[Spontaneous movement and brain catecholamines in mice].
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Animals↗
Biomedical subjects
K Kisara
Publications and source records attributed to K Kisara.
A new class opioid peptide, [D-Arg2, beta-Ala4]-dermorphin tetrapeptide; physical dependence liability in mice.
Development of morphine-like physical dependence of the [D-Arg2, beta-Ala4]-dermorphin tetrapeptide (H-Tyr-D-Arg-Phe-beta-Ala-OH) has been evaluated and compared with the physical dependence liability of morphine or pentazocine. Degree of the physical dependence was assessed by the naloxone-precipitated jumping behaviour in mice after treatment of a single dose of each compound. The number of jumps and the time of latency to first jump were recorded in this experiment. Number of jumps in a group pretreated with the peptide showed less than that in morphine-treated group. In addition, latency to the appearance of the first jump in the peptide-treated mice was later than that in the morphine-treated group. The present results indicate that the physical dependence induced by [D-Arg2, beta-Ala4]-dermorphin tetrapeptide may be less marked than that produced by morphine. It is also interesting to note that the antinociceptive effect of this opioid peptide is more powerful and of longer duration than that induced by morphine or pentazocine.
Analgesics, Opioid↗
Actions of intracerebroventricular administration of kyotorphin and an analog on thermoregulation in the mouse.
Intracerebroventricular (ICV) administration of kyotorphin (L-Tyr-L-Arg) and cyclo (N-methyl-L-Tyr-L-Arg), its analog, produced significant dose-dependent hypothermic responses in mice at an ambient temperature of 24 degrees C. The hypothermic action of kyotorphin was much greater than that of Met-enkephalin (Met-ENK) but less than that of cyclo NMTA. This action was slightly but not significantly reversed by intraperitoneally administered naloxone (8 mg/kg), an opioid receptor antagonist. Met-ENK utilized as a control peptide in this study also produced a dose-dependent hypothermia which was slightly antagonized by naloxone (8 mg/kg, IP). Thyrotropin releasing hormone (TRH) injected ICV produced hyperthermia dose-dependently. The hypothermia induced by kyotorphin, its cyclic analog and Met-ENK was prevented by a small dose of TRH (0.18 microgram = 0.5 nmol/animal) which by itself had little effect on body temperature. A TRH neuronal system in the brain may explain the mechanism of kyotorphin-induced hypothermia. However, there was little evidence of involvement of opioid receptors. The present study demonstrates a potent action of kyotorphin and its analog on thermoregulation.
Analgesics↗
A comparison of the antinociceptive and behavioral effects of D-Arg substituted dipeptides and tetrapeptides in mice.
Intracerebroventricular administration of D-Arg substituted dipeptides, H-Tyr-D-Arg-OMe and H-Tyr(Et)-D-Arg-OMe, and D-Arg2 substituted N-terminal tetrapeptides of dermorphin, H-Tyr-D-Arg-Phe-Gly-OEt and H-Tyr(Et)-D-Arg-Phe-Gly-OEt resulted in dose-related and naloxone-reversible antinociceptive effects. Among them, tetrapeptides not only exhibited much more potent and prolonged activities than dipeptides but also were significantly antagonized even by a low dose of naloxone. Spontaneous motor activity was lowered by dipeptides throughout the observation period, which was scarcely antagonized by naloxone. Tetrapeptides elicited locomotor hyperactivity following an initial locomotor suppression. Only the locomotor hyperactivity was significantly antagonized by naloxone. These results suggest that tetrapeptides induce the effects via opioid receptors, whereas the effects of dipeptides are involved in various systems non-specifically.
Animals↗
Antinociceptive cross-tolerance between [D-Arg2]-dermorphin tetrapeptide analogs and morphine.
Cross-tolerance between [D-Arg2]-dermorphin tetrapeptide analogs and morphine with respect to antinociception was examined in the present set of experiments. Systemic administration of H-Tyr-D-Arg-Phe-Gly-NH2 (TDAPG-NH2), H-Tyr-D-Arg-Phe-beta-Ala-OH (TDAPA) or morphine over a period of 5 days produced the development of tolerance. In the cross-tolerance study, antinociception after subcutaneous (SC), intracerebroventricular (ICV) and intrathecal (IT) administrations of TDAPG-NH2 and TDAPA in morphine-tolerant mice was not significantly different from their respective effects in saline-pretreated control mice. A marked tolerance to SC- and ICV-administered morphine was seen in mice made tolerant to TDAPG-NH2 and TDAPA. However, IT administration of morphine produced no significant decrement in the antinociceptive activity in mice made tolerant to TDAPG-NH2 and TDAPA. These data indicate that [D-Arg2]-dermorphin tetrapeptide analogs can produce significant antinociception in morphine-tolerant mice.
Amino Acid Sequence↗
Persistent erection in thiamine-deficient rats.
Male Wistar rats, maintained on a thiamine-deficient diet, showed a significant weight loss, decrease in heart frequency, disturbance of urinary excretion, and symptoms of polyneuritis. Once persistent erection ocurred in these rats, it continued throughout the study and subsided in most cases after the administration of thiamine HCl.
Animals↗
Changes of ejaculation due to suppression of noradrenaline biosynthesis by diethyldithiocarbamate.
The effects of diethyldithiocarbamate on manually induced erection and ejaculation and on monoamines in the brain and male reproductive organs were investigated in male mongrel dogs. From the results obtained in this study it was concluded that diethyldithiocarbamate suppresses ejaculation, although penile erection is maintained, and that the suppression is not mediated by the central nervous system but by the changes of the monoamine levels in the organs relating to sperm transport.
Animals↗
Changes of ejaculation due to suppression of noradrenaline biosynthesis by diethyldithiocarbamate in dogs: a supplemental report with reference to changes of posterior urethral pressure.
In the preceding paper (Kimura et al.-1979) it was reported that diethyldithiocarbamate suppresses ejaculation, although penile erection is maintained, and that the suppression is not mediated by the central nervous system but by the decrease of catecholamine contents in the organs relating to sperm transport. In this paper, changes of ejaculation following administration of diethyldithiocarbamate was studied with the posterior urethrogram; measurement of the posterior urethral pressure during hypogastric nerve stimulation. From the results obtained in this study the above results were confirmed. It was also confirmed that both seminal emission and ejaculation are under the influence of an alpha-adrenergic receptor mechanism. Also, a dopamine receptor mechanism was suspected to be present in the male accessory sexual glands.
Animals↗
On the brain monoaminergic systems relating to ejaculation. III) Further study by using a peripheral decarboxylase inhibitor.
In the previous papers it was reported that ejaculation is facilitated by the brain dopaminergic system, particularly by that in the anterior hypothalamus, and inhibited by the serotonergic system. In an attempt to clarify more precisely the results, a further study was done in dogs by using a peripheral cecarboxylase inhibitor, Ro 4-4602, in combination with tetrabenazine and L-dopa. As a result it was found that in addition to the brain dopaminergic system, the increase in 5-HT level in the limbic system and the decrease in 5-HT level in the brain stem facilitate ejaculation.
Animals↗
The spinal monoaminergic systems relating to ejaculation. I. Ejaculation and dopamine.
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Animals↗
The spinal monoaminergic systems relating to ejaculation. II. Ejaculation and serotonin.
The effects of Ro 4-4602 and L-5-hydroxytryptophan on manually induced ejaculation in dogs and on spinal monoamines in dogs were investigated. From the results obtained in the study it was concluded that the serotonergic system in the spinal cord is an intermediate mechanism which inhibits the occurrence of ejaculation. Both the results in this study and the results in our previous paper seem to indicate that ejaculation occurs with the reconciliation of the spinal dopaminergic and serotonergic system.
Animals↗
On suppression of ejaculation by Alpha-methyldopa.
Alpha-methyldopa caused inhibition of ejaculation. The cerebral mechanism which induced the inhibition was pursued by determining changes of brain monoamines in dogs. As a result, suppression of the dopaminergic system in the brain by alpha-methyldopa is found to be the origin of the inhibition of ejaculation. This inhibition was recovered by L-dopa with pretreatment with a peripheral decarboxylase inhibitor.
Animals↗
Role of the spinal monoaminergic systems in suppression of ejaculation by alpha-methyldopa.
Alpha-methyldopa causes inhibition of ejaculation by suppressing the dopaminergic system in the brain. The spinal mechanism which works together with this brain inhibitory mechanism was persued by determining the changes of spinal monoamines in dogs. As a result, it was found that suppression of the dopaminergic system by alpha-methyldopa is caused also in the spinal cord just as in the brain and that this suppression can be a direct origin of the inhibition of ejaculation.
Animals↗
The spinal monoaminergic systems relating to ejaculation ejaculation and monoamines after spinal cord transection.
The authors investigated the relationship between ejaculation and spinal monoamine levels by transecting the dog spinal cord at the various levels. From the results obtained in this study it was concluded that the lumbar and upper sacral segments of the spinal cord are important for ejaculation, and that the suppression of ejaculation by lower lumbar to upper sacral transection may be induced by increase in serotonin in the 5th lumbar-1st sacral segments.
Animals↗
Central action of 9-methyl-7-bromoeudistomin D (MBED), a derivative of eudistomin D isolated from Eudistoma olivaceum.
The behavioral responses of mice following intracerebroventricular (i.c.v.) injection of 9-methyl-7-bromoeudistomin D (MBED) were studied. Head-twitches were produced 20-90 min after the injection of 2, 20 and 200 nmol/mouse but such twitches were not significantly induced by caffeine (1000 nmol/mouse). The locomotor activity, as assessed by the Animex autometer, increased 0-120 min after the injection with doses of 2, 20 and 200 nmol/mouse, whereas a large dose of caffeine (500 nmol/mouse also increased the activity counts. Simultaneous injection of picrotoxin (3 mg/kg, s.c.) and MBED (50, 100 and 200 nmol/mouse) produced clonic and tonic extensive convulsions, but caffeine (1000 nmol/mouse) in combination with picrotoxin did not cause any type of convulsion.
Animals↗