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PubMed1997

Both ethanol toxicity and thiamine deficiency are necessary to produce long-term memory deficits in the young chick.

This series of studies revealed that a 2.5-mg dose of oxythiamine administered over 2 days yielded memory deficits from 10 min following passive avoidance learning. This result existed in association with slowing of righting reflex. Administration of thiamine reversed the memory deficit and the slowing of the righting reflex. A combination of oxythiamine and peripheral alcohol administration also resulted in memory deficits appearing from 10 min after training; however, in contrast to the effect of thiamine deficiency alone, the deficits induced by thiamine deficiency in association with acute administration of alcohol could not be reversed by thiamine resupplementation. The combination of alcohol and oxythiamine also slowed the righting reflex, but higher doses of thiamine also were unable to ameliorate the memory deficit caused by a combination of oxythiamine and alcohol; however, the slowing of righting reflex was reversed. The results suggest that preexistent thiamine deficiency may make the subject susceptible to the neurotoxicological effects of alcohol on memory function.

Animals↗

PubMed2003

The hypnotic and analgesic effects of 2-bromomelatonin.

2-bromomelatonin is an analog of melatonin with a higher melatonin receptor affinity. We tested the hypnotic and analgesic properties of 2-bromomelatonin and compared them with those of propofol. Sprague-Dawley rats were assigned to receive 2-bromomelatonin or propofol IV, or morphine intraperitoneally. Righting reflex and response to tail clamping were assessed. Both 2-bromomelatonin and propofol caused a dose-dependent increase in the percent of rats displaying loss of both the righting reflex and the response to tail clamping. 2-Bromomelatonin was comparable to propofol in terms of its rapid onset and short duration of hypnosis. The 50% effective dose (95% confidence interval) for loss of righting reflex for propofol and 2-bromomelatonin were 3.7 (3.4-4.0) and 38 (35-41) mg/kg, respectively. Corresponding values for loss of response to tail clamp were 2.9 (3.5-4.0) and 21 (15-30) mg/kg, respectively. 2-bromomelatonin is approximately 6-10 times less potent than propofol depending on the end-point used. Intraperitoneal 30 mg/kg morphine did not affect the righting reflex, but resulted in loss of response to tail clamping in all animals. 2-bromomelatonin can exert hypnotic and antinocifensive effects similar to that observed with propofol. Unlike propofol, the reduced nocifensive behavior persisted after the animals had regained their righting reflex. This study provides evidence that 2-bromomelatonin has properties that are desirable in anesthetics or anesthetic adjuvants.

Analgesics, Non-Narcotic↗

PubMedDate not supplied

Acute tolerance in inbred and selected lines of mice.

Mice of the C57Bl and C3H strains regained their righting reflex at higher brain ethanol levels than those at which they had lost their righting reflex, indicating that these animals developed acute tolerance. DBA mice did not develop acute tolerance. DBA mice "slept" significantly longer than C57Bl mice, but all mice lost their righting reflex at similar brain ethanol levels. Mice of SS and LS lines also showed no evidence for developing acute tolerance but differed significantly in brain ethanol levels upon loss of righting reflex. Both acute tolerance development and initial brain sensitivity to ethanol seem to determine duration of ethanol "sleep time" in mice.

Animals↗

PubMed2001

Differential modulation of GABA- and NMDA-gated currents by ethanol and isoflurane in cultured rat cerebral cortical neurons.

Ethanol and the volatile anesthetics share many features including effects on both GABA and NMDA receptors. To determine the degree of similarity between these compounds, we examined the concentration-response curves for ethanol and isoflurane on currents gated by GABA or NMDA. The effects of isoflurane and ethanol on the righting reflex of rats were also observed. The concentration of ethanol causing loss of the righting reflex of rats was 82.3+/-2.9 mM, whereas median concentration of isoflurane exerting that effect was 0.125 mM. Both isoflurane and ethanol inhibited NMDA-gated currents in cultured cerebral cortical neurons at concentrations well below those associated with loss of the righting reflex or anesthesia. However, the effect of isoflurane was greater than that of ethanol and the slope of the concentration-response curve for isoflurane less steep than that for ethanol. Isoflurane enhanced GABA-gated currents at anesthetic concentrations but there was a sharp concentration-response curve with only minimal effects of isoflurane on GABA-gated currents at concentrations associated with loss of the righting reflex. In contrast, ethanol had no effect on GABA-gated currents even at lethal concentrations, i.e. 300 mM or 1.2%. Comparison of the concentration-response curves for the effects of isoflurane on NMDA- and GABA-gated currents has revealed both EC50 and Hill slope for the potentiation of GABA-gated currents were significantly greater than those for inhibition of NMDA-gated currents. These results support the hypothesis that isoflurane has actions on both the GABA and NMDA systems that are not shared by ethanol.

Anesthetics, Inhalation↗

PubMed1983

Effects of in vivo ethanol administration on Ca2+/Mg2+ ATPase and ATP-dependent Ca2+ uptake activity in synaptosomal membranes.

Acute administration of ethanol (4 g/kg, i.p.) to mice inhibits the sequestration of calcium into endoplasmic reticulum-like organelles in synaptosomal membranes. Ethanol administration inhibits both Ca2+-stimulated adenosine triphosphate hydrolysis and ATP-dependent calcium uptake in the vesicles at time of loss of righting reflex. At recovery of righting reflex, the Ca2+-ATPase activity returns to normal levels, while the ATP-dependent uptake remains inhibited. The effect of ethanol is specific for the sequestration (active transport) of calcium since calcium binding to synaptic membranes is not altered. Alteration in mechanisms responsible for synaptosomal buffering of cytosolic Ca2+ levels by in vivo ethanol may contribute to altered transmitter release rates following ethanol administration.

Adenosine Triphosphate↗

PubMed1990

Sodium arsanilate-induced vestibular dysfunction in rats: effects on open-field behavior and spontaneous activity in the automated digiscan monitoring system.

Vestibular dysfunction was chemically induced in Long-Evans rats by intratympanic injections (30 mg per side) of sodium arsanilate (atoxyl). Following a one-week recovery period the rats were behaviorally assayed for integrity of the labyrinthine systems. All subjects were tested for presence of the air-righting reflex, the contact-righting reflex (by lightly holding a sheet of Plexiglas against the soles of the rat's feet), and body rotation-induced nystagmus. All animals were then tested for their ability to remain on a small (15 x 15 cm) platform. Next, the subjects were given two 10-min open-field tests during which ambulation, rearing, grooming, and defecation responses were recorded. Four to five weeks later all rats were tested twice (60 min per session) in the automated Digiscan Activity Monitor which provides a multivariate assessment of spontaneous motor activity. The rats with vestibular dysfunction (Group VNX) took significantly less time to fall off the platform (p less than 0.01). They also exhibited significantly more open-field ambulation but fewer rearing responses (ps less than 0.01). An examination of group correlation coefficients for open-field variables and the platform test scores revealed some interesting group differences (ps less than 0.05). In the Digiscan tests the atoxyl-treated rats exhibited fewer number of horizontal movements, but increased speed for these movements (ps less than 0.05). Vertical movements did not differ significantly in incidence, but these movements were greatly reduced in duration (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Effect of pyrethroids on pentobarbital-induced sleeping time in relation to the chemical structure.

The effect of pyrethroids on pentobarbital-induced sleeping time was examined in mice. Pentobarbital-induced sleeping time was defined as the time interval from loss of righting reflex to reappearance of righting reflex. Mice were administered pyrethroids orally 2 h before the intraperitoneal injection of pentobarbital at a dose of 45 mg/kg. Pyrethroids with a cyano group on the alcohol moiety, such as cyphenothrin, cypermethrin, fenvalerate and fenpropathrin shortened the pentobarbital-induced sleeping time, while pyrethroids with an ethynyl group on the acid moiety, such as prallethrin, furamethrin and empenthrin, prolonged sleeping time. Pyrethroids with neither a cyano nor an ethynyl group had no effect on sleeping time. We, thus, found a clear relationship between the chemical structure of pyrethroids and their effect on pentobarbital-induced sleeping time.

Administration, Oral↗

PubMedDate not supplied

Rat two-generation reproductive toxicity study of bisphenol A.

This study was conducted to determine the low-dose effects of bisphenol A (BPA) in a rat two-generation reproduction study. Groups of 25 male and 25 female Crj: CD (SD) IGS rats were given BPA at 0.2, 2, 20, or 200 microg/kg/day by gastric intubation throughout the study beginning at the onset of a 10- and 2-week premating period, in F0 males and females, respectively, and continuing through the mating, gestation, and lactation periods, for two generations. There were adult (F0, F1, F2) and postnatal day (PND) 22 (F1, F2) necropsies: the oldest F2 males and females being killed at postnatal weeks 7 and 14, respectively. No compound-related clinical signs or effects on body weight or food consumption were observed in any generation. There were no compound-related changes in surface righting reflex, negative geotaxis reflex, mid-air righting reflex, pinna detachment, incisor eruption, eye opening, testes descent, preputial separation, or vaginal opening in F1 and F2 generations, or behavior in the open field or water filled multiple T-maze in the F1 generation. No test compound-related changes in estrous cyclicity, copulation index, fertility index, number of implantations, gestation length, litter size, pup weight, pup sex ratio, pup viability, or other functional reproductive measures were noted in any generation. A few significant changes in the anogenital distance (AGD) per cube root of body weight ratio were found at 0.2 and 20 microg/kg in F1 males, at 2, 20, and 200 microg/kg in F1 females, and at 20 and 200 microg/kg in F2 females. However, the changes in the AGD were consistently small (within 5% of control values), and no continuous changes in the AGD or AGD/cube root of body weight ratio were detected. There were no compound-related changes in epididymal sperm counts or motility in F0 and F1 males. No compound-related necropsy findings or effects on organ weight including the reproductive organs were found in any generation. Histopathologic examinations revealed no evidence of compound-related changes in any organs including the reproductive organs of both sexes. The data indicate that oral doses of BPA of between 0.2 and 200 microg/kg over 2 generations did not cause significant compound-related changes in reproductive or developmental parameters in rats.

Administration, Oral↗

PubMed1995

Comparative developmental and maternal neurotoxicity following acute gestational exposure to chlorpyrifos in rats.

Chlorpyrifos (CPF), an organophosphorus (OP) insecticide, exerts toxicity through inhibition of acetylcholinesterase (AChE). In the present study, pregnant Sprague-Dawley rats were given CPF (200 mg/kg, sc) as a single dose on gestation d 12 (GD12) and then sacrificed on either GD16, GD20, or postnatal d 3 (PND3) for measurement of maternal and developmental indicators of toxicity. While most CPF-treated rats exhibited no overt signs, a subset (4/28) showed moderate to severe signs of "cholinergic" toxicity at 2-3 d after treatment, and these rats were omitted from further studies. Extensive AChE inhibition (82-88%) was noted in maternal brain at all three time points following acute exposures. At GD16 and GD20, fetal brain AChE activity was inhibited 42-44%. While some degree of recovery in AChE activity was noted in pup brain by PND3, AChE activity was still inhibited (30%) in treated pups cross-fostered to control dams. In vitro inhibition of maternal and fetal (GD20) brain AChE activity by the active metabolite, chlorpyrifos oxon, suggested that the prenatal brain AChE activity was somewhat more sensitive (IC50 at 37.0 degrees C, 20 min: dam, 26.6 +/- 1.8 x 10(-9) M; fetus, 6.7 +/- 0.4 x 10(-9) M). Maternal brain muscarinic receptor binding was more extensively reduced (30-32%) at GD20 and PND3 as compared to the developing brain at GD20 (16%) and PND3 (11%). A simple postnatal reflex test (righting reflex) was transiently altered by CPF. The results suggest that CPF exposure to dams during gestation produces more extensive neurotoxicological effects in the dam relative to the developing fetus.

Acetylcholinesterase↗

PubMed2000

Quantification of pharmacodynamic interactions between dexmedetomidine and midazolam in the rat.

The pharmacodynamic (PD) interaction between the benzodiazepine agonist midazolam and the alpha(2)-adrenergic agonist dexmedetomidine was characterized for defined measures of anesthetic action and cardiovascular and ventilatory side effects in 33 rats. For various combinations of constant plasma concentrations of midazolam (0.1-20 microg/ml) and dexmedetomidine (0.3-19 ng/ml) obtained by target-controlled infusion, the whisker reflex (WR), righting reflex (RR), startle reflex to noise (SR), tail clamp response (TC), and corneal reflex (CR) were assessed. EEG (power in 0.5-3.5-Hz frequency band), mean arterial pressure, and heart rate were recorded continuously. Blood gas values and arterial drug concentrations were determined regularly. The nature and extent of PD interaction was quantified by the model parameter synergy (SYN < 0, antagonism; SYN = 0, additivity; and SYN > 0, synergy). With increasing drug concentrations WR was lost first, followed by RR, SR, TC, and CR. These effects were accompanied by an increase of the EEG measure. The drug interaction was synergistic for all stimulus-response measures and the degree of synergy increased with deeper levels of central nervous system depression (SYN was 7.3, 145, 560, 374, and 1490 for WR, RR, SR, TC, and CR, respectively). The cardiovascular side effects of dexmedetomidine, evaluated at similar PD endpoints, were reduced in the presence of midazolam. Ventilatory side effects were minor for all drug combinations. The nature and extent of the PD interactions were not reflected in the EEG measure.

Adrenergic alpha-Agonists↗

PubMed1991

The relationship between brain temperature during intoxication and ethanol sensitivity in LS and SS mice.

The present study characterized the relationship between brain temperature, rectal temperature, and ethanol sensitivity in the selectivity bred long-sleep (LS) and short-sleep (SS) mice. Radiotelemetric brain probe implanted and nonimplanted LS/lbg and SS/lbg male mice were injected with 2.5 and 4.9 g/kg ethanol, respectively, before exposure to ambient temperatures of 15 degrees C, 22 degrees C, or 34 degrees C. Ambient temperature significantly affected rectal temperature, brain temperature, and ethanol sensitivity, measured by impairment of righting reflex. Brain and rectal temperatures at return of righting reflex (RORR) were highly correlated. In SS mice brain and rectal temperatures at RORR were significantly positively correlated with loss of righting reflex (LORR) duration and significantly negatively correlated with blood ethanol concentration (BEC) at RORR. In LS mice rectal temperature at RORR was significantly negatively correlated with LORR duration, while both brain and rectal temperature at RORR were significantly positively correlated with BEC at RORR. The strength of the correlations and r2 values generated from linear regression analysis indicates that body temperature during intoxication can explain up to 52% of the variability in ethanol sensitivity in SS mice, but only 19% of the variability in ethanol sensitivity in LS mice. The correlational analyses are consistent with previous results based on comparisons between rectal temperature and ethanol sensitivity and extend to direct brain temperature measurement the evidence that decreasing temperature during intoxication decreases ethanol sensitivity in SS mice and increases ethanol sensitivity in LS mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic Intoxication↗

PubMed1987

Morphine and fentanyl hypnotic interactions with thiopental.

The effects of morphine-thiopental and fentanyl-thiopental combinations on the righting reflex were studied in rats. Doses that block the righting reflex for the agents given alone and for their combinations were determined with a probit procedure and compared with an isobolographic analysis. Interaction between morphine or fentanyl and thiopental on blockade of the righting reflex were both found to be synergistic. The degree of synergism was relatively small for the fentanyl-thiopental combination; the maximal deviation from additive interaction (expected/observed ratio) for ED50 dose level was 1.15 (P less than 0.01). The degree of synergism was greater for the morphine-thiopental combination; the maximal deviation from additive interaction was 2.27 (P less than 0.001). Comparison of the results with the outcomes of opioid-barbiturate interactions in relation to blockade of purposeful movement response to tail clamping, which was antagonistic, shows that the combination of a barbiturate with an opioid gives different outcomes for different end-points of anesthesia. This suggests that the anesthetic effect of an agent is composed of several components, each with a different mechanism of action.

Animals↗

PubMed1992

Elucidation of dose-effect relationships for different opiate effects using alfentanil in the spontaneously ventilating rat.

In addition to producing antinociception and mild sedation, opiates diminish spontaneous movement and produce muscle rigidity. Examination of the relationship between different opiate effects may lead to a better understanding of the mechanism and sites of action of opiate anesthesia. Previous studies have compared the dose-effect relationships for morphine and fentanyl between antinociception and loss of righting reflex. However, neither muscle rigidity nor lack of spontaneous movement (as measured by catalepsy) has been fully examined or directly compared with either antinociception or loss of righting reflex. This study, therefore, compared five clinically relevant opiate endpoints (antinociception, muscle rigidity, catalepsy, loss of righting reflex, and respiratory depression) using the mu-selective agonist alfentanil in the spontaneously ventilating rat. Rats were randomized to receive alfentanil (0-500 micrograms/kg) subcutaneously. For muscle rigidity, 59 rats had electromyographic activity measured with percutaneous hindlimb electrodes. After alfentanil injection, electromyographic data were recorded for 60 min. For antinociception and catalepsy, 49 rats were studied for 120 min after alfentanil. Catalepsy was measured from the time the rat's forelimbs were placed on a 10-cm-high bar until either limb was removed. Antinociception was studied by measuring tail-flick response to hot (55 degrees C) water. For righting reflex, 40 rats were studied for 120 min. Alfentanil-induced respiratory depression was assessed in 40 rats with indwelling tail arterial catheters. Alfentanil was administered after baseline arterial blood gas measurements, and then additional samples were obtained for 45 min. For each effect, data were converted into quantal responses and were then transformed to probit-log dose-response curves for analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗

PubMed1994

Acceleration registrography of head movement during alternating inclination of the support platform.

The righting reflex, essential for maintaining equilibrium, keeps the head and trunk in a state of balance with regard to gravity. Because patients suffering from vestibular disorders almost always complain of dizziness during everyday movements such as rising and walking, the righting reflex should be evaluated within the context of these dynamic states. A new method of acceleration registrography was designed to enable the testing of this reflex as the subject stands upon a moving platform. Participating in the study were 49 normal control subjects and 80 patients with peripheral vestibular disorders. The test we devised proved to be more successful in detecting labyrinthine righting reflex dysfunction in patients than the tests of righting reflex and deviation evaluations used thus far, such as Romberg's, Mann's and the stepping test, and to more accurately represent the disequilibrium and/or dizziness experienced by patients in everyday movements.

Acceleration↗

PubMed1999

Methionine enhances alcohol-induced narcosis in mice.

Methionine is an essential amino acid that has been used as a therapeutic drug in some disorders. In this study we questioned whether methionine affects ethanol-induced loss of righting reflex (narcosis). One hour after IP methionine administration (60, 120, 240, 480, 720, 960, and 1280 mg/kg), mice were injected with ethanol (4.0 g/kg), and the duration of loss of righting reflex was recorded. Methionine, at the higher doses (960 and 1280 mg/ kg), significantly increased this effect on ethanol-treated animals. A time-course study revealed that methionine increased the duration of the loss of righting reflex induced by ethanol until 4 h after being injected. Because methionine did not affect blood ethanol levels, no change in peripheral alcohol can explain the observed effects. This potentiation was not specific for ethanol because methionine increased 3-methyl-1-butanol (0.6 g/kg) and 1-propanol (2.4 g/kg)-induced loss of righting reflex as well. Therefore, the results obtained in this study suggest the need for further investigation into methionine-ethanol interactions prior to the use of methionine as an agent that can be used as an antidepressant and to prevent damage to organic tissue in alcoholism.

1-Propanol↗

PubMed1988

Electroencephalographic changes after short-term exposure to agonists of benzodiazepine receptors in the rat.

Naive rats receiving IV diazepam (10 mg/kg), flunitrazepam (2.5 mg/kg) and clonazepam (2 mg/kg) show electroencephalographic (EEG) changes consisting of lengthening of the spindle bursts (7-12 Hz; 200-300 microV) and appearance of 15-30 Hz waves (beta-like activity). These EEG manifestations are associated with signs of behavioral sedation (crouched, eyes open and myorelaxation) and stimulation (gnawing, running, ear twitches and sometimes wet-dog shakes), respectively. Bursts of 2-4 Hz waves can be occasionally observed associated with either marked sedation (lying down, eyes closed and presence of righting reflex) or sleep (stretched in the side with absence of righting reflex). Measurements of the periods spent by the animals in the two EEG patterns within the first hour after intravenous injection show the large preponderance of the spindle bursts over the beta-like activity. After the triazolopyridazine Cl 218,872 (10 mg/kg) the beta-like activity is almost absent, and in no case loss of the righting reflex can be observed. These agonists of BDZ receptors have been injected at the above reported doses for 5 days, once-a-day. At the 5th day, animals receiving diazepam exhibit a preponderance of the EEG and behavioral activation within the first hour after injection. Rats receiving flunitrazepam show a significant increase of the periods of stimulation and a slight decrease of the periods of sedation. These phenomena of "habituation" are absent in animals treated with clonazepam and Cl 218,872.

Animals↗

PubMed1981

Are convulsant gases also anesthetics?

This study investigated whether the convulsant gas flurothyl deviates from the correlation between anesthetic potency and lipid solubility. Flurothyl (CF3CH2OCH2CF3) produced convulsions in 50% of mice at 0.122 +/- 0.006% atm. Mice often convulsed repeatedly after exposure to flurothyl, the maximum number of convulsions occurring when the concentration was 0.24% atm. Concentrations greater than 0.6% atm produced convulsions immediately after addition of flurothyl, but rarely at later times. An ED50 value for loss of the righting reflex was obtained when the concentration was 1.22 +/- 0.19% atm. The oil/gas partition coefficient was found to be 46.9 for flurothyl at 37 C. The product of righting-reflex ED50 and oil/gas partition coefficient (0.0122 atm x 46.9 = 0.57 atm) is similar to that found for conventional anaesthetics in mice. Therefore, flurothyl does not deviate from the correlation of anesthetic potency and lipid solubility. It was also found that 0.3 to 0.8% atm flurothyl increased isoflurane MAC in dogs, but that 3 to 4% atm flurothyl decreased it. The increase of isoflurane requirement at lower concentrations of flurothyl suggests that anesthetics with a potential to cause convulsions may partly antagonize their own anesthetic effect. The decrease in isoflurane MAC in dogs at higher concentrations of flurothyl also implies that this compound has an anesthetic effect. A structural isomer of flurothyl, iso-Indoklon [(CSF3)2CHOCH3], was only anesthetic and did not have convulsant properties. Its MAC in dogs was 4.60 +/- 0.45% atm, and its righting-reflex ED50 in mice was 2.65 +/- 0.13% atm. The product of iso-Indoklon MAC in dogs and its oil/gas partition coefficient (27.0) was 1.24 atm, and the product of iso-Indoklon righting-reflex ED50 in mice and oil/gas partition coefficient was 0.72 atm. These values are close to those found for conventional anesthetic agents in dogs and mice; thus iso-Indoklon also does not deviate from the correlation between anesthetic potency and lipid solubilities.

Anesthesia, Inhalation↗

PubMed1995

Glycine enhances the central depressant properties of ethanol in mice.

The interaction between ethanol and glycine in the central nervous system was investigated in male Swiss-Webster mice. The loss of the righting reflex (LORR) was used as a measure of central nervous system depression. Mice were injected with ethanol (4.0 g/kg, IP), causing an ethanol-induced LORR. Immediately after the animals regained the righting reflex from ethanol administration, they received an intracerebroventricular (ICV) injection of saline or glycine (1, 15, 25, or 50 mumol/kg) in a volume of 5 microliters. Upon ICV injection of glycine, the mice lost the righting reflex once again. This effect of glycine in the presence of ethanol occurred rapidly and in a dose-dependent manner. Glycine induced a return to the LORR of 12.6 +/- 0.7, 24.5 +/- 1.3, 32.8 +/- 2.0, and 46.8 +/- 4.5 min when doses of 1, 15, 25, and 50 mumol/kg, respectively, were injected. D-Serine (15, 25, or 50 mumol/kg), an amino acid precursor of glycine, was injected (ICV) after the animals regained the righting reflex following ethanol injection (IP). Serine caused a return to the LORR of 0.5 +/- 0.5, 6.0 +/- 1.0, and 6.5 +/- 0.9 min when doses of 15, 25, and 50 mumol/kg, respectively, were injected. Strychnine was used to attenuate the ability of glycine and serine to cause a return to the LORR in the presence of ethanol. Strychnine, a competitive antagonist of glycine, significantly reduced the ability of glycine and serine to enhance the depressant action of ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗