. The action of kynurenic acid and glutamic acid diethylester.

N-methyl-D-aspartate (NMDA) receptor antagonists are anticonvulsant drugs with specific activity against tonic-clonic pentylenetetrazol-induced seizures. However, they do not affect clonic seizures with preserved righting reflexes. In these experiments, we tested the anticonvulsant activity of strychnine-insensitive glycine receptor (at the NMDA site) antagonist kynurenic acid and nonspecific excitatory amino acid receptor antagonist glutamic acid diethylester (GDEE) in the pentylenetetrazol-induced seizure model in developing rats 7, 12, 18, 25, and 90 days old. Control rats were injected with pentylenetetrazol (100 mg/kg subcutaneously). Other rats were pretreated either with kynurenic acid (40, 80, or 240 mg/kg IP) or with GDEE (0.48-480 mg/kg IP), followed by pentylenetetrazol (100 mg/kg). In very young rats (7 and 12 days), both kynurenic acid and GDEE increased the incidence of clonic seizures, whereas the occurrence of tonic-clonic seizures was suppressed or delayed compared to controls. This effect is very similar to the anticonvulsant action of the competitive and noncompetitive NMDA receptor antagonists. In adult rats, the pretreatment with rather higher doses of kynurenic acid or GDEE suppressed or delayed clonic seizures as well as tonic-clonic seizures. Both drugs also induced behavioral side effects: repetitive orientation, wet dog shakes, and frequent jumping. Our data show that there are only weak and nonconsistent age-specific anticonvulsant effects resulting from the blockade of strychnine-insensitive glycine receptor often associated with serious side effects, thus decreasing chances to develop effective antiepileptic treatment in this drug class.

Age Factors↗

PubMed1984

Lack of behavioural teratogenic effect of phenytoin in rats.

A small battery of tests (static and air-righting reflexes, eye opening and a narrowing bridge test) was used to investigate the behavioural teratogenic potential of prenatal oral exposure (day 7-19 of gestation) of up to 100 mg phenytoin/kg/day to female rats. No treatment-related effects upon mother or offspring were detected. In order to validate our narrowing bridge test, neonatal old rats were tested over 4 weeks following early postnatal exposure to acrylamide (5 X 50 mg/kg/day i.p.). These animals showed a severe transient deficit compared with saline-treated controls. Despite the absence of an effect using phenytoin, the narrowing bridge test is considered worthy of further validation.

Acrylamide↗

PubMed1985

Inhibition of mouse liver alcohol dehydrogenase by methyl N-butyl ketone.

Methyl N-butyl ketone (MNBK) inhibited the activity of mouse liver alcohol dehydrogenase (LADH) in vitro. Ethanol elimination was reduced in MNBK-treated mice as compared to controls. Ethanol-induced induced loss of righting reflex was significantly prolonged in mice pretreated with MNBK.

Alcohol Dehydrogenase↗

PubMed1991

A symptomatological assessment of organophosphate-induced lethality in mice: comparison of atropine and clonidine protection.

A comprehensive symptomatological observational battery in conjunction with acute toxicity testing, evaluated with the method of a hyperbolic curve relating survival time (T) to dose (D), was used to characterize quantitatively the lethal toxicities of the organophosphorus (OP) compound, sarin, in mice. The experimental data observed with sarin (0.4-4.0 mg/kg s.c.), alone or in combination with atropine (ATR) (20 mg/kg i.p.), were plotted as a graph of D/T against D, a linearizing transformation of the hyperbolic function. This linearized plot gave two straight lines, deflecting at 1.2 mg/kg, in terms of latency to whole body tremor (BT) and loss of the righting reflex (LR). At lower lethal doses of sarin (0.4-1.2 mg/kg) with ATR pretreatment, the D/T vs. D curves of BT and LR were shifted in parallel to the left, while at high lethal doses (1.6-4.0 mg/kg) these curves interpolatedly converged. The sequelae and/or severity of symptoms were also comparatively different between the range of lower and high lethal doses as noted above. It has been claimed that the protective actions of ATR and clonidine (CLD) against the lethal effects of cholinesterase inhibitors are associated with different underlying mechanisms, i.e. presynaptic versus post-synaptic cholinergic inhibition. The protective effects of a single dose of ATR (20 mg/kg) and CLD (1.0 mg/kg), after 38 and 15 min of intraperitoneal pretreatment, respectively, alone or in combination, challenged with 2 x, 4x and 8x LD50's of sarin were also comparatively evaluated. ATR resulted in a nonsignificant increase in latency to onset of BT and LR. CLD significantly delayed the onset of these symptoms against all 3 dose levels of sarin intoxication, whereas ATR plus CLD additively increased the latency to the onset of these symptoms. The present results indicate that at lower dosages of sarin (less than or equal to 4 x LD50's) its mode of action appears to be mediated mainly by a/muscarinic mechanism, whereas at high doses it is mediated by some other non-specific actions superimposed on the cholinergic actions of sarin. The present study also lends support to the hypothesis of the existence of different forms of OP intoxication on the strength of lethal exposure. The possible mechanisms of both sarin lethality and ATR- and CLD-mediated protection are briefly discussed.

Animals↗

PubMed1990

Hepatoprotective effects of astraglus root.

Oral administration of an ethanol extract of the root of Astragalus membranaceus alleviated liver injury induced by stilbenemidine. Pre-administration in mice reduced elevated SGPT levels and subacute toxicity of stilbenemidine, decreased pentobarbital-induced loss of righting reflex and protected hepatic cells from pathological changes.

Alanine Transaminase↗

PubMed1990

Screening of Icacina trichantha extracts for pharmacological activity.

Some preliminary studies were conducted on the biological activities of Icacina trichantha in mice. In vitro tests performed with the 70% ethanol, petroleum ether and aqueous extracts of tubers, roots, stems and leaves did not show contraction of isolated guinea pig ileum up to a bath concentration of 40.5 mg/ml. Graded oral doses (100, 200, 400 and 800 mg/kg) of the aqueous extract of tubers produced wet faeces in mice with the number of wet faeces increasing with increasing dose up to 400 mg/kg. A time-course study of the purgative effect showed the maximum purgative response to be 7-8 h after oral dosing. The aqueous extract of tubers significantly potentiated pentobarbital-induced loss of righting reflex at a dose of 80 mg/kg i.p. but this dose did not protect mice from strychnine or leptazole convulsions and death.

Animals↗

PubMed1994

Some neuropharmacological effects of an ethanolic extract of Maprounea africana in rodents.

The ethanolic extract of the leaves of Maprounea africana (Euphorbiaceae), a medicinal plant in the Congolese traditional medicine, induced hypothermia and reduced the latency to the loss of the righting reflex and prolonged the sleeping time induced by pentobarbital in mice. It also significantly delayed the onset of clonic convulsions induced by pentylenetetrazole in mice. However, the extract did not affect either generalized convulsions induced by maximal electroshock and picrotoxin or limbic status epilepticus produced by pilocarpine and kainic acid.

Animals↗

PubMedDate not supplied

Revitalization of the AA and ANA rat lines: effects on some line characteristics.

After 37 generations, the AA and ANA rat lines developed for high and low voluntary alcohol consumption, were revitalized by crossing with hybrid (Brown Norwegian X Lewis) rats. The line difference in alcohol consumption continued, although initially diminished, after revitalization. The greater acetaldehyde accumulation and longer loss of righting reflex after ethanol administration of the ANAs persisted after revitalization, but significant line differences in motor impairment were no longer found. The line characteristics for open-field test behavior were also different than before revitalization. Of the previously-observed line differences that have now been reexamined, the level of blood acetaldehyde during ethanol metabolism appears to be the most closely related to the genetically-determined factors influencing alcohol consumption.

Acetaldehyde↗

PubMedDate not supplied

Effect of ethanol on tyrosine hydroxylation in brain regions of long and short sleep mice.

The effect of ethanol on the in vivo rate of tyrosine hydroxylation in 6 brain regions was examined in two lines of mice selectively bred for a differential sensitivity to ethanol. The mice are designated long-sleep (LS) and short-sleep (SS) and lose their righting reflex for a duration of 100 minutes (LS) and 13 minutes (SS) following an intraperitoneal dose of ethanol of 4.0 g/kg. DOPA accumulation after NSD-1015 administration was measured in the absence and presence of ethanol (4.0 g/kg, IP) in the periods 5-35 minutes and 85-115 minutes after saline or ethanol. There were no differences between the lines in either basal catecholamine levels or basal tyrosine hydroxylation rates (as measured by DOPA accumulation) in any brain region except the cerebellum, where the norepinephrine content in the SS mice is 33% greater and the tyrosine hydroxylation rate is 25% higher than that in the LS mice. In the presence of ethanol, there was a differential effect on the in vivo tyrosine hydroxylation rate. In the cerebellum of both LS and SS mice there was a decreased rate of tyrosine hydroxylation in the early period after ethanol, but the rate in the cerebellum of SS mice returned to the control value at 85-115 min. At that time, the rate in LS mice is still decreased. In the locus ceruleus, hypothalamus and frontal cortex, ethanol has no effect on the rate of tyrosine hydroxylation in either LS or SS mice during the early period, but ethanol decreases the rate during the later period in the LS mice only.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Temperature modulates ethanol sensitivity in mice: generality across strain and sex.

Findings in our laboratory indicate that body temperature alters ethanol potency as measured by sleep-time, wake-up brain ethanol concentration and mortality in male C57BL/6J mice. The current studies tested the generality of these results. Experiment one tested age-matched, drug-naive, male C57BL/6S and BALB/cS mice. Experiment two tested age-matched, drug-naive, male and female C57BL/6J mice. Each mouse was injected IP with 3.6 g/kg ethanol (20% w/v). After losing its righting reflex, the mouse was placed into a v-shaped sleep tray within a chamber kept at a designated temperature from 12 to 36 degrees C. Upon awakening, rectal temperature was measured and blood and brain samples were taken for gas chromatographic analysis. As in previous studies, ambient temperature modulated the body temperatures and sleep-times of intoxicated animals. More important, wake-up rectal temperatures were positively correlated with sleep-times and negatively correlated with wake-up ethanol concentrations in all animals tested. These results support the hypothesis that brain sensitivity to ethanol depression varies with body temperature in accordance with membrane perturbation theories of anesthesia.

Anesthetics↗

PubMedDate not supplied

A comparison of ethanol absorption and narcosis in long- and short-sleep mice following intraperitoneal or intragastric ethanol administration.

Blood ethanol concentrations (BEC) were determined in Long-Sleep (LS) and Short-Sleep (SS) mice during a 30 min period following ethanol (ETOH) administration. Absorption of ETOH was rapid and followed a similar time course in the two lines after intraperitoneal (IP) administration of 3.8 or 4.5 g/kg. Following intragastric (IG) administration, slower absorption and lower peak BECs were noted in both lines, but in LS mice this effect was more pronounced. The two routes of administration were not effective in altering duration of loss of the righting reflex (LRR), or waking BECs following 4.5 g/kg ETOH. LS mice had the expected longer LRR durations and lower BECs at waking than did SS mice. Differences in absorption rate and peak BEC are concluded to be unrelated to ETOH neurosensitivity in these mice.

Animals↗

PubMedDate not supplied

Genetic approaches to studying drug abuse: correlates of drug self-administration.

Some important issues in substance abuse are the relationship between propensity to self-administer a drug and neurosensitivity to that drug; similarities and differences between various models of drug-seeking behavior; and the commonality of drug-seeking behavior across drugs and genotypes. Findings related to these issues are now emerging from the areas of pharmacogenetics and operant drug self-administration. Ethanol has been readily established as a positive reinforcer in AA (Alcohol Accepting), P (Preferring) and LEWIS rats, as well as C57BL/6J and LS/Ibg mice. In low ethanol preferring F344 and NP (Non-Preferring) rats, ethanol maintains significant but low levels of responding. Ethanol does not maintain lever-pressing behavior in BALB/cJ or SS/Ibg mice, and is avoided in DBA/2J mice. This pattern of reinforcement from ethanol is only moderately correlated with ethanol preference, and is not correlated with neurosensitivity to ethanol, at least as measured by duration of loss of the righting reflex (LORR). However, these genotypic patterns of reinforcement from ethanol do appear to correlate highly with patterns of reinforcement from cocaine and opiates. From these findings it is concluded that: 1) there exist important genetic determinants of drug reinforced behavior; 2) ethanol preference is not a highly accurate measure of reinforcement from ethanol; 3) sensitivity to ethanol as measured by LORR and self-administration of this drug are not highly genetically correlated; and 4) drug-seeking behaviors maintained by ethanol, cocaine and opiates may have at least some common biological determinants.

Animals↗

PubMedDate not supplied

GM1 ganglioside reduces ethanol intoxication and the development of ethanol dependence.

The monosialoganglioside, GM1, protects the nervous system against a variety of insults. In this study, we evaluated the protective properties of GM1 on ethanol intoxication and development of dependence. GM1 (20-40 mg/kg, IP) reduced the extent and duration of ataxia produced by ethanol (2 g/kg, IP, 15-95 min), and delayed the onset of loss and reduced the duration of the righting reflex (LORR) produced by ethanol (4.2 g/kg, IP). GM1 did not alter ethanol-induced hypothermia or the rate of ethanol clearance. Rather, GM1 increased the waking blood ethanol concentration. In animals fed a complete liquid diet containing 4.5% ethanol, concurrent administration of GM1 (40 mg/kg/day) blocked the tremors, hypolocomotion, and anxiety-like behavior associated with ethanol withdrawal. These findings demonstrate that GM1 reduces both ethanol's acute intoxication and the signs and symptoms of ethanol withdrawal by a mechanism not related to ethanol pharmacokinetics.

Alcoholic Intoxication↗

PubMedDate not supplied

Nerve growth factor influences neurobehavioral development of newborn mice.

Thirty-six male pups of the CD-1 outbred strain received from postnatal day 2 to day 10 a daily subcutaneous injection of either highly purified murine Nerve Growth Factor (NGF; 5 mg/kg), cytochrome c (5 mg/kg), or saline solution. NGF-treated pups showed a slight, but significant, reduction in body weight gain and a concomitant acceleration in the appearance of early signs of neurobehavioral maturation such as righting reflex, cliff aversion, and response to tactile stimulation of the perioral area. Other responses, including the ultrasonic vocalization pattern on day 7, were unaffected or affected to a lesser extent.

Animals↗

PubMedDate not supplied

Diazepam and caffeine administration during the first week of life: changes in neonatal and adolescent behavior.

The male offspring of hooded Lister rats were fostered at birth into 23 experimental litters. One pup in each litter was allocated to each of the following treatment groups: vehicle control; caffeine (15 or 30 mg/kg); diazepam (10 mg/kg, alone or plus caffeine 15 or 30 mg/kg). Pups were given daily injections on neonatal days 1-7 and were observed for 15 min following each injection. Diazepam significantly increased paddling and forward walking, particularly on days 5 and 7; caffeine also increased these behaviors, but less markedly. Diazepam increased the incidence of clonic jerks, particularly on day 7 and increased the spontaneous loss of righting reflex. The pups were then left undisturbed until weaning at day 21 and testing from days 35-42. There were no lasting effects of the neonatal treatments in two tests of anxiety, or in passive avoidance performance. Rats that had been treated neonatally with diazepam had significantly lower motor activity scores and reared less in the holeboard than did controls, and neonatal treatment with caffeine also resulted in lower motor activity scores. Neonatal treatment with caffeine made rats more aggressive (increased kicking and pushing) when they were intruding into another rat's territory. Neonatal treatment with diazepam increased aggression in resident rats, and this was counteracted by neonatal treatment with caffeine. Neonatal caffeine treatment enhanced rats' unconditioned preference for the black chamber in a black-white preference test and neonatal diazepam treatment reduced it.

Aggression↗

PubMedDate not supplied

Sensorimotor maturation and alcohol responsiveness in rats prenatally exposed to alcohol during gestational day 8.

On gestational day 8, pregnant Sprague-Dawley derived rats received two intraperitoneal injections of 0.015 ml/g body weight of a 24% v/v ethanol solution representing an absolute alcohol dose of 2.82 g/kg per administration (ETOH Group). Control females were injected with similar volumes of saline (SAL Group) or did not receive any type of intraperitoneal administration of drugs (AC Group). In comparison with the control treatments, the ethanol treatment did not affect long-term maternal body weight gain during pregnancy, total length of gestation, probability of delivery, number of pups born per litter or the offsprings' preference of alcohol odor. Nevertheless, this ethanol insult was sufficient to significantly reduce body weights at birth and to retard the ontogeny of some sensorimotor patterns among offspring, as assessed through the Righting Reflex, Horizontal Screen Test and opening of the external auditory canals. The maturation of other reflexes (Cliff Aversion and Negative Geotaxis) appeared to be retarded indirectly as an outcome of the maternal injection procedure, with ETOH and SAL pups exhibiting similar developmental delays when compared with AC animals. During adulthood, rats prenatally exposed to alcohol exhibited a decreased hypothermic response to an intoxicating dose of alcohol as well as significant increases in voluntary alcohol consumption in comparison with both control conditions. Collectively, these results suggest that relatively acute alcohol exposure early in gestation may not only affect normal patterns of development but also later responsiveness to this pharmacological agent.

Animals↗

PubMedDate not supplied

Effects of perinatal ivermectin exposure on behavioral development of rats.

The antiparasitic agent ivermectin was administered to pregnant rats from days 6 to 20 of gestation and 2 to 20 of lactation at 1, 2 or 4 mg/kg/day. Reproductive performance and behavior of offspring in the preweaning period were observed. Ivermectin had no effect on reproductive performance and dams' growth. The highest dose induced 100% pup mortality. Later on, ivermectin at 4 mg/kg was administered only during gestation. At that dose, the drug induced 22% mortality and affected temporarily cliff avoidance, locomotion, negative geotaxis and swimming development. At 2 mg/kg, the drug induced offspring mortality (31%), retarded growth and delayed eye opening, cliff avoidance and surface righting reflex, negative geotaxis, locomotion and swimming development. Ivermectin at 1 mg/kg had no effect on mortality and growth but cliff avoidance and locomotion were retarded. Data suggest that newborn rats were highly susceptible to the neurotoxic action of ivermectin. Whether its effects were prenatal or by acute intoxication via mother's milk are discussed.

Animals↗

PubMedDate not supplied

Effects of sodium valproate on development and social behaviour in the Mongolian gerbil.

Sodium valproate is an anticonvulsant widely prescribed because of its broad spectrum of activity. While acute toxicity from high doses is well recognized, there have been few animal studies of its chronic toxicity at therapeutic dose levels. Sodium valproate given continuously in drinking fluid (600 mg/l) throughout pregnancy and lactation to breeding gerbils caused developmental delay of the self-righting reflex in their pups. Dams ingested 97 mg/kg daily during gestation and 151 mg/kg on average during lactation, a dose in the lower range of anticonvulsant effectiveness. Reproductive performance, birth weights and subsequent growth of the pups remained normal, as did brain weights in adulthood. Drug-treated offspring, continuing to receive valproate as drinking fluid after weaning (600 mg/l; 82 to 111 mg/kg) showed negligible behavioural alteration at 6 weeks of age as assessed by ethological procedures, although behavioural change did occur at 20 weeks in the female animals. These females were characterised by significant enhancement of exploration and scanning during dyadic encounters in an unfamiliar cage, and showed a concomitant reduction of other nonsocial activities. Short-term administration of this dose of the drug did not affect behaviour. These results suggest an increased reactivity to the environment which becomes evident only after long-term treatment with valproate and to which female animals are more susceptible than males. These findings of developmental delay and of modifications to behaviour later in life points to the need for more detailed clinical assessments of the effects of valproate in human patients.

Administration, Oral↗