Angular distributions of molecular photofragments emitted following K-shell excitation of N2.
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Journal Article↗
Biomedical subjects
M Ukai
Publications and source records attributed to M Ukai.
Multi-dimensional analysis of behavior in mice treated with the delta opioid agonists DADL (D-Ala2-D-Leu5-enkephalin) and DPLPE (D-Pen2-L-Pen5-enkephalin).
The effects of intracerebroventricular injection of the delta-selective opioid peptides, DADL (D-Ala2-D-Leu5-enkephalin) and DPLPE (D-Pen2-L-Pen5-enkephalin), on spontaneous locomotor activity were investigated in mice using multi-dimensional behavioral analysis, based upon a capacitance system. The analysers classified the movements into 9 sizes (1/1, 1/2, 1/4, 1/8, 1/16, 1/32, 1/64, 1/128 and 1/256). Specific patterns of behavior were each registered on these sizes of movement. At 1.0 and 3.0 micrograms, DADL produced a significant increase in circling (1/4 size of movements) within 15 min after the start of measurements, while it produced a marked increase in linear locomotion (1/2 size), circling (1/4 size), rearing (1/16 size) and grooming (1/32, 1/64 and 1/128 sizes) within 15-30 min after the start. At 10.0 micrograms, DPLPE decreased linear locomotion (1/1 size) and conversely increased circling behavior (1/4 size) within 15 min after the start, whilst this peptide at 3.0 or 10.0 micrograms, produced a marked increase in linear locomotion (1/2 size), circling (1/4 size) and grooming (1/128 size) within 15-30 min after the start. The behavioral effects induced by DADL (3.0 micrograms) and DPLPE (10.0 micrograms) were completely reversed by naloxone (1.0 and 2.0 mg/kg). These results obtained with DPLPE, a delta-selective peptide and DADL, a less delta-selective peptide, indicate a common pattern of activity which was presumably delta receptor-mediated. However, one component (linear locomotion, at times immediately after administration of the peptide) did clearly differ between these two peptide analogues.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Inhibition of drinking by naltrexone in the rat: interaction with the dopamine D-1 antagonist SCH 23390 and the D-2 antagonist sulpiride.
The involvement of dopamine receptors in water intake was investigated in the rat deprived of water for 24 hr. A 0.03 mg/kg dose of SCH 23390 markedly enhanced naltrexone (0.1 and 10.0 mg/kg)-induced hypodipsia, whilst the drug alone significantly decreased water intake at doses of 0.01 to 3.0 mg/kg, accompanied by marked motor dysfunction. Sulpiride (20.0 and 40.0 mg/kg) did not markedly affect water intake and naltrexone-induced hypodipsia. Consistent with previous results, apomorphine (0.3 mg/kg) alone was without marked effects, while it produced a marked potentiation of naltrexone (1.0 and 10.0 mg/kg)-induced hypodipsia. SCH 23390 (0.003 mg/kg) and sulpiride (40.0 mg/kg) completely antagonized the enhancing effects of apomorphine on naltrexone-induced hypodipsia. Similar effects were also seen in the latency to begin drinking. In contrast to the effects on naltrexone-induced hypodipsia, it appears that both dopamine D-1 and D-2 receptors play a key role in the effects of apomorphine on naltrexone-induced hypodipsia in the rat.
Animals↗
Discriminative stimulus properties of the mixed agonist-antagonist pentazocine in the rat using two-choice discrete-trial avoidance paradigm.
The discriminative stimulus effects of pentazocine were evaluated in the rat trained to discriminate 3.0 mg/kg of pentazocine from vehicle in a two-choice discrete-trial avoidance paradigm. The rats used could discriminate 3.0 mg/kg of pentazocine from vehicle within 20 sessions after the start of discrimination training. The stimulus effects lasted 30 to 90 min and disappeared thereafter except for one rat in which the discriminative effects lasted 30 to 150 min. Pentazocine produced dose-dependent stimulus effects at 0.3 to 3.0 mg/kg doses. The stimulus effects of pentazocine were fully reversed by higher doses of naltrexone. Butorphanol, nalorphine, morphine, levorphanol, SKF 10,047, and methamphetamine generalized to pentazocine cue. However, ethylketocyclazocine, dextrorphan or pentobarbital did not produce stimulus effects in common with pentazocine. These results suggest that the discriminative stimulus effects of pentazocine (3.0 mg/kg) are mediated through an opioid but non-mu and nonspecific mechanism.
Animals↗
Effects of intrahypothalamic administration of opioid peptides selective for mu-, kappa, and delta-receptors on different schedules of water intake in the rat.
The effects of opioid peptides selective for mu, kappa, and delta-opioid receptors were investigated on 3 different schedules of water intake in the rat: spontaneous, deprivational (12 h), and hypertonic saline-induced drinking. Peptides were injected into the paraventricular and supraoptic hypothalamic nuclei, D-Ala2-NMePhe4-Gly(ol)-enkephalin, a mu-selective opioid agonist, tended to increase water intake in non-deprived rats, but 0.01 and 0.1 microgram significantly decreased water intake for 45 min in deprived rats, and for up to 60 min in hypertonic saline-injected rats when injected into the paraventricular hypothalamic nucleus. The kappa-selective agonist, dynorphin A1-13 (0.1, 0.3, 1.0 and 3.0 micrograms)and the delta-selective agonist, [D-Pen2,L-Pen5]enkephalin (0.3 and 3.0 micrograms) did not affect spontaneous, deprivational or hypertonic saline-induced water intakes when injected into either the paraventricular or supraoptic hypothalamic nuclei. Thus, a mu-selective opioid peptide produced dose- and time-dependent effects on drinking that were pharmacologically and anatomically specific, and dependent upon the schedule of water intake.
Animals↗
Effects of beta-funaltrexamine on ingestive behaviors in the rat.
The effects of beta-funaltrexamine (beta-FNA), an irreversible mu-opioid receptor antagonist, were determined on water and food intake of non-deprived rats. Intracerebroventricular administration of 1.25 or 2.5 micrograms of beta-FNA did not affect drinking or eating. However, 5.0 micrograms first transiently increased food intake and then reduced both water and food intake for at least 72 h. Locomotor activity was unaffected by 5.0 micrograms of beta-FNA; thus, changes in ingestive behavior were not a secondary consequence of drug-induced behavioral stimulation or depression. The early increase in food intake may be due to the short lived and reversible kappa-agonist activity of beta-FNA. On the other hand, selective blockade of mu-opioid receptors appears sufficient to reduce the intake of water and food.
Animals↗
Apomorphine markedly potentiates naltrexone-induced hypodipsia in the rat.
This article describes the effects of apomorphine on naltrexone-induced decreases in water intake of the rat deprived of water for 24 h. Apomorphine alone at reasonable doses (0.03, 0.1, 0.3 and 1.0 mg/kg) failed to affect water intake of the rat, but a higher dose (3.0 mg/kg) abolished water intake completely, accompanied by marked stereotypy. Naltrexone (0.1, 1.0 and 10.0 mg/kg) produced a dose-dependent reduction in water intake. A 0.3-mg/kg dose of apomorphine which is considered to activate preferentially presynaptic dopamine autoreceptors enhanced markedly naltrexone (1.0 and 10.0 mg/kg)-induced decreases in water intake. Only apomorphine at 1.0 mg/kg caused a significant prolongation of the latency to start drinking. Apomorphine (0.3 mg/kg), naltrexone (0.1, 1.0 and 10.0 mg/kg) or their combinations did not produce a marked effect on locomotor activity in the rat. These results suggest that apomorphine is capable of potentiating naltrexone-induced decreases in water intake through the mediation of presynaptic dopamine autoreceptors without causing motor dysfunction.
Animals↗
Morphine-like discriminative stimulus effects of opioid peptides: possible modulatory role of D-Ala2-D-Leu5-enkephalin (DADL) and dynorphin A (1-13).
The role of the different opioid receptors was studied in rats trained to discriminate SC injections of 3.0 mg/kg morphine from saline by tests for generalization to graded doses of morphine and receptor-selective peptides administered into the lateral cerebral ventricle. Dose-dependent morphine-like stimulus effects were produced over a wide range of doses (0.001-30 micrograms), depending upon ligand and animal, by morphine, by the mu-selective peptides DAGO[D-Ala2-NMePhe4-Gly(ol)-enkephalin] and FK33824[D-Ala2,NMePhe4-Met(O)5-(ol)-enkephalin], and by the delta-selective peptide, DADL[D-Ala2,D-Leu5)enkephalin]. The order of relative potency of these substances was: FK33824 greater than DAGO greater than morphine greater than DADL. In contrast, DPLPE[D-Pen2,L-Pen5)enkephalin], which has much greater delta receptor selectivity than does DADL, and dynorphin A(1-13) (0.1-10 micrograms), a kappa-receptor agonist, engendered choice responding appropriate for saline. When 1.0 micrograms DADL, a dose lacking morphine-like discriminative effects, was administered concurrently with SC morphine, the stimulus effects of morphine were potentiated. Concurrent administration of 10 micrograms dynorphin A(1-13) and morphine attenuated the stimulus effects of morphine inconsistently. These results support previous findings that mu-opioid receptors are of primary importance in mediating the morphine-like discriminative effects of opioid peptides. They also suggest that morphine-like discriminative effects can be modulated by other types of opioid receptors.
Animals↗
The opioid antagonist, MR2266, specifically decreases saline intake in the mouse.
The effects of the opioid antagonist, Mr2266 [(-)-(1R,5R,9R)-5,9-diethyl-2-(3-furyl-methyl)-2'-hydroxy-6,7-benzomo rph an] on the intake of water and saline (0.9%) were investigated in the mouse, deprived of water for 24 hr. In an attempt to evaluate motor functions, the behavior after treatment with Mr2266 was also examined by using multi-dimensional behavioral analyses. Although smaller doses (1.0, 3.0 and 10.0 mg/kg) of Mr2266 failed to affect significantly the intake of water, a larger dose (30.0 mg/kg) elicited a significant attenuation in the intake of water. During a 30 min observation, Mr2266 (30.0 mg/kg) depressed markedly linear locomotion, while other behavioral responses, such as rearing and grooming, remained unchanged. In contrast, 1.0-30.0 mg/kg doses of the drug produced a significant reduction in the intake of saline. The drug Mr2266 had no significant effects on the latency to start drinking at any doses tested. These results suggest that Mr2266 specifically blocks the intake of saline of the mouse through the mediation of opioid systems.
Animals↗
Restricted feeding does not modify discriminative stimulus effects of morphine in the rat.
An experiment was performed to determine if the discriminative stimulus effects of morphine are modified by mild food deprivation, a condition that increases drug-reinforced behavior. Rats were trained to discriminate between SC injections of saline and morphine (3.0 mg/kg) in a discrete-trial shock-avoidance procedure. Stimulus generalization curves for morphine were then determined on three occasions by a cumulative-dosing procedure: before, during and after the body weight of the rats had been reduced to 86-87% of normal by restricted feeding. Food deprivation had little or no effect on the morphine generalization curve. Despite a close relationship between the reinforcing and discriminative stimulus properties of opioid drugs, stimulus control of behavior by morphine was not modified by a condition that enhances opioid-reinforced behavior.
Animals↗
Effects of the infraorbital nerve-transection on the formation of Ia fibers in muscle spindles of the masseter muscle in developing mice.
The effect of the transection of the infraorbital nerve on d 20 after birth on the formation of the annulospiral ending of Ia fibers of muscle spindles in the masseter muscle was investigated in developing mice. On the 20th d after the operation, there were significant differences between control and treated animals in the ratio of muscle spindles with non-coiled endings to all muscle spindles, and the ratios of muscle spindles with non-coiled endings in the masseter muscle on the operated and sham-operated sides were about equal to each other. On the 30th d after the operation, the ratio for the masseter muscle on the operated side was approximately twice that for the one on the sham-operated side. The ratio for the operated side was about equal to that for 15-d-old control mice, and about twice that for 20-d-old control animals. Thus, the present results indicate that disorder of sensory inputs following the transection of the infraorbital nerve leads to degeneration and/or inhibition of the formation of annulospiral endings in muscle spindles of the masseter muscle, and suggest that disorder of the masticatory mechanism may be caused by the degeneration and/or inhibition of the formation of the endings in many muscle spindles of the masseter muscle.
Animals↗
Postnatal development of the annulospiral endings of Ia fibers in muscle spindles of the mouse temporal muscle.
The formation of the annulospiral endings of Ia fibers in muscle spindles was investigated in the temporal muscle of developing mice. From 15 to 20 d after birth, there were only a few spindles with "++" sensory endings. With growth of mice, the primary endings of the Ia fiber began to develop its spiral endings. And by the 30th postnatal day (that is, after weaning), almost all of the Ia fibers had completely coiled endings though the formation was still continuing in some spindles at this time. Formation of the annulospiral endings of the Ia fibers of muscle spindles in the temporal muscle was completed earlier than that of fibers in the spindles in the masseter muscle.
Animals↗
Ex vivo repair and renal autotransplantations for renovascular disease.
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Adult↗
Suppression of deprivation-induced water intake in the rat by opioid antagonists: central sites of action.
The effects of naltrexone methobromide, a quaternary derivative of the opioid antagonist naltrexone, were investigated on deprivation (24 h)-induced water intake in the unilaterally cannulated rats. Naltrexone methobromide reduced post-deprivational water intake with an ED50 of 7.3 micrograms when tested at 30 min (peak effect) after intracerebroventricular administration. It also dose-dependently (0.3-10 micrograms) depressed water intake, with peak effects at 15 min, after microinjection into the paraventricular hypothalamic nucleus and into the supraoptic hypothalamic nucleus. The drug did not produce any other effects on behaviors. The ED50S were 1.4 micrograms when given into the paraventricular nucleus, and 3.3 micrograms when given into the supraoptic nucleus, respectively. Although injections of higher doses (1.0, 3.0 and/or 10 micrograms) of the drug into the preoptic area, zona incerta, and corpus callosum significantly suppressed water intake, other behavioral manifestations, such as rotational behaviors, convulsions, body shakes, head swaying, and/or backward locomotion were manifested simultaneously with the reduction in drinking. When injected into the lateral hypothalamic area, water intake was not significantly affected by the drug. These findings suggest that the paraventricular and supraoptic hypothalamic nuclei are important sites of action in the naltrexone-induced suppression of water intake.
Animals↗
Effects of ethylketocyclazocine on behaviors in mice using multi-dimensional behavioral analyses.
The effects of ethylketocyclazocine, a relatively selective kappa opioid agonist on the behaviors in mice were examined by using multi-dimensional behavioral analyses. Within 15 min after the measurements, ethylketocyclazocine (0.03, 0.1 and 0.3 mg/kg) dose-dependently decreased the linear locomotion, rearing, and grooming behaviors in mice. Fifteen to 30 min ethylketocyclazocine (0.3 mg/kg) decreased most of the behaviors in mice. The ethylketocyclazocine (0.3 mg/kg)-induced behavioral effects were antagonized by naloxone (1 and 2 mg/kg). These data suggest that the decreases in the linear locomotion, rearing and grooming behaviors are mediated via kappa opioid system.
Analysis of Variance↗
Anatomical and functional differences in the Adductor mandibulae muscle between Zaco platypus and Carassius gibelio langsdorfi of the Cyprinidae family.
A histological study has been made on the jaw-closing muscle, Adductor mandibulae, of 2 species of Cyprinidae, Zaco platypus and Carassius gibelio langsdorfi, which show completely different feeding behaviour. The former swims up to the food with its mouth open in rapid current, and the latter sucks food from the bottom into its mouth by enlargement of the buccal and opercular cavities in quite mild current. The latter's feeding behaviour was made repeatedly. The A. mandibulae was divided into its anterior and posterior parts in both fish. The anterior part in Z. platypus was divided into 2 portions, and that of C. gibelio langsdorfi into 3 portions. In each portion of the muscle of both fish, SDH activity in the muscle fibers decreased from the medial to the lateral side. Both fish had 3 types of the fibers on the basis of SDH activity, whereas the combinations of each fiber type were more complex in C. gibelio langsdorfi than in Z. platypus. Moreover, the ratio of fibers with higher SDH activities was larger in C. gibelio langsdorfi than in Z. platypus. And, differences in the number of capillaries per fiber in the same fiber type between the 2 fish suggest a complex adaptation of the jaw-closing muscle to the environmental circumstances of the fish.
Animals↗
Multi-dimensional analyses of behavior in mice treated with U-50,488H, a purported kappa (non-mu) opioid agonist.
The effects of U-50, 488H (trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl ]-benzeneacetamide, methane sulfonate, hydrate), a purported selective kappa (non-mu) opioid agonist on spontaneous locomotor activity were investigated using a multi-dimensional behavioral analyzer (Animex II). U-50,488H (1 mg/kg) failed to affect behavior in mice, however, 3 mg/kg significantly reduced rearing and grooming. In addition, 10 mg/kg markedly reduced linear locomotion, rearing and grooming. The behavioral depression induced by U-50,488H (10 mg/kg) was reversible by the opioid antagonist Mr2266 (10 mg/kg). These results suggest that the selective activation of the kappa (non-mu) opioid receptor by U-50,488H decreases linear locomotion, rearing and grooming in mice.
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
Naloxone specifically blocks the linear locomotion in mice.
The effects of naloxone on mouse behavior were investigated by using a multi-dimensional behavioral analyzer. No significant changes in behavior were seen after 1, 3 and 10 mg/kg doses of naloxone. Within 15 min following the start of observation, however, naloxone significantly suppressed linear locomotion at the 30 mg/kg dose, while the same dose of naloxone did not markedly affect other behaviors such as rearing and grooming. These results suggest that naloxone specifically disrupts linear locomotion in the mouse.
Animals↗