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PubMedDate not supplied

Altered responsiveness to alcohol after exposure to organic lead.

Ethyl alcohol is known to effect the functional integrity of the limbic system, particularly the hippocampus, and to alter behaviors which are thought to be mediated through limbic function. Organometals also compromise the limbic system and result in deficits in learning and memory. Since both alcohol and organoleads are present in the environment and seem to influence limbic integration, the interaction of these two compounds was assessed in the present experiment. Thirty male rats of the Fischer-344 strain were divided into three equal groups and were given injections of trimethyl lead (TML) (8.0 or 17.0 mg/kg/ml SC) or the saline vehicle. Fourteen days later, all animals were challenged with a single hypnotic dose of ethanol (3.5 g/kg IP). The 20% v/v solution of alcohol was prepared in water from a stock solution of 95% ethanol. The latency to loss of the righting reflex and duration of sleep time were recorded while the rats were kept in sound-attenuating chambers. The rats treated with the highest dose of TML manifested significantly longer latencies to lose the righting reflex and shorter durations of sleep than did controls. These results suggest that exposure to environmental lead may alter the biological and behavioral responsiveness of an animal to alcohol.

Animals↗

PubMed1960

Anaesthesia in new-born animals.

Pentobarbitone was more toxic to new-born than to adult rabbits and rats, produced a longer loss of righting reflex in new-born animals but did not anaesthetize them effectively in less than toxic doses. Urethane did not anaesthetize new-born animals in doses which anaesthetized adults. Ether produced loss of righting reflex at lower concentrations for new-born than for adults, but the new-born animals became anaesthetized more slowly.

Analgesia↗

PubMed1977

beta-Endorphin: endogenous opiate or neuroleptic?

The opiatelike neuropeptide beta-endorphin produces a spectrum of effects that contrasts with that induced by the neuroleptic haloperidol. Rats injected intraventricularly or directly into the periaqueductal gray with beta-endorphin (0.5 to 50 micrograms) exhibited rigid immobility accompanied by the loss of righting reflex; the period of rigidity was preceded or followed (depending upon dose) by a state of hyperactivity. In contrast, no dose of haloperidol tested (0.5 to 12 milligrams per kilogram) produced rigidity, loss of righting reflex, or behavioral excitation. Furthermore, whereas animals injected with haloperidol remained stationary on a vertical grid, rats injected with beta-endorphin typically slid off the grid. Moreover, combined beta-endorphin and haloperidol treatment produced flaccidity in most animals. These results do not support the contention that this opiatelike peptide may be a naturally occurring neuroleptic.

Animals↗

PubMed1990

Isobolographic characterization of drug interactions incorporating biological variability.

Isobolograms have been widely used to characterize the nature of the interaction between combinations of drugs or chemicals. Some authors have applied this technique without accounting for the variability in the data or without adjusting for multiple comparisons to the line of additivity. This paper develops a graphical procedure which takes into account the variability of the data and which maintains favorable statistical properties. The isobolographic procedure utilized is illustrated by using three classical pharmacological drug combinations in female ICR mice. An additive relationship is illustrated with the loss of righting reflex after combinations of doses of sodium hexobarbital with itself. An antagonistic relationship is illustrated with the protection by mecamylamine of nicotine-induced lethality. A synergistic relationship is illustrated with the loss of righting reflex after combinations of ethanol and chloral hydrate. The procedure's statistical properties (level of significance and power) were determined using a simulation study. The isobolographic procedures developed here are applicable for quantal, continuous and count data. These procedures are applicable for identifying beneficial drug combinations, or conversely, identifying hazards resulting from exposure to multiple toxicants.

Animals↗

PubMed1985

The role of gamma-aminobutyric acid (GABA) in the regulation of ethanol and acetaldehyde self-administration.

Laboratory rats were presented with ethanol and water in a free-choice paradigm to determine each animal's preference for ethanol. Following a three week ethanol free period, it was observed that the duration of gamma-butyrolactone induced loss of righting reflex was negatively correlated to voluntary ethanol intake. It was also observed that the rate of intracerebroventricular self-administration of acetaldehyde was positively correlated with the latency to gamma-butyrolactone induced loss of righting reflex. These findings indicate that high ethanol drinking rats and high acetaldehyde self-administrating rats are less sensitive to the sedative action of gamma-butyrolactone.

4-Butyrolactone↗

PubMed2001

Acute and subchronic neurotoxicological evaluation of tetrahydrofuran by inhalation in rats.

Groups of adult male and female rats received exposure to tetrahydrofuran (THF) vapor by inhalation in acute or subchronic exposure scenarios. Acute exposure concentrations were 0, 500, 2500, or 5000 ppm for 6 hr. Evaluations conducted immediately after exposure included clinical observations, motor activity assessments (MA), and a battery of functional tests (FOB) designed to reveal nervous system dysfunction. During exposure to 2500 and 5000 ppm, rats had a diminished or absent startle response to a punctate auditory alerting stimulus. Following exposure to 5000 ppm, male and female rats were lethargic, exhibited abnormal gait or mobility, and splayed rear feet. Lethargy and splayed rear feet were also observed in females exposed to 2500 ppm. During the subsequent FOB, males exposed to 5000 ppm had a lower incidence of palpebral closure, higher incidences of slow or absent righting reflex, and a biphasic pattern of reduced motor activity followed by increased motor activity. Females exposed to 5000 ppm had increased incidences of palpebral closure in the open field, increased incidences of slow or absent righting reflex, and decreased motor activity. During the 14-week subchronic exposure series, daily THF exposure concentrations were 0, 500, 1500, or 3000 ppm, and neurobehavioral evaluations occurred on non-exposure days at approximately monthly intervals. Diminished startle responses to an auditory alerting stimulus were observed during exposure to 1500 or 3000 ppm; however, repeated exposures did not cause additional neurobehavioral or pathological effects. This pattern of effects is suggestive of transient sedation. Despite daily reinstatement of acute sedative effects during repeated exposure with up to 3000 ppm, THF did not produce any persistent or cumulative effects on nervous system structure or function. The demonstrated no-observed-effect level of THF for both acute and subchronic exposure was 500 ppm.

Administration, Inhalation↗

PubMed2001

Influence of naloxone on the increased sensitivity to propofol during hypovolemia in the rat.

OBJECTIVE: Hypovolemia has been shown to decrease the dose requirement for propofol. This increased effect has been explained partially by an increased end organ sensitivity to the anesthetic effect of propofol. We used the opioid blocking agent naloxone to test the hypothesis that endogenous opioids may be involved in this increased sensitivity. SUBJECTS: Thirty-two chronically instrumented rats were assigned randomly to either the hypovolemia (n = 16) or the control (n = 16) group. INTERVENTIONS: After pretreatment of each rat in the two groups with either intravenous saline (n = 8) or naloxone (3 mg/kg; n = 8), an intravenous infusion of propofol (150 mg x kg(-1) x hr(-1)) was given until 5 secs of electrical suppression of the electroencephalographic signal was observed. Return of righting reflex was used to assess depth of anesthesia, and the propofol blood concentration was determined simultaneously with high-performance liquid chromatography. MEASUREMENTS AND MAIN RESULTS: The mean propofol blood concentrations at the return of righting reflex were significantly lower in the hypovolemic animals compared with the controls within both naloxone-treated (2.1 +/- 0.2 microg/mL vs. 2.9 +/- 0.2 microg/mL; p < .01) and saline-treated (2.2 +/- 0.1 vs. 3.0 +/- 0.2 microg/mL; p < .01) rats. The mean concentrations were not different between the saline- and naloxone-treated rats either within the hypovolemic group or within the control group. CONCLUSIONS: The results of our study indicate that it is unlikely that the increased end organ sensitivity to propofol during hypovolemia is mediated by endogenous opioids, because it was not reversed by naloxone.

Anesthetics, Intravenous↗

PubMed1990

Development of tolerance to the CNS effects of aminoglutethimide in mice.

Initially, there is a high incidence of CNS-depressant side-effects when the aromatase inhibitor, aminoglutethimide, is used in the treatment of patients with advanced breast cancer. Tolerance to these effects develops with continued dosing. This study examines the development of tolerance to various indices of CNS depression with the drug in mice. Single doses of aminoglutethimide induced a dose-dependent depression of spontaneous locomotor activity, rotarod performance, righting reflex and body temperature and a dose-related antileptazol activity. On repeated dosing with the drug, tolerance to these various activities occurred. The tolerance was found to be dose-dependent in the rotarod and righting reflex tests and time-dependent in the locomotor and body temperature tests. Although the results do not allow a determination of whether this clearly demonstrated phenomenon in the mouse is primarily functional or dispositional, the slow onset (14 days) for complete tolerance may be indicative of a functional mechanism.

Aminoglutethimide↗

PubMed2000

Inhaled nonimmobilizers do not alter the middle latency auditory-evoked response of rats.

UNLABELLED: General anesthetics cause surgical immobility and oblivion (unconsciousness and amnesia). A class of compounds known as "nonimmobilizers" were predicted to be anesthetic, based on their physiochemical properties, but found to cause only amnesia. In humans, cerebrocortical electrical activity after auditory stimulation is depressed by concentrations of anesthetics which impair auditory recall. We sought to use these evoked responses to characterize the effects of the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N) and conventional inhaled anesthetics on early sensory processing in rats. Unrestrained rats with chronically implanted epidural silver screw electrodes were put into a chamber. On separate days, the same population of rats were exposed to isoflurane, desflurane, nitrous oxide, or 2N, each at several subminimum alveolar concentration of anesthetic required to eliminate movement in response to a noxious stimulus concentrations. After equilibration at each concentration, auditory-evoked responses were obtained. The behavioral state (activity and righting reflex) and electroencephalogram were also examined. 2N did not significantly change the middle latency auditory-evoked response, whereas the anesthetics all slowed conduction and depressed amplitude in a dose-dependent fashion. 2N neither depressed the righting reflex, nor induced epileptiform activity. IMPLICATIONS: Although the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (2N) suppresses learning, we find that 2N does not depress middle latency auditory-evoked responses. This suggests that 2N may suppress learning by depressing transmission through rostral subcortical structures, such as the amygdala, rather than by acting on the brainstem or neocortical structures.

Anesthetics↗

PubMed1991

Stress in mice increases intrinsic pentobarbitone sensitivity by a predominantly pharmacodynamic mechanism.

1. Mice were swum for 3 min at room temperature. 2. After this stress 'sleeping time' in response to pentobarbitone was increased by over 70%. 3. Loss of 'righting reflex' occurred in these stressed animals at brain concentrations of pentobarbitone which were 40% lower than those needed for 'sleep' in the unstressed mice, indicating a true increase in sensitivity to the drug. 'Waking' (the return of the righting reflex) occurred at identical levels in both groups. 4. Kinetic analysis showed that the rates of absorption, elimination and transfer between plasma and brain were slower in the swum than in the unswum mice, probably because of the reduced body temperatures produced by the swimming.

Animals↗

PubMed2003

Defective balancing ability and hyperactivity in the CLX (circling behavior linked to the X-chromosome) mutant rat.

We have reported that the recently described circling behavior rat (CLX) is a hereditary mutant controlled by a single sex-linked recessive gene (gene symbol: clx). This mutant shows intermittent circle walking and/or running and head tossing with the neck twisted. The abnormal behavior begins to appear around weaning and continues throughout life. In the present study, behavioral tests were performed during the suckling and post-weaning periods and when the rats reached maturity, and the following peculiar abnormalities were revealed: (1) in the righting reflex test, the CLX young show a tendency to take a longer time to revert to normal posture; (2) in the negative geotaxis test, they had difficulty moving upward at 12 days of age; (3) in the air righting reflex test, they frequently fell on their backs or shoulders even after weaning; (4) almost none of the CLX rats showed nystagmus, which is invariably observed in normal rats after rotating stimulation, at 20 weeks of age; and (5) they showed hyperactivity in the open field test at the age of 5 or 6 weeks and a higher degree of locomotor activity in the home cage at the age of 7 and 15 weeks. These results suggest that CLX mutant rats may have some defect in vestibular function (balance sense) or abnormalities in an area of the central nervous system responsible for posture control, e.g., in the dopaminergic or GABAergic neurons.

Animals↗

PubMed1990

Site-specific enhancement of gamma-aminobutyric acid-mediated inhibition of neural activity by ethanol in the rat medial septal area.

Because of uncertainty concerning the interaction of ethanol with gamma-aminobutyric acid (GABA) receptor-mediated events, the present work was designed to investigate the effect of ethanol on GABA transmission in the rat septal area using behavioral and electrophysiological techniques. Microinjection of the GABAA agonist muscimol into the medial septal area (MSA) enhanced, and bicuculline administration antagonized, ethanol-induced impairment of the aerial righting reflex. Microinjection of these drugs into the lateral septum (LSi) did not influence this measure of ethanol-induced sedation. Furthermore, intraseptal injections of muscimol or bicuculline in saline-treated rats had no effect on the aerial righting reflex. These data suggest that the MSA plays a critical modulatory role in the sedative actions of ethanol. To assess the effect of ethanol on muscimol responses in the MSA and LSi at the cellular level, GABA was applied by iontophoresis to rhythmically bursting neurons of the MSA and to cells in the LSi. The magnitude of the resultant inhibition by GABA on these cells was assessed before and after systemic administration of ethanol. Ethanol enhanced GABA-mediated inhibition of MSA neural activity, but did not alter GABA-mediated inhibition of cellular activity in the LSi. In contrast, the inhibition of cellular activity in the MSA, caused by a maximally effective concentration of the benzodiazepine flurazepam, was not altered by ethanol. Other work in the MSA demonstrated that electrical stimulation of the fimbria caused an inhibition of ongoing single unit activity that was reduced by concurrent application of bicuculline. The duration of this electrically elicited inhibition in the MSA was enhanced after ethanol injection and then recovered to base-line levels. In addition, ethanol (1.5 mg/kg) caused an enhancement of the inhibition induced by nipecotic acid, a GABA uptake inhibitor. These findings demonstrate that GABA-mediated neural inhibition is enhanced by ethanol in the MSA but not the LSi, indicating that the actions of ethanol on GABA-induced inhibition can be site specific. It is proposed that the cellular action of ethanol may depend upon a specific molecular composition of the GABA receptor complex which may vary at selected sites in the brain.

Animals↗

PubMedDate not supplied

Influence of opioid receptor antagonists on motor-impairing effects of benzodiazepines.

The influence of naloxone and naltrexone on the motor-impairing effects of diazepam, chlordiazepoxide, clonazepam and estazolam were studied in the aerial righting reflex test (mice, rats), and the first two drugs were examined in the rota-rod test (mice). Benzodiazepine-induced motor incoordination was significantly decreased by naloxone and naltrexone (4-16 mg/kg) in mice and rats in aerial righting reflex test. The motor-impairing effects of diazepam and chlordiazepoxide observed in rota-rod test were significantly diminished only by naltrexone (8-16 mg/kg). These data seem to confirm some interactions between benzodiazepines and opioid system.

Animals↗

PubMed1989

Mechanisms of general anesthesia: brain regional responses to baclofen.

The GABAB agonist baclofen is reported to produce general anesthesia when administered either centrally into the lateral ventricles of rats or peripherally to mice. Previously we demonstrated that beta-endorphin given intracerebrally produces anesthesia in rats, a response localized to sites in or adjacent to the inferior third and fourth ventricles. In order to compare the anatomical localization of these two anesthetic responses, we administered baclofen into the inferior or superior lateral or third ventricles, the aqueduct, or fourth ventricle in rats. Although 10 micrograms baclofen infusions into several regions caused loss of the righting reflex, in no case did animals exhibit an unconscious state which satisfied strict criteria of anesthesia. Infusions of 20 micrograms into the inferior third and fourth ventricles elicited seizures followed by a postictal depression. Although unresponsive to some stimuli, these animals showed no impairment in the corneal reflex. Since this dose was often lethal, higher doses not tested. Baclofen, given to mice intraperitoneally at doses of 25, 50, or 75 mg/kg, failed to elicit strictly defined anesthesia, although, to varying degrees, animals exhibited analgesia, loss of the righting reflex, and loss of behavioral responses to loud sounds. Animals continued to show motor responses when handled and retained corneal reflexes. Baclofen does not evoke an unconscious anesthetic state when administered centrally or systemically, emphasizing the need for strict criteria to define general anesthesia and to categorize drugs that promote this state.

Anesthesia, General↗

PubMed1987

Ethanol-induced sleep time: interaction with taurine and a taurine antagonist.

In male Swiss-Webster mice sleep time (hypnosis) was used as an index of ethanol-induced central nervous system depression. Ethanol (4 g/kg, IP) was administered to animals and the onset to sleep time (loss of the righting reflex) and the duration of sleep time were recorded. At the end of the ethanol-induced sleep time, taurine (7.5, 15 or 25 mumol/kg, ICV) was injected. Immediately after the ICV injection of taurine the mice again lost the righting reflex. This effect of taurine occurred in a dose-dependent fashion. In the absence of ethanol, taurine (25 mumol/kg, ICV) did not produce a significant sleep time. In another experiment when TAG, 6-amino-methyl-3-4H-1,3,4-benzothiadiazine-1,1-dioxide HCl, (a taurine antagonist) was given to mice, TAG (0.9 mumol/kg, ICV) significantly reduced the effect of taurine (7.5, 15 and 25 mumol/kg, ICV) to reinstate a sleep time in the presence of ethanol. TAG, however, did not alter ethanol-induced sleep time. These results indicate that taurine (ICV) can enhance the central depressant action of ethanol and that this effect of taurine can be attenuated by TAG. The antagonism of taurine by TAG appears to be noncompetitive in nature.

Animals↗

PubMedDate not supplied

Motor impairment, narcosis and hypothermia by ethanol: separate genetic mechanisms.

The AT and ANT rat lines, developed by selective outbreeding for differential ethanol-induced motor impairment, were tested for their sensitivity to the hypothermic and narcotic (loss of righting reflex) effects of ethanol. In contrast to the large differences between the lines in their degree of motor impairment, as measured with both the tilting-plane and rotarod tests, only minor differences were observed in duration of loss of righting reflex or hypothermia. Therefore, we suggest that genetically determined factors influencing motor impairment are for the most part dissociated from the factors determining the hypothermic and narcotic effects of ethanol.

Alcoholic Intoxication↗

PubMed1975

Neurotological studies on the role of the sympathetic nervous system in the formation of traumatic vertigo of cervical origin.

To test the validity of the hypothesis that irritation of the cervical sympathetic nerves is a cause of hypertonicity of the cervical soft supporting tissues, especially the deep nuchal muscles, and that this hypertonicity is a cause of traumatic vertigo of cervical origin, we examined 44 vertigo cases with whiplash injury by testing equilibrium function and EMG discharges from the neck before and after administration of drugs affecting the sympathetic receptors. The results obtained were as follows: 1. Administration of iso-proterenol (beta-receptor stimulant) caused a significant increase in the EMG's from the injured neck muscles, in parallel with increased impairment of the righting reflex. The blindfolded vertical writing test showed the appearance or intensification of ataxia or deviation in writing when this drug was given. In contrast, administration of propranolol (beta-receptor depressor) had the opposite effects on the EMG's, the righting reflex and blindfolded vertical writing. Furthermore, the resulting changes in the EMG's and equilibrium functions were parallel with alterations in subjects' complaints, i.e., increase or decrease in neck pain and vertigo. 2. Administration of drugs affecting the alpha receptors, such as noradrenaline (alpha-receptor stimulant) and phentolamine (alpha-receptor depressor) had no appreciable effect on the EMG's, equilibrium function or the subjects' complaints. These results show that in vertigo due to whiplash injury hypertonicity of the cervical erector muscles can be induced sympathetically, and that this hypertonicity is based on over-excitement of beta receptors in the injured neck muscles, which results in vertigo of cervical origin.

Adolescent↗

PubMed2001

Effects of prenatal styrene exposure on postnatal development and brain serotonin and catecholamine levels in rats.

Maternal reproductive effects in Wistar rats exposed to 0, 50, or 300 ppm styrene for 6 h/day during gestational days 6 to 20 were evaluated. Their offspring were observed postnatally for neurochemical changes, growth, and physical landmarks of development. Mothers exposed to styrene were compared with pair-fed and ad-lib-fed controls in order to adjust nutrient conditions. Prolongation of the gestational period, food intake, and the number of neonatal deaths or stillbirths in 300-ppm-exposed dams showed evidence of styrene-related effects. Other reproductive parameters, such as litter size, birth weight, and sex ratio, were found to exhibit no effects within the variation range studied. A neurochemical effect was observed in that the 5-HT and HVA concentrations in cerebrum were significantly decreased. Incisor eruption (mandible), eye opening, and the air-righting reflex were delayed in rat pups born to dams receiving 300 ppm styrene exposure compared with the pair-fed and ad lib control groups. Pups born to dams exposed to 50 ppm styrene also had a significantly delayed air-righting reflex compared with ad lib controls. These results suggest that the offspring were susceptible to the effects of styrene on a few developmental landmarks even when nutritional effects were controlled.

Animals↗