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PubMed1991

Comparison of the anti-scorbutic activity of L-ascorbic acid and Ester C in the non-ascorbate synthesizing Osteogenic Disorder Shionogi (ODS) rat.

The Osteogenic Disorder Shionogi (ODS) rat, Clea Inc., Tokyo, Japan lacks the ability to synthesize L-ascorbic acid (AA). As with man, monkey and the guinea pig, this rat lacks L-gulonolactone oxidase necessary for the synthesis of AA from glucose. This study shows this animal to be an alternative to the guinea pig in AA studies. The anti-scorbutic potency of Ester C (EC), a calcium ascorbate and calcium threonate mixture, was compared with an AA dose of equal ascorbate activity equivalents (AAE) for anti-scorbutic activity in the ODS rat. The minimal anti-scorbutic dose of EC was determined to be 0.44 mg/kg/day (AAE), while an AA dose of 0.51 mg/kg/day (AAE) was not anti-scorbutic in a 24 day study. At 24 days EC rats gained 125% of initial body weight (BW) and the AA rats only 45% BW. Scorbutic signs at 24 days were scored on a 0 (min) to 3 (max) scale. The EC/AA ratio scores were: hemorrhage 0/1.4, behavior change 0/2.0, piloerection 0/2.2, mobility 0.4/2.2, dysbasia 0.6/2.8 and ataxia 0.4/1.0. Pearson's correlation coefficient for BW versus AAE was r = .34 for the AA group and r = .90 for the EC group. The morbidity index for EC was 0/5 and for the AA group 2/5. The AAE dose of AA which was 16% higher/day than the EC AAE dose was not anti-scorbutic, while the EC dose was anti-scorbutic. EC rats had 3.5X greater weight gain, a sensitive indicator of scurvy, than the AA rats. EC rats had 3-4 times less, if any, scorbutic signs than AA rats. The results clearly show that, based on ascorbate activity equivalents, EC has more available ascorbate activity/potency than AA. The mechanism of this increased potency is believed to be due to the facilitated transport of AAE into the cell by the threonate (a normal in vivo metabolite of AA) present in the EC product. In addition, previous studies have shown EC (AAE) to be higher in plasma and excreted less rapidly than the AAE derived from AA administered orally.

Animals↗
PubMed1984

Anticonvulsant actions of DS 103-282. Pharmacological studies in rodents and the baboon, Papio papio.

The anticonvulsant actions of DS 103-282 [5-chloro-4-(2-imidazolin-2-yl-amino)-2,1,3- benzothiadazole , tizanidine], have been evaluated after intraperitoneal administration in DBA/2 mice (seizures induced by sound), in Swiss S mice (seizures induced by N-methyl-D,L-aspartate; NMDLA ) and following intravenous or oral administration in Papio papio (seizure responses to intermittent photic stimulation). Protection against sound-induced seizures occurred after intraperitoneal administration of DS 103-282 (0.66-3.33 mg/kg). The ED50 doses for suppression of the tonic, clonic and wild-running phases of sound-induced seizures were 0.53, 0.79 and 1.3 mg/kg respectively. This protective effect of DS 103-282 (1.5 mg/kg, i.p.) was maximal after 30 min and was maintained for 60-120 min. Seizures induced by NMDLA were not suppressed by DS 103-282 (3.3-10 mg/kg, i.p.). In the baboons, a transient protection against photomyoclonic responses was observed 1 hr after intravenous administration of DS 103-282 (2-4 mg/kg). A similar profile of action was seen after oral administration of larger doses of DS 103-282 (16-32 mg/kg). Unwanted effects of DS 103-282 included transient piloerection, slight disturbance of gait and a fall in rectal temperature in mice, and muscular hypotonia and signs of sedation in baboons. These studies demonstrate an anticonvulsant action of DS 103-282, in both rodent and primate models of epilepsy, but do not support a postsynaptic blockade in excitatory neurotransmission as the mechanism of this action.

Acoustic Stimulation↗
PubMed1985

Effect of ambient temperature on thermoregulation in rats following preoptic/anterior hypothalamic injection of physostigmine.

This experiment was designed to study the effect of ambient temperature (Ta) on the thermoregulatory response after the injection of the acetylcholinesterase blocking agent, physostigmine, into the preoptic/anterior hypothalamic area (POAH) of the rat. Three doses of physostigmine (3.0, 30.0 and 60.0 micrograms) were injected in a volume of 1.0 microliter in the preoptic/anterior hypothalamic area of unrestrained rats at three different ambient temperatures (15, 25 and 35 degrees C). Brain temperature (Tbr) and gross changes in behavior were monitored continuously throughout the duration of each experiment. Physostigmine induced hypothermia at ambient temperatures of 15 and 25 degrees C but not at 35 degrees C. Immediately prior to and during the hypothermic response the animals displayed behavioral reflexes such as fur licking and a sprawled posture which presumably enhanced heat loss. Generally, soon after the peak of the hypothermic response (approximately 30 min), the rats displayed heat-conserving behavior (huddled position, piloerection of the fur). These data indicate that the activity of cholinergic synapses within the preoptic/anterior hypothalamic area increases with decreasing ambient temperature. The behavioral observations suggest some role for the cholinergic system in the activation of heat-dissipating responses in the rat.

Animals↗
PubMed1985

The cumulative effects of estrogen on precopulatory behavior in the female Mongolian gerbil.

Differences in responsiveness of precopulatory patterns to estradiol were investigated in the female Mongolian gerbil. Administration of five daily injections of 6 micrograms estradiol benzoate (EB) to ovariectomized females demonstrated that the precopulatory patterns differ in their responsiveness to EB. Estradiol benzoate shortened the latency to the first significant increase in frequency above post-ovariectomy levels for a group of precopulatory patterns (investigation of male's anogenital area, allogrooming and ventral gland marking) in comparison with a second group (approaching, leaving, investigation of the male's head, sand rolling, the present and piloerection postures). One component of precopulatory behavior (foot stomping) was not affected by EB. We suggest that the first group of more estrogen-sensitive patterns increases rapidly during early estrus as plasma estradiol-17 beta (E2) rises, whereas the second group shows peak levels later in estrus following the rise in plasma progesterone. We conclude that separable hormonal mechanisms may govern component precopulatory patterns.

Animals↗
PubMed1986

Intermale social aggression: suppression by medial preoptic area lesions.

The intermale social aggressive behavior of male rats cohabiting with a female rat was quantitatively scored weekly in response to the introduction of an unfamiliar intruding male. Resident male rats whose aggressiveness toward an intruder reached a criterion level were subjected to either sham lesions or bilateral lesions in the region of the medial preoptic area. The lesioned rats continued to exhibit levels of piloerection and lateral attack that were not significantly lower than those of sham-lesioned animals. However, the lesioned animals did emit significantly fewer bites and spent significantly less time in the "on-top" position than did sham-lesioned animals. The lesioned animals also displayed significantly less sexual behavior than the sham-lesioned animals but were not different in terms of defensiveness toward the experimenter. It is suggested that bilateral lesions in the region of the medial preoptic area cause a decrease in the intensity of intermale social aggression but do not prevent external stimuli from eliciting the aggression.

Aggression↗
PubMed1986

Testosterone removal in rats results in a decrease in social aggression and a loss of social dominance.

Alpha male rats from mixed sex colony groups were tested for aggressiveness toward nonaggressive male intruders. Afterward, they were castrated and implanted with testosterone filled Silastic tubes, castrated and implanted with empty tubes, or sham castrated and implanted with empty tubes. There were significant declines in the aggressiveness (lateral attacks, bites, and piloerection but not on-top) of castrated rats without testosterone replacement but not in castrated rats with testosterone replacement. At a second operation, castrated animals had their testosterone capsules removed or had their empty capsules replaced with testosterone filled capsules. When tested for aggression toward nonaggressive intruders, those alpha males which had testosterone removed declined in aggressiveness while those which had it implanted returned to a level of aggressiveness close to that emitted by sham castrated control animals. Subordinate males became dominant when alpha males were castrated and not given testosterone replacement. In a final series of observations, sham castrated males were found to be more aggressive than castrated males when pitted against one another. It is argued that testosterone plays a primary role in intermale social aggression and that the decline in aggressiveness following castration is typically accompanied by a loss of social dominance.

Aggression↗
PubMed1987

Intermale social aggression: reinstatement in castrated rats by implants of testosterone propionate in the medial hypothalamus.

Male hooded rats were castrated, subcutaneously implanted with testosterone-filled silastic tubes, and individually housed with an intact adult female rat. An unfamiliar male intruder was introduced into each colony on a weekly basis and the aggressive behavior of the resident male was recorded. When the intermale social aggressive behavior of the resident male toward the intruder reached a high level in terms of a composite aggression score, the subcutaneous testosterone tubes were removed. Weekly tests of aggression toward unfamiliar intruders continued until the aggression of the resident male dropped to a low level for two successive weeks in terms of our composite aggression score. Bilateral implants of pellets of testosterone propionate were then made into the medial hypothalamus or adjacent tissue. A control group was implanted with cholesterol pellets into the medial hypothalamus. During four weekly tests following the implant, rats with testosterone propionate implants in the medial hypothalamus showed increases in lateral attacks, lateral attack duration, bites, and piloerection. The increase in aggression was not consistently displayed by animals with testosterone propionate implants dorsal or anterior to the medial hypothalamus or by animals with cholesterol implants in the medial hypothalamus. These results suggest that the medial hypothalamus or closely adjacent tissue contains testosterone-sensitive neural circuitry modulating intermale social aggression.

Aggression↗
PubMed1987

Intermale social aggression in rats: suppression by medial hypothalamic lesions independently of enhanced defensiveness or decreased testicular testosterone.

Medial hypothalamic lesions or sham lesions were made in castrated adult male rats with subcutaneous implants of testosterone-filled silastic capsules. Seven days following surgery all animals were given a test of defensiveness (reactivity) toward an experimenter. The following day, groups composed of one lesioned male rat, one sham-lesioned male rat, and one intact female rat were placed in large cages. Beginning two weeks later, unfamiliar intruders were introduced into each colony on a weekly basis and the aggressive behavior of the residents recorded. All 12 of the sham-lesioned animals but only 2 of 12 lesioned animals displayed substantial intermale social aggression toward intruders. Analysis of individual elements of intermale social aggression indicated that the lesioned animals were deficient in attack, bite, and piloerection but not in on-top behavior. The deficit in intermale social aggression was not correlated with defensiveness toward the experimenter or body weight of the lesioned animals. It is argued that the medial hypothalamus plays a role in the modulation of intermale social aggression which is independent of its role in modulating defensiveness or testosterone production. These results also demonstrate that intermale social aggression develops even when testosterone levels are held relatively constant by replacing testicular testosterone with an artificial testosterone source.

Aggression↗
PubMed1988

Cohabitation with a female activates testosterone-dependent social aggression in male rats independently of changes in serum testosterone concentration.

Male hooded rats (350 to 450 g) were sham-castrated, castrated and implanted with testosterone-filled, or castrated and implanted with empty Silastic tubes. Twenty-four hours postoperatively the animals in each group were housed with a female or a male similar in size to the female. Beginning one week following surgery and continuing for three weeks thereafter, the female or male cagemate was removed once each week while a 15-min test of aggression toward an unfamiliar male intruder was conducted. During the aggression tests, lateral attacks, lunge attacks, bites, on-top, and piloerection were recorded. At the first aggression test, males housed with females were significantly more aggressive than their counterparts housed with males. In contrast, different testosterone regimes did not consistently influence the initial activation of intermale social aggression. At the second and third tests, males with testicular testosterone or a replacement were significantly more aggressive than their castrated controls on most measures but males housed with females continued to be more aggressive than the comparable group housed with males. These results suggest that normal fluctuations in serum testosterone concentration associated with sexual interaction are not necessary for the initial activation of intermale social aggression. Both repeated exposure to unfamiliar males as well as cohabitation with a female are effective stimuli for activation of testosterone-dependent social aggression.

Aggression↗
PubMed1988

Defensive aggression and testosterone-dependent intermale social aggression are each elicited by food competition.

Castrated rats with medial hypothalamic lesions or sham lesions and castrated rats with testosterone implants or sham implants were placed on a 23-hr food deprivation schedule, adapted to a highly palatable liquid food, and then housed in pairs. The pairs were observed in competition for the highly palatable food over a 4-min period on each of six days. On the first three days, the food was dispensed in a way that allowed only one animal at a time to drink while during the second three days both animals could drink simultaneously. The pairs of animals were then separated, individually adapted to a bland liquid food, and paired with a different animal for a second series of competition tests. With highly palatable food as the incentive, rats made hyperdefensive by medical hypothalamic lesions were more successful at maintaining access to the food and more aggressive than their sham-lesioned competitors on tests when food access was restricted to a single animal but not on tests when both animals could drink simultaneously. With bland food as the incentive, lesioned animals were not consistently more successful in maintaining access to the food but were significantly more aggressive than their cagemates. With the highly palatable food, castrated males with testosterone implants were neither more successful in maintaining access to the food nor more aggressive than their cagemates with sham implants. However, when paired with an unfamiliar cagemate in preparation for competition tests with the bland food, most rats with testosterone implants attacked the new cagemate using a lateral attack and displaying piloerection.(ABSTRACT TRUNCATED AT 250 WORDS)

Aggression↗
PubMed1988

No change in intermale aggression after amygdala lesions which reduce freezing.

Long-Evans rats with bilateral lesions in the area of the amygdala, or operated controls, were tested with strange male intruders into the subjects' home cages. Various measures of attack toward the intruder, including piloerection, lateral attack, on-top-of and biting showed no difference between the experimental and control animals. However, subjects with amygdaloid damage showed a substantial and significant reduction in freezing in the presence of a cat. This finding of reduced defensiveness to a predator is consistent with previous findings for amygdala lesions, while the failure to find decrements in conspecific offensive attack agrees with some, but not all, previous work in this area. The finding that a clear decrement in defense occurs in the same amygdala-lesioned subjects showing no suggestion of a reduction in offense adds to a body of data which indicates that offense and defense respond differentially to manipulation of a number of important neural and neurochemical systems.

Aggression↗
PubMed1988

Activation of aggression in female rats by normal males and by castrated males with testosterone implants.

Female hooded rats were continuously housed with an intact male, a castrated male with subcutaneous testosterone implants, or two other females. At weekly intervals over a 10-week period, the cagemate(s) and pups were removed and aggression by the female toward an unfamiliar female intruder was observed over a 15-min period. On the 11th week each female was subjected to this intruder test in an unfamiliar cage. On the 12th week, a final test was conducted in each female's living cage with a male rather than a female as the intruder. The aggressive behaviors recorded were attacks, bites, on-top, and piloerection. Females housed with normal males displayed a significant increase in aggression prior to parturition. Their aggressiveness persisted through the 10th test with peaks at parturition and the start of lactation. Females housed with castrated males also displayed significant increases in aggression but without the peaks associated with parturition and lactation. Their aggressiveness also persisted throughout the test period. Females housed with other females showed a small increase in aggression over weeks. All groups showed virtually no aggression in the unfamiliar cage. All females displayed some aggression toward a male intruder but the level of aggression was highest in maternal females. The results demonstrate that aggression qualitatively similar to that displayed following parturition and during lactation can be elicited in nulliparous females.

Aggression↗
PubMed1989

Ovariectomy attenuates aggression by female rats cohabiting with sexually active sterile males.

Female rats were individually housed with a single castrated male with a testosterone implant that maintained sexual and aggressive behavior. At weekly intervals, the resident male was removed and an unfamiliar female intruder was introduced into the colony. Attacks, bites, on-top, and piloerection of the resident female toward the intruder were scored. Females whose level of aggression toward the intruder was substantial and stable were either ovariectomized or sham-ovariectomized. Aggression tests resumed 1 week postoperatively and continued for an additional 3 weeks. The results confirm that female cohabiting with a sterile male become aggressive. They also demonstrate that ovariectomy greatly attenuates but does not entirely abolish aggression toward an unfamiliar female intruder. The results appear to contribute to a growing body of evidence suggesting that the biological substrate and behavioral form of aggression by females housed with males (including that following parturition) is a hormone-dependent aggression which parallels testosterone-dependent social aggression of males housed with females.

Aggression↗
PubMed1990

Behavioral study in rats of paired accumbens-lesioned residents and intact intruders.

Behavior in accumbens-lesioned male Wistar rats during paired encounters was assessed by several parameters, scores and cluster analysis based on similarity between patterns. Encounters were videotaped and analyzed by an ethogram and a software package previously elaborated. Residents were lesioned (n = 23) or sham operated (n = 10). A reactivity score was used to corroborate the effectiveness of the lesions. Although accumbens lesions produced the well-known increase in reactivity and enhancement of piloerection, only subtle changes were elucidated by the ethological analysis. Dendrograms revealed postoperative changes in the lesioned rats as well as in the intruders paired with them. Threat category in the lesion group dissociated in threat with arched-back attitude and threat with erect posture. In intruders paired with lesioned rats, compared with those paired with sham-operated animals, the patterns of freezing and on-back became mainly associated with immobile-crouch instead of upright defense posture, and the category of defense/submission was not observed in dendrograms.

Aggression↗
PubMed1992

Ovariectomy does not attenuate aggression by primiparous lactating female rats.

Nulliparous female hooded rats were allowed to cohabit with a sexually active male in a large living cage. Aggression toward an unfamiliar female was assessed during the second and third week of pregnancy. Within 12 to 24 h following parturition females were ovariectomized (n = 7) or sham-ovariectomized (n = 6) in a manner that balanced previous aggression scores. Aggression was assessed at 48 h following ovariectomy and at three weekly intervals thereafter. Ovariectomized and sham-ovariectomized females did not differ in the number of attacks, number of bites, duration of on-top, or frequency of piloerection on any test day following parturition. These results indicate that circulating levels of ovarian steroids do not influence the level of aggression by a primiparous lactating female toward an unfamiliar female conspecific.

Aggression↗
PubMed1984

Pharmacological activity of the basic fraction of marihuana whole smoke condensate alone and in combination with delta-9-tetrahydrocannabinol in mice.

This basic fraction (BF) of marihuana whole smoke condensate was subjected to pharmacological testing in males, Swiss-Webster mice. In a general pharmacological activity screen looking at behavioral, neurologic, and autonomic parameters, BF, at iv doses of 5, 10, and 20 mg/kg, caused impairment of visual placing, increase in tail pinch response, decrease in tail elevation, and induction of piloerection. These effects, although statistically significant, were slight and not consistently dose dependent. In a second study with doses ranging from 10 to 29 mg/kg, BF caused a decrease in spatial locomotion, rearing behavior, and urination incidence. In a third study, body temperatures of mice were measured periodically for 2 hr following administration of BF (1.2, 2.4, and 4.8 mg/kg) alone or in combination with 1.0 mg/kg delta-9-tetrahydrocannabinol (THC). BF did not alter body temperature, nor did it affect THC-induced hypothermia. These results, although suggesting that the basic fraction of marihuana whole smoke condensate has pharmacological activity in mice, offers little evidence for the presence of highly active compounds.

Animals↗
PubMed1989

Acute and subchronic effects of methylenedioxymethamphetamine [(+/-)MDMA] on locomotion and serotonin syndrome behavior in the rat.

Specific behaviors comprising the serotonin syndrome (low body posture, forepaw treading, headweaving) and the autonomic signs of piloerection and salivation were determined and analyzed with locomotor activity in response to MDMA at three doses (2.5, 5.0, and 7.5 mg/kg). All behaviors were dose-responsive. Serotonin syndrome behaviors increased in both intensity and duration of response with increasing doses. In contrast, locomotion varied only in intensity. Subchronic injections, in the same group of animals, permitted an analysis of acute vs. subchronic effects on these same behaviors. Both the serotonin syndrome and locomotor behaviors were augmented on subsequent testing, indicating that, (+/-)MDMA, like amphetamine, is capable of producing behavioral sensitization.

3,4-Methylenedioxyamphetamine↗
PubMed1989

Acute intracerebroventricular injections of the mast cell degranulator compound 48/80 and behavior in rats.

The intracerebroventricular (ICV) injection of the mast cell degranulator Compound 48/80 (2.5-2.0 micrograms/kg) produced a marked behavioral syndrome in normotensive rats. The behaviors included head and body shakes, paw tremor, excessive grooming, unusual posture and gait, mild diarrhoea, piloerection, extreme agitation and irritability to touch, and a later phase of sedation. The highest doses (15 and 20 micrograms/kg) also produced catalepsy and episodes of "barrel rolling" (continuous rolling of 1-8 turns around the longitudinal axis). These behaviors were observed for approximately 15-30 min although the sedation and catalepsy were maintained for 90-120 min. A second ICV injection of the 10 micrograms/kg dose of Compound 48/80 given 2 hr after an initial injection of this dose, produced a much reduced response and the numbers of head and body shakes, and episodes of paw tremor and grooming were between 20-30% of those produced by the first injection. The reduced effect of the second injection indicates that the behavioral effects of Compound 48/80 may arise from the acute degranulation of mast cells rather than direct effects on neuronal populations or the cerebral vasculature.

Animals↗