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PubMed1990

Kinetics of drug action in disease states. XXXIX. Effect of orally administered activated charcoal on the hypnotic activity of phenobarbital and the neurotoxicity of theophylline administered intravenously to rats with renal failure.

The central nervous system (CNS) sensitivity to the hypnotic (general anesthetic) action of phenobarbital and to the neurotoxic (convulsive) action of theophylline is greater in rats with acute renal failure than in normal animals, consistent with clinical observations. In the case of phenobarbital, this increased sensitivity can be produced in normal rats by infusion of a solution of the lyophilized dialysate of serum from rats with renal failure. It was hypothesized that the relevant constituent(s) of this dialysate may circulate between the blood and the intestinal lumen and that it (they) can be adsorbed by orally administered activated charcoal and thereby removed from the body. If so, treatment of renal failure rats with activated charcoal should partly reverse the increased CNS sensitivity to phenobarbital and to other drugs similarly affected. Accordingly, rats with renal failure produced by bilateral ligation of ureters were given an aqueous suspension of activated charcoal, about 1 g per kg body weight, orally every 8 hr for six doses. Uremic controls received equal volumes of water. About 2 hr after the last dose, the animals were infused i.v. with phenobarbital to onset of loss of righting reflex or with theophylline to onset of maximal seizures. In the phenobarbital study, charcoal treatment partly reversed the hypothermia associated with renal failure and caused a reduction of creatinine and total bilirubin concentrations in serum. The cerebrospinal fluid (CSF) concentration of phenobarbital at onset of loss of the righting reflex was significantly higher in charcoal treated rats than in their controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Delayed postnatal behavioral development in spontaneously epileptic rats and tremor rats, and poor operant performance in spontaneously epileptic rats.

Postnatal behavioral development and learning ability of operant performance were examined in spontaneously epileptic rats (SER: zi/zi, tm/tm), and the original tremorous mutant strains of rats, tremor rats (tm/tm) and zitter rats (zi/zi) and their controls. Before the eyes opened, the increase in body weight and the age of achieving the righting reflex on a surface were no significantly different between the SER and their littermates without epileptic seizures (SER-N: zi/zi, tm/+ or zi/zi, +/+), and between tremor rats and the original strain Kyo: Wistar rats. After the eyes opened, the increase in body weight, age of achieving the righting reflex in air and traction performance, and the development of rotarod performance, were delayed in SER and tremor rats in comparison with other groups of rats. The zitter rats were apparently inferior in their development of rotarod performance in comparison with the same zitter homozygous SER-N. Operant performance was more inferior in SER than in SER-N and in tremor rats than in Kyo: Wistar rats. The differences were much more marked between SER and SER-N than between tremor and Kyo: Wistar rats. Thus, homologous tm genes and the coexistence of homologous tm and zi genes have an inhibitory effect on postnatal behavioral development and learning ability.

Animals↗

PubMed2003

[Effects of +Gz exposure time on memory and behavior in rats].

OBJECTIVE: To explore the effect of +Gz exposure time on memory and behavior in rats. METHOD: Twenty-four male SD rats were randomly divided into control group (A), +10 Gz/3 min group (B) and +10 Gz/5 min group (C). Rats in group A and B were exposed to +10 Gz for 3 min or 5 min respectively. Changes of memory and behavior in rats were observed after +Gz exposure. RESULT: As compared with control, percentage of right reflex decreased significantly and reaction time lengthened significantly immediately, 1 d, 2 d, 4 d and 6 d after +10 Gz/5 min exposure (P<0.01); reaction time lengthened significantly immediately and 2 d after +10 Gz/3 min exposure (P< 0.01). As compared with +10 Gz/3 min, percentage of right reflex decreased significantly and reaction time lengthened significantly at 1 d, 2 d, 4 d and 6 d after +10 Gz/5 min exposure (P<0.01). As compared with control and +10 Gz/3 min, time stayed in center grille lengthened significantly immediately after +10 Gz/5 min exposure (P<0.01); balancing function decreased significantly immediately and 2 d after +10 Gz/5 min exposure (P< 0.01). CONCLUSION: It is suggested that +10 Gz/ 3 min exposure may induce a provisional disturbance in memory function and a change in behavior in rats, and +10 Gz/5 min exposure may induce a sustained disturbance in memory function and an obvious change in behavior in rats.

Acceleration↗

PubMed2002

Pharmacological evidence for GABAergic regulation of specific behaviors in Drosophila melanogaster.

We have identified several GABAergic-modulated behaviors in Drosophila melanogaster by employing a pharmacological approach to disrupt GABA transporter function in vivo. Systemic treatment of adult female flies with the GABA transport inhibitors DL-2,4-diaminobutyric acid (DABA) or R,S-nipecotic acid (NipA), resulted in diminished locomotor activity, deficits in geotaxis, and the induction of convulsive behaviors with a secondary loss of the righting reflex. Pharmacological evidence suggested that the observed behavioral phenotypes were specific to disruption of GABA transporter function and GABAergic activity. The effects of GABA reuptake inhibitors on locomotor activity were dose dependent, pharmacologically distinct, and paralleled their known effects in mammalian systems. Recovery of normal locomotor activity and the righting reflex in DABA- and NipA-treated flies was achieved by coadministration of bicuculline (BIC), a GABA receptor antagonist that supresses GABAergic activity in mammals. Recovery of these behaviors was also achieved by coadministration of gabapentin, an anticonvulsant agent that interacts with mammalian GABAergic systems. Finally, behavioral effects were selective because other specific behaviors such as feeding activity and female sexual receptivity were not affected. Related pharmacological analyses performed in vitro on isolated Drosophila synaptic plasma membrane vesicles demonstrated high affinity, saturable uptake mechanisms for [3H]-GABA; further competitive inhibition studies with DABA and NipA demonstrated their ability to inhibit [3H]-GABA transport. The existence of experimentally accessible GABA transporters in Drosophila that share conserved pharmacological properties with their mammalian counterparts has resulted in the identification of specific behaviors that are modulated by GABA.

Animals↗

PubMed1980

Effects of gamma-butyrolactone, amphetamine, and haloperidol in mice differing in sensitivity to alcohol.

Gamma-butyrolactone (GBL) induced longer loss of righting reflex in mice (LS-line) selectively bred for greater sensitivity to ethanol than in less sensitive SS-line mice. GBL also induced a three-fold greater increase of brain dopamine levels in LS than in SS mice. Among three inbred strains, GBL-induced loss of righting reflex was greater in BALB/c, and greater in DBA/2 than in C57BL/6 mice. A low dose of GBL produced biphasic effects on locomotor activity. Both an initial depressant action and a later increase in activity were greater in LS than in SS mice. These GBL effects on activity were modified in a genotype-dependent fashion by amphetamine. Results of these experiments as well as greater catalepsy-inducing properties of haloperidol in SS mice suggest that genotypic influences on motor reactivity to ethanol may be modeled by GBL effects on brain dopamine systems.

4-Butyrolactone↗

PubMed2003

Mapping quantitative trait loci mediating sensitivity to etomidate.

Long- and Short-Sleep (LS and SS) mice were selectively bred for differences in ethanol-induced loss of the righting reflex (LORR) and have been found to differ in LORR induced by various anesthetic agents. We used a two-stage mapping strategy to identify quantitative trait loci (QTLs) affecting duration of LORR caused by the general anesthetic etomidate and brain levels of etomidate (BEL) following regain of the righting reflex. Analysis of recombinant-inbred strains derived from a cross between LS and SS mice (LSXSS) yielded a heritability estimate of 0.23 for etomidate-induced LORR and identified one marker that showed suggestive linkage for a QTL, on mouse Chromosome (chr) 12. Mapping in an F(2) population derived from a cross between inbred LS and SS (ILS and ISS) revealed a significant QTL for etomidate-induced LORR on Chr 12, and two significant QTLs mediating BEL on Chrs 6 and 12. Several QTLs showing suggestive linkage for etomidate-induced LORR and BEL were also identified in the F(2) population. Brain levels of etomidate in the RI and F(2) mice suggested that differences in LORR were due to differential central nervous system sensitivity, rather than differential etomidate metabolism. Interestingly, the region on Chr 7 has also been identified as a region influencing ethanol-induced LORR, suggesting the possibility of a common genetic mechanism mediating etomidate and ethanol sensitivity. These QTL regions need to be further narrowed before the testing of candidate genes is feasible.

Analysis of Variance↗

PubMed2004

Effects of 4-methylpyrazole on ethanol neurobehavioral toxicity in CD-1 mice.

OBJECTIVES: 4-Methylpyrazole (4-MP), an alcohol dehydrogenase (ADH) antagonist, is used for the treatment of ethylene glycol and methanol ingestions. However, ethanol is frequently co-ingested by those who ingest these more toxic alcohols. Several in vitro and in vivo studies have shown a decrease in the elimination rate of ethanol after the administration of 4-MP, but none has evaluated the effects of 4-MP administration on the neurobehavioral toxicity of ethanol. This was a study to determine whether ADH blockade with 4-MP prolongs ethanol neurobehavioral toxicity in a murine model. METHODS: D-1 mice were pretreated with 4-MP, with observation of its effect on ethanol dose-response curves. 4-MP (25 mg/kg) or an equal volume of saline was administered intraperitoneally. Ten minutes later, incremental ethanol doses of 1-5 g/kg were administered intraperitoneally. Pretreated and control groups were composed of ten mice each for each dose of ethanol tested. Outcomes for assessing ethanol neurobehavioral toxicity were successful performance on the rotarod test and presence of the righting reflex, two established and validated outcome measures for ethanol-induced neurobehavioral toxicity in mice. RESULTS: The dose of ethanol at which 50% of the animals failed a particular outcome test (toxic dose 50 [TD(50)]) was decreased with 4-MP administration for both the rotarod test and the righting reflex. The TD(50) intergroup differences (control vs. 4-MP) were statistically significant at 60, 120, and 180 minutes (p < 0.05). CONCLUSIONS: Pretreatment with 4-MP significantly prolonged ethanol neurobehavioral toxicity in CD-1 mice, presumably by inhibiting its metabolism by ADH. Further investigation is warranted to evaluate this interaction.

Alcohol-Induced Disorders, Nervous System↗

PubMedDate not supplied

Behavioral effects of chronic toluene exposure in the developing rat.

The effects of acute and chronic toluene exposure on the hypnotic effect, the righting reflex latencies and the blood and tissue toluene contents were studied in rats during development. The data showed a progressive significant prolongation of the hypnotic effect latencies until the third and fourth postnatal weeks, followed by a significant continuous declining trend until the eighth week postpartum. The measure of the righting reflex latencies followed an opposite temporal course compared to that of hypnotic effect measurements. The acute and chronic toluene exposure did not reveal significant differences in toluene concentrations of blood, brain and liver tissues. The data suggest that chronic toluene treatment may probably be inducing behavioral manifestations of a tolerance phenomenon combined with maturational influences in the developing rat.

Age Factors↗

PubMed2000

Protection by Osbeckia aspera against carbon tetrachloride-mediated alterations in microsomal drug metabolizing enzyme activity.

Previous investigations have confirmed the protective effect of Osbeckia aspera leaf extract on carbon tetrachloride-mediated liver injury in rat models. It is well known that the earliest alterations in liver cell structure and function following carbon tetrachloride poisoning involve the endoplasmic reticulum and its drug metabolizing enzymes. Therefore, we investigated whether an aqueous leaf extract of O. aspera could offer protection against carbon tetrachloride-induced changes in the microsomal drug metabolizing enzymes aniline hydroxylase and p-aminopyrine N-demethylase. This enzyme activity was compared with phenobarbital-induced righting reflex and lipid peroxidation. Treatment of rats with the aqueous leaf extract of O. aspera (before or after the administration of carbon tetrachloride) resulted in a marked decrease in carbon tetrachloride-mediated alterations in aniline hydroxylase and p-aminopyrine N-demethylase activity, phenobarbital-induced loss of righting reflex and malondialdehyde formation due to lipid peroxidation. The Km value of these enzymes in control and Osbeckia-treated rats were the same. These results show that the plant extract can markedly decrease the carbon tetrachloride-mediated reduction in aniline hydroxylase and p-aminopyrine N-demethylase activity and inhibit peroxidative damage to the cell membrane. Phenobarbital-induced sleeping time in rats and kinetic enzyme studies suggested that the effects of the plant extract was neither due to an induction of the drug-metabolizing enzymes under investigation, nor due to an alteration in the Km values of these enzymes.

Aminopyrine N-Demethylase↗

PubMed1987

Interaction between flurazepam and ethanol.

The interaction of a representative benzodiazepine, flurazepam, and ethanol has been assessed in ICR albino mice. Tests done included loss of "rotarod" performance, light sedation, deep sedation, loss of righting reflex, anesthesia, and lethality. LD50 and ED50s were plotted as isobolograms (plots of equieffective dose combinations). Data for anaesthesia and lethality showed little or no interaction between the two drugs. In contrast, the four motor and behaviour tests showed synergism, especially with higher doses of ethanol (over 2 g/kg) for righting reflex, and (over 1.5 g/kg) for deep sedation. Synergism occurred over all doses for light sedation and rotarod performance. It is expected that concurrent use of benzodiazepines and ethanol can result in a significantly higher accident risk in humans, but little additional risk of death from simple overdose.

Anesthesia↗

PubMed1985

Activities of thiamine-dependent enzymes in two experimental models of thiamine-deficiency encephalopathy: 1. The pyruvate dehydrogenase complex.

Chronic thiamine deprivation in the rat leads to selective neuropathological damage in brainstem structures whereas treatment with the central thiamine antagonist, pyrithiamine, results in more widespread damage. In order to further elucidate the neurochemical mechanisms responsible for this selective damage, the thiamine-dependent enzyme complex pyruvate dehydrogenase (PDHC) was measured in 10 brain structures in the rat during progression of thiamine deficiency produced by chronic deprivation or by pyrithiamine treatment. Feeding of a thiamine-deficient diet to adult rats resulted in 5-7 weeks in ataxia and loss of righting reflex accompanied by decreased blood transketolase activities. PDHC activities were selectively decreased by 15-30% in midbrain and pons (lateral vestibular nucleus). Thiamine treatment of symptomatic rats led to reversal of neurological signs and to concomitant reductions of the cerebral PDHC abnormalities. Daily pyrithiamine treatment led within 3 weeks to loss of righting reflex and convulsions and to decreased blood transketolase of a comparable magnitude to that observed in chronic thiamine-deprived rats. No significant regional alterations of PDHC, however, were observed in pyrithiamine-treated rats.

Animals↗

PubMed1986

Age-dependent enhancement of diazepam sensitivity is accelerated in New Zealand Black mice.

Separate age groups of C57BL/6 and autoimmune New Zealand Black (NZB) mice were compared for diazepam-induced ataxia and barbiturate-induced loss of righting reflex. Between 1 and 3 months of age, both strains showed a similar age-related decrease in ED50 for diazepam-induced ataxia. However, between 3 and 12 months the decrease in ED50 was markedly greater in NZB mice. In contrast, age-related increases in the durations of loss of righting reflex following hexobarbital or barbital were similar in both strains. The results suggest that NZB mice show relatively accelerated age-related increases in sensitivity to benzodiazepine, but not to barbiturates.

Aging↗

PubMed1989

A new alcohol antagonist: phaclofen.

The ability of the GABA(B) receptor antagonist, phaclofen to alter behavioral effects of ethanol was evaluated by loss of righting reflex (sleep time), motor incoordination (bar holding), spontaneous locomotion (open field activity) and hypothermia. Pretreatment with phaclofen significantly decreased the effects of ethanol on motor incoordination, locomotor activity and hypothermia. However, phaclofen had no effect on either pentobarbitalor diazepam-induced motor incoordination. Phaclofen slightly increased the ED50 for loss of the righting reflex but did not alter either the duration of reflex loss produced by ethanol or blood ethanol levels at awakening. Our results suggest phaclofen is rapidly inactivated resulting in difficulty in observing antagonism of long duration ethanol effects. These findings suggest that the GABA(B) system may play a role in mediating several important actions of ethanol.

Animals↗

PubMed2005

Long-term effects of lanthanum intake on the neurobehavioral development of the rat.

The effects of subchronic exposure to lanthanum on rats' physical and neurobehavioral development were investigated. Wistar rats were exposed to lanthanum through oral administration at 0, 0.1, 2, and 40 mg/kg concentrations from gestation day 0 through 5 months of age. Prior to weaning of the pups, physical parameters and neurobehaviors were assessed, including body weight gain, pinna detachment, eye opening, surface righting reflex and swimming endurance. At 30 days of age, DNA concentration and protein/DNA ratio of the whole brain were determined. At 150 days of age, the Morris water maze test was carried out to study the memory and learning abilities of the rats. Differences were found in the body weight gain, surface righting reflex and swimming endurance. Moreover, lanthanum exposure significantly altered the DNA concentration and Protein/DNA in brain. The Morris water maze test showed that lanthanum exposure at 40 mg/kg significantly impaired memory and learning abilities. These findings indicate that lanthanum is a potential behavior teratogen. The information provided by this work should be considered in future applications of lanthanides.

Animals↗

PubMed1995

Antinociception and side effects of L- and D-dipalmitoylphosphatidyl choline liposome-encapsulated alfentanil after spinal delivery in rats.

We have observed that spinal liposome administration in the rat resulted in in an allodynia evoked by light touch. We later determined that liposomes composed of D-isomer phospholipids were essentially non-toxic. This study examines the effects of alfentanil encapsulated in liposomes made from the natural L-isomer and synthetic D-isomer of dipalmitoyl phosphatidyl choline on antinoceiception, side effects, and algogenic behaviour. Both unilamellar and multilamellar liposomes were studied. Rats prepared with chronic intrathecal catheters received intrathecal injections of alfentanil (5 or 50 micrograms) in saline or encapsulated in liposomes composed of either L- or D-isomers of dipalmitoyl phosphatidyl choline (DPPC) in unilamellar or multilamellar liposome formulations. Antinociception was measured using the hot plate test (52.5 degrees). Side effects were measured by catalepsy, corneal responses, pinna response, righting reflex, and paw step. Allodynia was measured by lightly stroking the animal's back. Intrathecal alfentanil in saline or in the liposomes produced a dose-dependent increased latency in the hot plate response. Encapsulation of alfentanil in the liposomes produced a significant decrease in the loss of corneal, paw step and righting reflex and a slight decrease in catalepsy and loss of the pinna response. There was no significant difference between liposome preparations in preventing side effects. L-multilamellar-DPPC produced allodynia in 100% of the animals whereas significantly less allodynia was observed with the other preparations. This study indicates that liposomal preparations can significantly enhance the therapeutic ratio of a lipid soluble opioid after spinal delivery. However, the choice of lipids for the formulation of liposomes intended for spinal drug delivery must be considered since the L-isomer and larger lipid load of multilamellar liposomes have a direct spinal effect leading to alledynia. Previous studies have in fact shown that spinal lysolecithin can yield focal demyelination.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1994

Synergistic sedative effect of selective MAO-A, but not MAO-B, inhibitors and melatonin in frogs.

Total suppression of righting reflex in frogs (Rana pipiens, 25-35 mg b.w.) was observed after combined administration of melatonin (12.5 mg/kg) and selective inhibitors of MAO-A: clorgyline (2.5 mg/kg) and moclobemide (50 mg/kg) but not MAO-B: selegiline (25 mg/kg) and Ro-19-6327 (50 mg/kg). None of these drugs alone affected the righting reflex. Clorgyline and selegiline selectively inhibited brain MAO-A and MAO-B activity (by more than 90%), resp. Frogs might represent a convenient model to study the selective MAO-A and B type inhibitors since they provide the opportunity to correlate behaviour and biochemical changes induced by MAO inhibitors.

Animals↗

PubMed2004

[Dexmedetomidine hydrochloride (Precedex), a new sedative in intensive care, its pharmacological characteristics and clinical study result].

Dexmedetomidine hydrochloride (Precedex) is a potent and highly selective central alpha(2)-adrenoreceptor agonist. In a test of affinity to receptors in rat brain cortex, this drug showed a high affinity and selectivity to the alpha(2)-adrenoreceptor. This drug induced a dose-dependent decrease in activity, loss of righting reflex, an increase in sedation score, and a dose-dependent prolongation of the latent time of escape from pain in various animal models. The site of action for the sedative action of this drug is considered to be the locus coeruleus. With administration of this drug into the locus coeruleus, loss of righting reflex was observed in almost all animals. Test results using mice with variant alpha(2A)-receptor suggested that the sedative action of this drug is expressed through the alpha(2A)-receptor subtype. This drug is promptly eliminated from blood. In the phase II/III multi-center placebo-controlled double blind bridging study conducted in Japan, efficacy and safety were examined in patients brought to the ICU. As regards sedative action, the ratio of patients who did not require additional propofol medication (>50 mg) while intubated was taken as the effective rate. The drug group showed a significantly high effective rate (90.9%; placebo group, 44.6%). Similarly, with analgesic action, the ratio of patients who did not require additional morphine medication during intubation was taken as the effective rate. The effective rate for the drug group was significantly high (87.3%; placebo group, 75.0%). The main adverse events observed in the drug group were hypertension and hypotension.

Adrenergic alpha-2 Receptor Agonists↗

PubMed1983

Encephalopathic effect of phenol in rats.

The coma-inducing effect of phenol was studied in normal 300 +/- 50 gm Sprague-Dawley rats. Dose-response curves were developed which showed that one-half the animals became deeply comatose with 540 mumol of intraperitoneal phenol and 100% with 600 mumol. Five stages of encephalopathy were readily distinguished. In stage I, spontaneous activity was noticeably decreased, posture was upright, back-leg control normal, muscle tonus slightly increased, and response to stimuli normal. In Stage V, activity was gone, the rats were deeply unconscious, righting reflex and back-leg control were gone, muscles were completely relaxed, and there was no response to stimuli. With a coma-inducing dose of phenol, spontaneous activity decreased. After 1 min a body tremor developed interspersed with unpredictable jumping, and all four limbs began to shake. Leg control and then the righting reflex were lost by 2 min. Within 5 min rats were deeply unconscious and muscles completely relaxed while shaking of limbs continued until recovery 20 to 60 min later or death. With 480 mumol or less, none of the rats became comatose, but the shaking of limbs was present. The coma-inducing dose of phenol was reduced by 10% to 20% with simultaneous injection of subcoma doses of NH4+ or OA and by 20% to 30% with simultaneous DMDS leads to 2 methanethiol. Conversely, a subcoma dose of phenol reduced the coma-inducing doses of NH4+, OA, and DMDS by approximately 20% to 25%. Thus phenol, which accumulates in human hepatic failure, induces coma by itself in rats and acts synergistically with other hepatic failure toxins.

Animals↗