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PubMed1993

Behavioral and electrophysiological comparison of ketamine with dizocilpine in the rat.

We have compared the effects of MK 801 and ketamine on a measure of anesthesia (loss of righting reflex) and two measures of basal ganglia dopamine (DA) function: apomorphine (APO)-induced stereotypy and APO-induced excitation of type II globus pallidus (GP) neurons. As expected, ketamine induced anesthesia. High-dose MK 801 administered IP induced ataxia, but not anesthesia. When administered i.v., high-dose MK 801 induced anesthesia in only three of five rats. Using a modified stereotypy scale, it was found that pretreatment with MK 801 blocked APO-induced stereotypic sniffing. Intravenous ketamine also blocked APO-induced stereotypy, but IP ketamine did not. Similar results were observed in neurophysiological studies; MK 801 altered the excitation of type II GP neurons by APO. Intravenous ketamine (5 mg/kg) also altered the responsiveness of these cells to APO, but ketamine anesthesia (150 mg/kg, IP) had no effect. These findings suggest that MK 801 is not an effective anesthetic in rats, and the method of administration of ketamine plays a role in its ability to exert NMDA receptor blockade.

Animals↗

PubMed1996

Comparison of the renal effects of six sedating agents in rats.

This study was designed to compare the renal effects of sedation with alphaxalone-alphadolone, etomidate, propofol, midazolam, fentanyl-fluanisone, and thiopental in rats. The sedative dose was defined as the highest dose that abolished the escape response without affecting the righting reflex. Female Wistar rats were chronically catheterized with a jugular vein catheter, and urine flow rate and renal clearances of inulin (glomerular filtration rate = GFR), sodium, and lithium (used as an index of proximal tubular function) were measured in the conscious, unrestrained state (n = 107 experiments). In a separate series (n = 70 experiments), the effect of sedative doses of each drug on the nociceptive threshold was tested with the tail-flick test. Responses in sedated animals were compared to responses in animals infused with the vehicle. Fentanyl-fluanisone and thiopental had hypoalgesic actions in sedating doses. Propofol, fentanyl-fluanisone, and thiopental reduced GFR by 20-30%. Urine flow rate was significantly decreased by propofol (-24%) and thiopental (-48%). Propofol and fentanyl-fluanisone reduced fractional lithium excretion by 9-13%. Only alphaxalone-alphadolone, etomidate, and midazolam produced sedation without affecting renal function in rats. Because midazolam produced the most consistent degree of sedation, we conclude that midazolam is the least confounding sedative agent for renal function studies in conscious rats.

Animals↗

PubMed1985

Comparative ototoxicity of netilmicin, gentamicin, and tobramycin in cats.

Netilmicin, a semisynthetic aminoglycoside antibiotic, is less ototoxic in a variety of species than other aminoglycosides currently in therapeutic use. In this study, mixed-breed cats (four/group) were given daily sc injections of netilmicin (20, 40, and 80 mg/kg), gentamicin (20 and 40 mg/kg), or tobramycin (20, 40, and 80 mg/kg) for up to 30 weeks or until ototoxicity was observed. The animals were examined throughout the study for effects on cochlear and vestibular function. Hematologic, serum chemical, and drug-serum (24-hr postdose) assays were performed at approximate monthly intervals during the dosing period. The cochleae, kidneys, and liver were examined microscopically. The mean number of dose days required to produce vestibulotoxic effects, demonstrated by impaired righting reflex or locomotor ataxia, was from 41 to 61 in cats dosed with tobramycin (40 and 80 mg/kg) or gentamicin. No vestibular dysfunction was observed in any of the netilmicin 20-mg/kg-dosed cats, in two cats each of the tobramycin 20-mg/kg and netilmicin 40-mg/kg groups, and in one netilmicin 80-mg/kg-dosed animal. Histologic examination of the cochleae revealed degeneration of the hair cells and supporting sensory structures in the majority of cats dosed with gentamicin at 20 and 40 mg/kg and tobramycin at 40 and 80 mg/kg. Less than 50% of the tissues from cats of the tobramycin 20-mg/kg and netilmicin 40- and 80-mg/kg-dosed groups had similar degenerative cochlear changes. No cochlear damage was noted in any of the cats given netilmicin at 20 mg/kg. Results of the clinical laboratory determinations were generally unremarkable. Proximal tubular degeneration was the principal finding observed in the kidneys of the animals. Under the conditions of this study, at least a twofold (vestibular) to fourfold (cochlear) relative safety margin for ototoxicity was established in favor of netilmicin over tobramycin and gentamicin.

Animals↗

PubMed1986

Behavioral changes in preweaning and adult rats exposed prenatally to low ionizing radiation.

Seven behavioral tests were used to evaluate the postnatal behavior of rats after exposure on gestational Day 15 to 0, 25, 50, 75, or 125 r, whole body irradiation of the pregnant rat. Three tests were administered in the first 2 postnatal weeks (righting reflex, negative geotaxis, and reflex suspension); three tests were administered on postnatal Day 21 (modified open field, spatial maze, and continuous corridor). As adults, the rats were retested with the same tests as at 21 days and also in the running wheel. Dose-response decreases in body weight were greater in the younger rats. Some behavioral tests were not altered by irradiation, while others showed clear dose-response relationships, starting as low as 25 r. The early changes were characterized by light body weight, delays in behavioral development and hypoactivity, followed by recovery of some parameters with maturation. Eventually hyperactivity developed in adult rats after gestational irradiation. However, it cannot be concluded that either morphological or behavioral tests are more sensitive than neonatal body weight change for detection of damage from gestational irradiation.

Animals↗

PubMed1989

The lethal principle of Poa huecu (coiron blanco): a plant indigenous to Argentina.

The lethality of Poa huecu, a plant toxic to cattle and sheep, was followed by injection of chromatographic fractions in mice. The lethal aqueous extract was administered i.p. to Rockland mice of either sex and produced motor incoordination, transient ataxia, rough hair coat, tremors and muscle contractions and, occasionally, blindness. Doses greater than 1.5 g/kg mouse were always lethal. Fractionation of this lethal extract included dialysis, column chromatography on Sephadex G-25 and fractional precipitation with ethanol. Precipitates obtained with 70% and 85% ethanol were further purified on a DEAE-cellulose column. Eight fractions were obtained, each was injected into mice. Only fractions 3-6 were toxic. Fraction 3 produced slight hepatosis and hyperemia in the liver and gliosis in the brain. None of the other tissues exhibited histological lesions. Fractions 4 and 5 caused death of all animals within 30 min to 4 hr after injection. Polyacrylamide gel electrophoresis and acid hydrolysis showed that fractions 4 and 5 contained a glycoprotein of nearly the same mol. wt (67,000-94,000). Microscopic pathology in the mice treated with the lethal glycoprotein of fraction 4 included hyperemia in the kidneys, megakaryocytes in the spleen, slight hepatosis and focal coagulative necrosis with nuclear pyknosis and karyonexis in the liver, gliosis, intracellular brain edema with axon degeneration and swollen astrocytes in the brain. These brain injuries may relate to the motor incoordination of cattle that causes a delayed righting reflex. The major monosaccharides of the lethal glycoprotein are glucose and mannose, while rhamnose, arabinose, xylose and galactose are present in low percentages. Proline and the acidic amino acids (glutamic and aspartic acids) are the most abundant in the peptidic residue.

Amino Acids↗

PubMed1976

Effects of TRH on the central nervous system of the rabbit.

Thyrotropin releasing hormone (TRH) administered intraventricularly to rabbits produces tachypnea, hyperthermia, behavioral excitation and, with larger doses, compulsive scratching. These effects of TRH were unaffected by various catecholamine and serotonin antagonists or depleting agents. When TRH was administered to pentobarbital-narcotized animals, tachypnea and rapid recovery of the righting reflex occurred. The antagonism of narcosis or sedation was evident against other barbiturates, diazepam, chlorpromazine, and reserpine, but not against morphine. Morphine actually appeared to antagonize the excitatory actions of TRH. Scopolamine pretreatment prevented the arousal from pentobarbital narcosis, but not the tachypnea or hyperthermia. TRH represents a new class of psychoactive chemical which may play a role in brain function.

Animals↗

PubMed1980

Calcium enhancement of alcohol and drug-induced sleeping time in mice and rats.

Calcium injected intracerebroventricularly (IVT) at various times before a hypnotic dose of ethanol significantly enhanced the duration of sleeping time (loss of righting reflex, LRR) in mice and rats. This cation also enhanced the duration of LRR induced by t-butanol and chloral hydrate, but not that induced by sodium pentobarbital. Other cations injected IVT (manganese, cadmium, and zinc) also enhanced ethanol-induced LRR. The synergistic effects of the ionophores X537A and A23187 on calcium-enhanced LRR, and the antagonism of ethanol-induced LRR by EDTA and EGTA suggest the involvement of a membrane-associated calcium pool in the hypnotic effect of ethanol. These studies show the generality of cation enhancement of alcohol-induced sleeping time in mice and rats, and confirm earlier reports which suggested that calcium is involved with the central nervous system depressant effects of alcohols.

Animals↗

PubMed1980

Interaction between phencyclidine (PCP) and GABA-ergic drugs: clinical implications.

Pretreatment (IP) of mice with (-) baclofen, muscimol, 4,5,6,7-tetrahydroisoxazolo (S,4-c) pyridin-3-ol hydrate (THIP), aminooxyacetic acid (AOAA) or gamma-acetylenic GABA caused a dose-dependent inhibition of thelocomotor stimulant effect of phencyclidine (PCP, 8 mg/kg). Although (-) baclofen was found to be the most effective PCP antagonist, its (+) isomer was inactive. The maximum blocking effect of AOAA was seen in animals treated 3 and 6 hr earlier. Except for gamma-acetylenic GABA, none of these drugs significantly blocked the locomotor stimulant effect of d-amphetamine (3 mg/kg, IP). Diazepam reduced d-amphetamine response, but failed to influence PCP-induced stimulation. The locomotor stimulant effect of PCP, unlike that of d-amphetamine, may be the result of a specific GABA antagonistic effect at certain dopamine-rich areas of the brain. It seems that (-) baclofen may prove to be useful in the management of PCP intoxication. Administration of higher doses of PCP (20 and 50 mg/kg) in mice pretreated with (-) baclofen resulted in the development of surgical anesthesia manifested as the loss of a) righting reflex, b) pain sensation and c) corneal reflex. The duration of the general anesthetic response was found to be a function of the doses of both (-) baclofen and PCP. The possible use of (-) baclofen as an adjuvant to general anesthetic is discussed.

Aminooxyacetic Acid↗

PubMed1981

Oxidation of alcohol in free-moving mice from high and low preference strains.

Free-moving mice from the high-alcohol preference C57BL/6J strain and low-preference DBA/2J strain were slowly fed [2-14C]ethanol intragastrically until anesthesia was achieved. Behavior was monitored in a Plexiglas metabolic chamber while 14CO2 was simultaneously trapped to determine the rate of ethanol metabolism. Average time to the loss of the righting reflex in the DBA/2J was 21.9 min and 27.9 min for the C57BL/6J strain (p less than 0.005). Elimination of 14CO2 was slightly higher (n.s.) in the DBA/2J strain for the entire monitoring period. Infusion of ethanol via the tail vein yielded identical results indicating that the slower elimination rate in the C57BL/6J strain could not be the result of slower absorption across the gut wall. Infusion via the tail vein with radioactive sodium bicarbonate indicated that the DBA/2J strain has a higher rate of CO2 expiration (n.s.). Consequently, the higher rate of 14CO2 expiration from ethanol oxidation may not reflect a higher rate of metabolism. These results are discussed in terms of the apparent differences between these strains in neural sensitivity to ethanol.

Alcohol Drinking↗

PubMed1982

Evidence for genetic correlation of hypnotic effects and cerebellar Purkinje neuron depression in response to ethanol in mice.

In the present study, we compared phenotypic differences in behavioral and neurophysiological responses to acute ethanol administration among eight inbred strains of mice. Genetic variation for behavioral sedation, as measured by loss of the righting reflex (sleep time) after a hypnotic dose of ethanol, was shown to be present among the inbred strain population. In addition, a large genetic component of variation in the depressant action of ethanol on the spontaneous discharge of cerebellar Purkinje neurons was found. Results from an analysis of covariance of the behavioral and electrophysiological phenotypes, measured on each mouse among the inbred strains, provided strong evidence for a high genetic correlation between sleep time and inhibition of cerebellar Purkinje neuron discharge in response to acute ethanol administration. Taken together with our previously reported data on ethanol-induced electrophysiological changes in selectively bred lines, the results described here strongly support the hypothesis that the cerebellar Purkinje neuron is one important locus for the acute soporific effects of alcohol.

Animals↗

PubMed1982

Alcohol and morphine induced hypothermia in mice selected for sensitivity in ethanol.

We have used changes in body temperature as an index of responsiveness to alcohol and morphine in mice selectively bred for differential sensitivity to ethanol. In agreement with other laboratories, we found that mice which show longer duration of loss of righting reflex following hypnotic doses of ethanol (long sleep; LS) also showed greater loss in body temperature following subhypnotic doses of ethanol than did the less sensitive short sleep (SS) mice. This effect was dose dependent in both lines. In contrast, SS mice were more sensitive than LS mice to the hypothermic effects of morphine, although the difference was only evident 30 min after morphine administration. Naloxone attenuated morphine induced hypothermia in mice of both genotypes, but attenuated alcohol induced hypothermia only in SS mice. Thus, SS mice may be more sensitive to an opiate agonist and an antagonist, at least as indexed by changes in body temperature, and may prove to be a useful population for evaluating both alcohol-opiate interactions and genetic differences in opiate responsiveness.

Animals↗

PubMed1983

Cerebellar role in the differential ethanol sensitivity of long sleep and short sleep mice.

Two lines of mice have been selectively bred for differential sleep time responses to ethanol. Long sleep (LS) mice sleep over an order of magnitude longer than short sleep (SS) mice. We have found that these behavioral sensitivities are also reflected in the responsiveness of cerebellar Purkinje neurons in those two mouse lines in situ and in intraocular cerebellar brain grafts. The differential sensitivity of Purkinje cells to the depressant effects of ethanol appears to be an intrinsic property of the cerebellum and shows a high genetic correlation with the hypnotic effects of this drug as measured by sleep time. Sleep time studies of neonatally cerebellectomized LS and SS mice indicate that the cerebellum is not the primary determinant of the sensitivity of these mice to the soporific effects of ethanol. The sleep time of SS, but not LS mice, was altered by cerebellectomy suggesting that the cerebellum has different influences on the ethanol-induced loss of righting reflex in these two mouse lines.

Animals↗

PubMed1983

Initial sensitivity and acute tolerance to ethanol in the P and NP lines of rats.

We recently reported that selectively bred, alcohol-preferring (P) and alcohol-nonpreferring (NP) rats differ in sensitivity to a single sedative-hypnotic dose of ethanol, as measured by performance in the jump test. The present study examines the contributions of initial sensitivity and acute tolerance development to this difference. Initial sensitivity, assessed by brain alcohol content upon loss of the aerial righting reflex, was not significantly different between P and NP groups given 3 g ethanol/kg body weight intraperitoneally. Acute tolerance was indexed from blood alcohol concentrations (BAC) upon recovery of jumping performance following two successive ethanol doses. Practiced P and NP rats were required to jump 35 cm to a descending platform following the IP injection of 2.0 g ethanol/kg. The NP group took significantly longer (74 min) than the P (33 min) group whereupon BAC1 of NP rats (234 mg%) was significantly lower than that of P rats (250 mg%). A second injection (1.0 g/kg) was given immediately after the animals reached the 35 cm criterion. Again, NP rats took significantly longer (124 min) than P rats (52 min) to jump 35 cm and BAC2 of NP animals was lower (295 mg%) than that of P rats (343 mg%). The difference between BAC2 and BAC1, the measure of tolerance development, was significantly larger for P rats (90 mg%) than for NP rats (61 mg%). No significant differences in blood ethanol elimination were observed between the groups. The data indicate no difference in initial sensitivity between P and NP animals but that P rats develop acute tolerance more rapidly and/or to a greater degree than do NP rats. The results are consistent with a relationship in these selectively bred lines of rats between alcohol preference and the development of acute tolerance.

Animals↗

PubMed1984

Apomorphine effects on behavioral response to ethanol in mice selectively bred for differential sensitivity to ethanol.

Two lines of mice selectively bred for differences in response to a hypnotic dose of ethanol were administered apomorphine alone or in combination with ethanol. When administered by itself, apomorphine produced similar dose-dependent depression of locomotor activity and increases in stereotypy in the two lines. Doses of apomorphine (0.5 microM/kg and 2 microM/kg) thought to bind only presynaptic dopamine receptors blocked the slight locomotor activation to 1.5 g/kg ethanol in the ethanol-sensitive Long-Sleep (LS) mice; in the ethanol-insensitive Short-Sleep (SS) mice which show marked activation to all subhypnotic doses of ethanol, these doses of apomorphine only attenuated the activation. A higher apomorphine dose (8 microM/kg) antagonized the locomotor depressant effects of 2.0 and 2.5 g/kg of ethanol in LS mice but did not alter the shape of the SS ethanol dose response curve for locomotor activity. Apomorphine (2 and 8 microM/kg) potentiated ethanol-induced loss of the righting reflex in LS mice in a dose dependent fashion, but did not alter this soporific effect of ethanol in SS mice. These findings extend the data base suggesting a role for dopamine both in the mechanism(s) differentiating the LS and SS mice and the stimulant and intoxicating properties of ethanol.

Animals↗

PubMed1984

Lithium, rubidium and cesium: cerebral pharmacokinetics and alcohol interactions.

The distribution of exogenously administered Li+, Rb+ and Cs+ in distinct mouse brain regions was studied as a function of time subsequent termination of a short-term daily treatment with these alkali metal salts. The resulting distribution profiles were compared with that obtained from the corresponding endogenous alkali metals. Endogenous Rb+ and Cs+ were readily measurable in all 6 brain regions studied compared to traces of measurable Li+. The Rb+ concentration was greater than that of Cs+. Short-term treatment with equal doses of the alkali metals studied showed greater brain accumulation of Rb+ and Cs+ than Li+ with a prolonged brain regions preference for Cs+ storages as a function of time. Duration of ethanol-mediated narcosis was reduced from saline controls by pretreatment with RbCl or CsCl as contrasted with prolongation by LiCl. The narcotic dosage of ethanol used reduced endogeneous Li+ and increased Cs+ levels in the cerebellum. This massive ethanol dosage exerted little effect on the distribution of exogenously administered Cs+ with exception of the striatum which continued to show a high content of Cs+. This may have contributed to partial antagonism of ethanol-depressant action and to restoring of motor function, i.e., rapid regaining of righting reflex. The results showed that Cs+ possessed longer biological life time in the brain than Rb+ or Li+ which may be of therapeutic value, i.e., in the use of Cs salts in treatment of brain tumors and in conjunction with psychoactive agents provided the respective chemotherapeutic and antidepressant properties of CsCl have been established.

Animals↗

PubMed1984

Metronidazole influences the development of neural tolerance to ethanol.

The duration of the loss of the righting reflex (LoRR) was measured in Swiss Webster (SW) and DBA/2 mice following intraperitoneal injection of ethanol or metronidazole alone or together. A single injection of ethanol induced to short LoRR in SW mice and a long LoRR in DBA/2 mice. Metronidazole did not induce LoRR in either strain. When the mice were exposed daily to ethanol for five days, the duration of the LoRR was prolonged in SW mice and shortened in DBA/2 mice. This indicates the development of increased neural sensitivity to ethanol in SW mice and of neural tolerance to ethanol in DBA/2 mice. The response in SW mice to administration of ethanol and metronidazole together did not differ from their response to ethanol alone. However, the duration of the LoRR in DBA/2 mice injected repeatedly with the two drugs was longer than that observed with ethanol alone. Thus metronidazole appears to inhibit the development of neural tolerance to ethanol in DBA/2 mice but has no effect on ethanol induced LoRR in SW mice.

Animals↗

PubMed1986

Reversible disruption of lordosis via midbrain infusions of procaine and tetrodotoxin.

Behavioral effects of bilateral intracranial infusions of tetrodotoxin (1, 3.3 or 10 ng/rat), 50% procaine (2 microliters/rat) or phosphate-buffered saline (PBS-2 microliters/rat) into the dorsal midbrain of conscious, lightly-restrained female rats were evaluated. High levels of lordotic responsiveness were induced in ovariectomized animals treated with estradiol (E2) capsules or subcutaneous injections of estradiol benzoate (EB) followed by progesterone (P). The effect of each of the 3 infusates on lordosis was determined using manual stimulation and lordosis quotient determinations. In addition, the vocalization by an animal during lordosis measurements, paw withdrawal to pinch, righting reflex latency and recognition of a platform edge were also monitored. Within 2 minutes following procaine or tetrodotoxin (TTX) infusions in E2 implanted rats, lordotic responsiveness declined sharply. Whereas procaine-treated animals returned to control levels of responsiveness within 20 minutes, TTX infusions induced a more prolonged depression of lordosis lasting up to 8 hours. Infusions of PBS had no effect on any of the behaviors. In a separate group of animals treated with either E2 or EB + P and infused with 10 ng TTX the time course of the decline in lordotic responsiveness was identical for both steroid treatments. Paw withdrawal was unaffected by TTX while all other measured behaviors were disrupted along the same time course as lordosis. Collectively the above results implicate the requirement of sodium-dependent neuronal activity within dorsal midbrain for the maintenance of the lordosis reflex, along with other behavioral responses influenced by this brain region.

Animals↗

PubMed1986

Calcium influence on neuronal sensitivity to ethanol in selectively bred mouse lines.

Sensitivity to ethanol, as measured by blood ethanol concentration at loss of righting reflex, was increased significantly in SS but not LS mice following intracerebroventricular (ICV) administration of calcium chloride or A23187, a calcium ionophore. Magnesium chloride or lanthanum chloride, ICV, did not alter sensitivity to ethanol in either SS or LS mice, further indicating a specificity for calcium cation. Calcium was without effect on sensitivity to halothane narcosis in LS or SS mice. Endogenous brain calcium content was similar in these mouse lines, and ethanol administration either in vivo or in vitro did not alter brain calcium concentration. These results indicate that differences in brain sensitivity to ethanol are mediated, in part, by genetic differences in calcium-related processes and support the hypothesis that ethanol-induced narcosis may be due to alterations in calcium metabolism in the CNS.

Animals↗