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PubMed1988

Phenobarbitone: adverse effects on reproductive performance and offspring development in the Mongolian gerbil, (Meriones unguiculatus).

Phenobarbitone at a concentration of 500 mg/l in drinking fluid of gerbils during pregnancy (60 mg/kg) and lactation (136 mg/kg) markedly reduced the proportion of animals bearing litters, decreased pup weights at birth and during later life and delayed development of the self-righting reflex, auditory startle reaction, eye opening and full fur coverage. It also prolonged the period of suckling. Scars of implantation were evident in uterine horns of 60% of treated and in none of control females that had failed to give birth. Treated offspring after weaning were given phenobarbitone (500 mg/l; 42-124 mg/kg) as their drinking fluid throughout life and a further group of gerbils received this concentration of the drug from the time of weaning. Seizure susceptibility was unaltered by the drug treatment, and the only evidence of behavioural change was seen in offspring gerbils at 6 weeks when the bout length of social investigation during encounters was increased. Drug-treated offspring showed no abnormality in brain weight relative to body weight. Weight gain and brain weight remained normal among the gerbils given phenobarbitone after weaning. The drug treatment reduced scent gland size in breeding males, though not in the offspring, and had no effect on weights of the testes or ovaries and uterus. no effect on weights of the testes or ovaries and uterus. Plasma concentrations of phenobarbitone in females of the postweaning group amounted on average to 4.4 mg/kg. Most of the adverse effects of this dose of phenobarbitone in the gerbil can thus be seen to be associated either with reproductive impairment or with exposure during sensitive periods of early development.

Animals↗

PubMed1992

Local spiking interneurons controlling the equilibrium response in the crayfish Procambarus clarkii.

1. In the crayfish brain, the responses of local spiking interneurons to body roll simulated by bending of statocyst hairs, were investigated with intracellular recording and staining techniques. The neurons had two separate branching portions in the protocerebrum and the deutocerebrum. They were named as type-I local neurons and further classified into 5 types (ac-U, vplc-U, vplc-B, vupc-U, vupc-B). 2. Vupc-U neurons showed excitatory responses and vplc-U neurons showed inhibitory responses to inward hair deflection of the statocyst ipsilateral to their deutocerebral branches. The other 3 types were of mixed populations of the interneurons showing either excitatory or inhibitory responses to the stimulation. 3. Of 10 type-I local neurons showing excitatory responses to inward hair deflection, 6 interneurons had output effects on oculomotor and/or descending neurons. All these 6 interneurons showed large EPSPs and much higher frequency of spikes to the hair stimulation than those of the other 4. All 8 type-I local neurons that showed inhibitory responses had no output effects. 4. Type-I local neurons controlled two equilibrium responses, compensatory eye movement and righting reflex, either simultaneously or independently.

Acoustic Stimulation↗

PubMed1991

N-butyl benzenesulfonamide: a neurotoxic plasticizer inducing a spastic myelopathy in rabbits.

N-Butyl benzenesulfonamide (NBBS), a plasticizer used commercially in the polymerization of polyamide compounds, is neurotoxic. Young adult New Zealand white rabbits, inoculated repeatedly with NBBS by the intracisternal or intraperitoneal routes, developed a dose-dependent motor dysfunction characterized by limb splaying, hyperreflexia, hypertonia, gait impairment, and abnormal righting reflexes. Histopathological changes consisted of intramedullary thickening of the ventral horn axons, random neuroaxonal spheroids confined to brain stem nuclei and spinal motor neurons, and swollen dendritic processes of spinal motor neurons. Immunoreactivity to a monoclonal antibody against microtubule-associated protein-2 (MAP-2) was markedly increased in the dendrites of spinal motor neurons following thrice weekly intraperitoneal inoculations of NBBS for 4 months, whereas after 12 monthly intracisternal inoculations, MAP-2 immunoreactivity was absent or strikingly reduced in the same neuronal populations. Ultrastructurally, postsynaptic zones contained vacuoles and multilamellar bodies. These findings raise questions about the safety of NBBS to humans.

Animals↗

PubMed1977

Tolerance to ethanol: effect of congeners present in bourbon.

Fish were exposed to water and to ethanol or bourbon solutions of the same ethanol concentration (0.1, 0.2, 0.4, 0.6, or 0.8 g/100 ml) during 6 h and then tested in 3.1 g/100 ml ethanol for loss of righting reflex or overturn point. The content of ethanol in the brain at overturn was determined for each fish. Although the ethanol brain levels at overturn of bourbon-exposed fish were higher than those of the ethanol group, no significant differences were observed between the two groups. Moreover, there was a tendency for the bourbon fish to take longer times to overturn than the ethanol fish. These findings indicate that the congeners present in bourbon did not affect significantly the development of tolerance to ethanol in goldfish.

Acetaldehyde↗

PubMed1979

Hypnotic susceptibility to various depressants in rats selected for differential ethanol sensitivity.

MA rats, bred for greater motor impairment following subhypnotic doses of ethanol, were found to be more sensitive to the hypnotic effects of phenobarbital and chloral hydrate than were LA rats. In addition, the previously reported finding of a difference between the two lines of rats in duration of loss of righting reflex following a hypnotic dose of ethanol was replicated. The results are discussed in terms of a phenotypic difference in central nervous systems sensitivity to a range of sedative-hypnotics.

Animals↗

PubMed1979

Effects of delta-aminolaevulinic acid administration on social behaviour in the laboratory mouse.

Ethologic analysis has been used to study the behavioural effects following injection of delta-aminolaevulinic acid (ALA) in mice. After a dose level of 1.6 mmol ALA/kg, male and female mice showed periods of immobility and scanned less frequently than saline-injected controls. Exploration of the cage was significantly reduced in frequency in treated males, many elements of social and sexual investigation were reduced in treated females, and no elements of aggression were seen in treated males. Gait was abnormal and movement lethargic in animals showing the greatest degree of immobility. Righting reflexes and the response to stimuli of noise and touch remained normal. After a dose level of 0.8 mmol ALA/kg, no significant behavioural effects were detectable.

Aminolevulinic Acid↗

PubMed1979

Effects of physostigmine, scopolamine, and mecamylamine on the sleeping time induced by ketamine in the rat.

Male Sprague-Dawley rats weighing 116--241 g were injected i.p. with ketamine hydrochloride, 80 mg per kilo of body weight. Immediately after loss of righting reflex, scopolamine, physostigmine, and mecamylamine were administered i.p. to different groups of rats. Control animals received sterile saline by the same route. The ketamine-induced sleeping time was significantly prolonged by physostigmine and scopolamine, but not by mecamylamine. After the delayed injection of physostigmine, the ketamine sleeping time was longer. These results, although too preliminary for a mechanistic interpretation, suggest that multiple neurotransmitter systems, probably including the cholinergic system, are involved in the mechanism of action of ketamine-induced narcosis.

Animals↗

PubMed1978

Differential tolerance to pentobarbital in rats bred for differences in alcohol sensitivity.

Two lines of rats bred for differences in motor impairment following alcohol treatment were also found to be differentially affected by sodium pentobarbital in three experiments. The most affected (MA) animals, bred for sensitivity to alcohol, showed a decrement in stabilimeter activity at doses of 8 mg and 16 mg pentobarbital per kg body weight. The least affected (LA) animals, bred for insensivity to alcohol, were affected only by the higher dose, at which the resulting impairment was still less than that of the MA group. This finding was partially replicated in a second study designed to test the possibility of an activating effect of pentobarbital on LA animals at 8 mg/kg. In a final study, MA animals were more likely to lose their righting reflex than LA animals at a dose of 18 mg/kg, and 'slept' longer following this dose. These results indicate that the differential sensitivity shown by these animals is not specific to alcohol, but can be generalized to another depressant.

Animals↗

PubMed1983

Drug interactions in goldfish tolerant to ethanol and pentobarbital.

The interactions between short- and long-term exposure to ethanol and pentobarbital were characterized in goldfish tolerant to one of these drugs. The effects of ethanol and pentobarbital were measured by the overturn test as the time of onset of the loss of the righting reflex and the corresponding drug concentration in brain of fish immersed in 674 mumol/ml ethanol or 1.21 mumol/ml sodium pentobarbital (challenge solutions). The chronic treatment consisted of 6- or 24-h preexposure to 130 mumol/ml ethanol or 0.06 mumol/ml sodium pentobarbital in Tris buffer solution. Fish preexposed to ethanol for 6 or 24 h or to pentobarbital for 24 h were rendered more tolerant to pentobarbital or ethanol, respectively. Preexposure to pentobarbital for 6 h, however, produced in goldfish the same degree of tolerance to ethanol and to pentobarbital.

Animals↗

PubMed1982

The effect of prenatal exposure to diazepam on aspects of postnatal development and behavior in rats.

In the present study the effects of chronic treatment of pregnant rats with diazepam on the physical and behavioral development of their offspring were investigated. Rats that were diazepam-exposed prenatally were compared to age-matched controls in terms of the following: number of littermates; birth weight and weight gain until weaning: motor development and coordination; simple motor learning; open field activity; performance on learning tasks of varying complexity; retention of these tasks. Nulliparous Wistar rats were injected s.c. for 16 days of their pregnancy was either 2.5, 5, of 10 mg/kg diazepam or an equal volume of vehicle. Prenatal diazepam treatment did not alter litter size, birth weight, or the righting reflex, but seemed to retard early motor development transiently. Diazepam pups showed longer latencies and less rearing in the open field. There were no differences between animals exposed to drug and vehicle in simple motor learning or in acquiring a simple successive discrimination task. However, there were significant dose-dependent differences on a complex six-choice simultaneous discrimination learning task, the diazepam-exposed rats making more errors and taking more time to reach the goal. A significant difference was seen again between diazepam- and vehicle-exposed rats on the retention test 10 days later. The results indicate that diazepam administered to pregnant rats has long-range effects on the behavior of the offspring, some becoming manifest even in maturity.

Animals↗

PubMed1975

The effect of ouabain and digitoxin on hexobarbitone sleeping time in the mouse.

The effect of ouabain and digitoxin upon the duration of loss of righting reflex produced by hexobarbitone in mice pretreated with the liver microsomal enzyme inhibitor SKF 525 A was studied. Both ouabain and, to a greater extent digitoxin, produced a dose dependent potentiation of the activity of hexobarbitone. These results confirm and extend previous observations and may be explained by a direct interaction at the level of the CNS and by a modified distribution of the barbiturate. Furthermore, they re-emphasize the possibility of such an interaction in the clinic.

Animals↗

PubMed1975

Induction of physical dependence upon ethanol and the associated behavioral changes in rats.

This paper reports findings relative to a simple, rapid and reproducible technique for the induction of physical dependence upon ethanol in the rat. The dependence was induced by intragastric intubation of 20% (w/v) ethanol solutions at 9-15 g/kg in 3-5 fractional doses daily for 4 days, maintaining blood ethanol concentrations above a threshold level sufficient to sustain observable sedation throughout the entire period of intubation. Two phases were distinguished during the withdrawal period: 1. Prodromal detoxication, characterized by a spectrum of signs and responses of diminishing severity, related to the decline in blood ethanol concentrations (mg/dl): death, greater than 640; coma, 780-460; loss of righting reflex, 640-400; ataxia 3-1, 570-250; sedation 340-190; neutrality, 220-130; 2. Ethanol dependence, characterized by a spectrum of withdrawal signs and reactions of progressively increasing severity as blood ehtanol concentration approached 100 mg/dl: hyperactivity, tremors, akinesia, spastic rigidity, and induced and spontaneous convulsions. A rapid sucession of two diverse clusters of signs and reactions represents a reversal of the central nervous system function from the extremes of ethanol intoxication (CNS depression) to the extremes of ethanol dependence (CNS hyperexcitability) during the withdrawal period. Both extremes may terminate in death.

Alcoholic Intoxication↗

PubMed1976

Temporal relationship of the induction of tolerance and physical dependence after continuous intoxication with maximum tolerable doses of ethanol in rats.

Rats were treated by intragastric intubation of a 20% ethanol solution in doses of 9-15 g/kg in 3-5 fractions for 1-7 days. Both tolerance and physical dependence were demonstrated after this treatment with the maximum tolerable doses to only a few days. Tolerance was assessed by signs of severity of intoxication: coma, loss of righting reflex, ataxia-3, ataxia-2, ataxia-1, sedation, and neutrality. During withdrawal, as blood ethanol concentrations approached 100 mg/dl the ethanol dependence phase was characterized by the onset of signs and responses of progressive severity: hyperactivity, tremors, spastic rigidity, and spontaneous convulsive seizures. A significant degree of tolerance was demonstrated for all signs of intoxication after 4 days of treatment, but did not reach maximum level even after 7 days. The severity of the withdrawal reactions intensified progressively to a maximum intensity after 4 days of treatment when as many as 72% of animals exhibited severe withdrawal signs and reactions including convulsive seizures. These different time courses suggest that tolerance and physical dependence are mediated through different mechanisms.

Alcoholism↗

PubMed1983

The effects of neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors in mice.

The effects of the three peptides neurotensin, beta-endorphin, and bombesin on ethanol-induced behaviors were studied in mice. Intracisternal administration of these peptides to mice prolonged the duration of sleep induced by ethanol (5.2 g/kg). Neurotensin and beta-endorphin also enhanced ethanol-induced hypothermia. None of the peptides, when administered alone, produced sleep. However, all three compounds impaired the aerial righting reflex and induced sleep when followed by an IP dose of ethanol (3.5 g/kg), which alone did not induce sleep. These results, taken together with previous findings, suggest that neuropeptides may be involved in the complex mechanisms of action of ethanol on the CNS.

Animals↗

PubMed1980

Attenuation of the effects of punishment by ethanol: comparisons with chlordiazepoxide.

Ethanol (ETOH), like chlordiazepoxide (CDZ), significantly attenuated the suppressive effect of punishment on licking behavior in water-deprived rats and mice. In rats, the greatest effects of ETOH (1.5 g/kg) were observed between 30 and 60 min following IP administration. tert-Butanol also attenuated the effects of punishment, suggesting that acetaldehyde was not contributing to this effect of ETOH. Since a dose of ETOH that increased punished drinking did not increase unpunished drinking, alteration in thirst motivation would not appear to be responsible for its antipunishment action. However, doses of ETOH or CDZ that significantly increased punished responding increased jump thresholds to aversive shock, suggesting that decreased sensitivity to aversive stimulation may contribute to the anti-punishment action of both agents. In addition to these similarities between ethanol and CDZ, several differences were noted in their effects. For example, CDZ decreased serum corticosterone concentration, whereas ETOH did not. Further, ETOH impaired aerial righting reflex and reduced rectal temperature, whereas CDZ had no effect on these parameters at doses that had anti-punishment activity. Finally, specific binding of [3H]flunitrazepam to crude brain cortical membranes was decreased by CDZ, but not ETOH. Although ETOH and CDZ similarly alter punished behavior, results suggest that ETOH does not act through a direct interaction with a benzodiazepine binding site.

Animals↗

PubMed1979

Behavioral activities of opioid peptides and morphine sulfate in golden hamsters and rats.

The behavioral effects of beta-endorphin, [D-Ala2, D-Leu5]-enkephalin and morphine were investigated in golden hamsters and in rats. In golden hamsters, beta-endorphin and [D-Ala2, D-Leu5]-enkephalin induced loss of righting reflex, whereas morphine caused no such effect. Both opiate peptides and morphine caused the inhibition of tail-flick response and catalepsy in rats. beta-Endorphin was the most potent, followed by [D-Ala2, D-Leu5]-enkephalin and then by morphine. The catalepsy induced in rats by [D-Ala2, D-Leu5]-enkephalin was different from that of beta-endorphin and morphine in that it produced catalepsy without muscular rigidity. beta-Endorphin and [D-Ala2, D-Leu5]-enkephalin caused hypothermia in golden hamsters; morphine was less active in altering the body temperature. beta-Endorphin caused hypothermia at high doses and hyperthermia at low doses in rats. These heterogenous behavioral responses indicate that multiple types of receptors mediate the effects of opiates in the central nervous system.

Animals↗

PubMed1981

Decreased 3H-L-quinuclidinyl benzilate binding and muscarine receptor subsensitivity after chronic gamma-butyrolactone treatment.

A significant decrease in the number of 3H-quinuclidinyl benzilate (3H-QNB) binding sites in striatal membranes was observed in rats exposed to gamma-butyrolactone (GBL) during 3 weeks. This decrease in 3H-QNB binding was not due to a direct effect of GBL on muscarine receptors since no alterations of binding were produced by high concentrations of GBL or of its active metabolite gammahydroxybutyric acid (GHB) when added in vitro. Challenge doses of pilocarpine were less effective in producing catalepsy and tremors in rats chronically treated with GBL. It is proposed that the partial inhibition of the nigro-striatal dopaminergic pathway produced by chronic GBL treatment leads to a persistent activation of the intrastriatal cholinergic interneurons, which are tonically inhibited by dopaminergic nigrostriatal neurons. The activation of striatal cholinergic interneurons results in a decreased number of muscarine receptors and in a lower sensitivity to cholinomimetic agents. Moreover, tolerance to the anesthetic effect of GBL was found to occur after chronic treatment with this drug. The brain levels of GHB at the time of regaining of the righting reflex were 50% higher in GBL pretreated animals then in controls. Indicating the tolerance to GBL-induced "sleep" is due to a decrease sensitivity of the effector to GHB rather than to a faster inactivation of elimination of the drug.

4-Butyrolactone↗

PubMed1989

Involvement of noradrenergic system in a remarkably rapid tongue clonus produced by acute hypnotic doses of ethanol in Fischer F344 rats.

Ethanol (2.95 g/kg, IP) eliminated the righting reflex and induced vigorous tongue clonus spontaneously or following tactile tongue stimulation in Fischer F344 rats. Responses normally lasted 30-60 min, and was reinstated by tactile stimulation in those cases where it subsided quickly. Sub-hypnotic (1.95 g/kg) or high (3.95 g/kg) doses failed to elicit clonus, even after tactile stimulation. A lipophilic alpha 1-adrenergic agonist (St 587) promptly initiated tongue clonus in rats treated with a 3.95 g/kg dose of ethanol. Prazosin, a selective alpha 1-adrenergic antagonist, blocked clonus, while the dopamine selective antagonist pimozide failed to modify this response. We infer an alpha 1-adrenergic effect in which norepinephrine is released by ethanol.

Animals↗