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Biomedical subjects

K Kisara

Publications and source records attributed to K Kisara.

At least 181 records · Page 10Linked to original sources
PubMed1979

Effect of 5-hydroxytryptophan on muricide response induced by thiamine deficiency.

Male Wistar rats maintained on a thiamine deficient diet showed the mouse-killing response (muricide). On the 30th day of experimental feeding, the incidence of the muricide response was 78% in the thiamine deficient group. Intraperitoneal (i.p.) injection of 5-hydroxytryptophan (5-HTP) suppressed the muricide response in a dose-dependent manner. The suppressive effect of 5-HTP on the muricide response was potentiated by pretreatment with Ro4-4602. On the 20th day of experimental feeding, the incidence of the muricide response was 42.9% in the thiamine deficient group, 14.3% in the pair-fed group and 0% in the control group, respectively. The incidence increased to 92.5% in the thiamine deficient rats 24 hr after the i.p. injection of 100 mg/kg parachlorophenylalanine. The results of the present sutdy indicate that the injection of 5-HTP was effective in suppressing the muricide response induced by thiamine deficiency.

5-Hydroxytryptophan↗
PubMed1978

[Muricide induced by thiamine deficiency in the rats (author's transl)].

The emotional behavioral aspects and the interaction between the changes of the polyamine contents and muricide response in thiamine deficient rats were investigated. In the thiamine deficient group, there was evidence of muricide and such increased progressively with advanced thiamine deficient feeding. This muricide was characteristic in the following respects; 1) the killer-rats did not eat but only kill a mouse and it was quite difficult to remove a sacrificed animal from the cage. 2) they bit at random into any body region of the mouse. 3) the killer-rats did not bite inanimate objects such as nails nor chalk. 4) the muricide induced by thiamine deficiency could not be suppressed by a single injection of thiamine HCl. On the 30th day of the experimental feeding, both spermidine and spermine levels in the brain of the thiamine deficient group decreased significantly as compared to the control and the pair-fed groups. Both spermidine and spermine levels were reversed to the control levels with a intraperitoneal administration of thiamine. There were no significant differences in spermine and spermidine levels between the killer-rats and non-killer-rats in the thiamine deficient group.

Aggression↗
PubMed1978

[Persistent erection in thiamine deficient rats (author's transl)].

Male Wistar rats weighing 75 to 85 g and maintained on a thiamine deficient diet for 33 days showed growth inhibition with the principal manifestation of significant weight loss from about the 28 day of experimental feeding. Symptoms of polyneuritis were also evident. On the 20th day of feeding and thereafter, rats on the thiamine deficient diet had a persistent erection. This was observed in 7% of the rats on a thiamine deficient group on day 20, 30.7% on day 25, 63.6% on day 30, and 100% on day 33. Effects of thiamine hydrochloride, in a single dose of 1 mg/kg given subcutaneously on the symptoms of thiamine deficiency were investigated. The treated rats recovered from the polyneuritic symptoms, and persistent erection disappeared in one out of 5 rats on the 3rd day and in 2 more rats on the 7th day. Persistent erection disappeared completely in rats maintained on a thiamine sufficient diet 3 days after single subcutaneous administration of thiamine HCl. These observations suggest that persistent erection was brought on as a consequence of thiamine deficiency.

Animals↗
PubMed1978

Effects of intraventricularly administered polyamines spermidine and spermine on sleep-wakefulness cycles in rats.

Freely moving rats with chronically implanted electrodes were used and the electroencephalogram (EEG) from the occipital cortex and the dorsal hippocampus, the electromyogram (EMG) and the electrooculogram (EOG) were simultaneously recorded. The REM (rapid eye movement) sleep stage was significantly shortened without a marked change of the Non-REM sleep from the 24th to the 32nd hr following injection of 40 microgram of SPD. The waking stage significantly increased, and the Non-REM sleep and REM sleep markedly decreased immediately after the injection of 40 microgram of SPM to the 8th, and from the 24th to the 32nd hr. The amount of total sleep significantly shortened from the 72nd to the 80th hr following injection of 40 microgram of SPD. The administration of 40 microgram of SPM significantly reduced the amount of total sleep in every period measured for 8 hr. Marked change was observed from the 24th to the 32nd hr following injection of 100 microgram of PUT, and Non-REM sleep and total sleep produced a significant decrease. These results show that the intraventricular administration of polyamines including PUT inhibits the amount of normal sleep.

Animals↗
PubMed1978

[Effects of diazepam on evoked potential recorded from basal medial amygdaloid nucleus, lateral hypothalamus and midbrain reticular formation (author's transl)].

The evoked potential in the lateral hypothalamus (LH) recorded by stimulation of basal medial amygdaloid nucleus (Abm) showed a triphasic pattern and diazepam (2 mg/kg, i. p.) decreased the late component. The evoked potential in the midbrain reticular formation (MRF) recorded by stimulation of Abm showed a fast component with a relatively short latency followed by a biphasic late component and diazepam decreased the late component. Though the evoked potential in the Abm recorded by stimulation of LH showed a triphasic pattern, diazepam had no influence on the amplitude. Diazepam increased markedly the amplitude of evoked potential in the MRF recorded by stimulation of LH. Diazepam was ineffective on the evoked potential in the Abm recorded by stimulation of MRF. Diazepam decreased markedly the late component of evoked potential in the LH recorded by stimulation of MRF. These results suggest that the depression of emotional behavior by diazepam may be particularly related to the fact that the evoked potential in the LH recorded by stimulation of Abm was decreased by diazepam.

Amygdala↗
PubMed1977

[Effects of morphine on the single unit activity of nucleus dorsal raphe].

Effects of morphine were studied in 36 gallamine triethiodide immobilized adult cats under light N2O anesthesia. Single units were recorded from the nucleus dorsal raphe using a stainless steel microelectrode. Dorsal raphe neurons were divided into two types; one was a clock-like (CL) neuron which was typically slow in rate, rhythmic and stable throughout recording time, and the other was a non-clock like (NCL) neuron which was relatively irregular in pattern as compared with CL neuron. Out of 36 neurons recorded in this experiment, 13 were CL neurons and 23 were NCL neurons. Mean discharge rates (spikes per sec) of CL neuron and NCL neuron were 2.84 (range of 2.01 approximately 3.68) and 4.11 (range of 0.10 approximately 35.09), respectively. None of the 13 CL neurons responded to the nociceptive (pinch and/or brdaykinin) and non-nociceptive (hair bending and/or tapping) stimuli. On the contrary, out of 23 NCL neurons, 13 responded to both nociceptive and non-nociceptive stimuli, 4 were responsive to only non-nociceptive stimuli and 6 were not responsive to these stimuli. Receptive fields of NCL neurons were wide with various somatic modalities. The latency for bradykinin (3 microgram) was 6.46 +/- 0.77 sec. Effects of morphine were examined in 6 CL neurons and 12 NCL neurons. After morphine, no nociceptive neuron responded to nociceptive stimuli, although there was no appreciable change in the responsiveness to non-nociceptive stimuli. Firing frequency and pattern of all CL neurons were unaffected by morphine. Out of 12 NCL neurons, 7 were unaffected in firing frequency and 5 were decreased after morphine.

Action Potentials↗
PubMed1977

[Effects of morphine on evoked potential recorded from pain-afferent pathways (author's transl)].

Effects of morphine (1 mg/kg i.v.) were examined on evoked potential of somatosensory afferent pathways elicited by tooth pulp stimulation in cats. Results were as follows: In central gray (CG) of the midbrain which has a triphasic evoked potential with a short latency, morphine decreased the amplitude. In nucl. lateralis posterior(LP) and nucl. medialis dorsalis(MD) of the thalamus, association relay nuclei, which have a late component followed by a fast component with a relatively short latency, morphine decreased the amplitude of the late component but not that of fast component of the evoked potential. In nucl. centralis lateralis(CL) of the thalamus, intralaminar nuclei, and pre-central association area(PCA) of the cortex, which have monophasic and triphasic evoked potentials with a long latency, respectively, morphine markedly decreased the amplitude of both evoked potentials. In nucl. ventralis posteromedialis(VPM) and somatic sensory area I (SI), lemniscal system, which has biphasic and mutiphasic evoked potentials with a short latency, respectively, morphine had no effect on these evoked potentials. As these depressant effects of morphine on evoked potentials were antagonized by naloxone (0.2mg/kg i.v.), a specific morphine action is suggested.

Afferent Pathways↗
PubMed1977

[Effects of capsaicin on spontaneous unit discharges in medial thalamic single neurons of cats (author's transl)].

The effect of capsaicin was studied in gallamine triethiodide immobilized adult cats. Single neurons were recorded from the medial thalamus with a stainless steel microelectrode. Out of 21 neurons recorded in this experiment, 10 were responsive to both nociceptive (pinch) and non-nociceptive (hair bending and/or tapping) stimuli. Six neurons were responsive to only non-nociceptive stimuli and 5 were not responsive to these stimuli. Out of 10 neurons responding to both nociceptive and non-nociceptive stimuli, 9 were responsive to both bradykinin (3 microgram) and capsaicin (3 microgram). Out of 6 neurons responding to only non-nociceptive stimuli, 5 were not responsive to either bradykinin and capsaicin. All neurons responding to bradykinin were also responsive to capsaicin. The latency for bradykinin and capsaicin was 7.64 +/- 1.12 sec and 0.97 +/- 0.07 sec, respectively. The increased in firing frequency produced by capsaicin was depressed by morphine. However, these depressant effects of morphine on single unit activity were antagonized by naloxone.

Action Potentials↗
PubMed1977

Effects of p-chlorophenylalanine (p-CPA) on sleep in olfactory bulb lesioned rats.

The effect of p-CPA and 5-HTP followed by p-CPA on sleep was studied in rats with olfactory bulb lesions (O.B. lesioned rats). In these rats, electrodes were chronically implanted to record the EEG (frontal cortex and dorsal hippocampus), the cervical electromyogram and eye movements. The REM sleep stage was selectively decreased from 24 to 32 hours after 200 mg/kg of p-CPA in the sham lesioned rats, whereas both the slow wave sleep and REM sleep stages were markedly decreased by the same dose of p-CPA in the O.B. lesioned rats. In both sham and O.B. lesioned groups, the slow wave sleep and REM sleep stages decreased from 24 to 32 hours after 400 mg/kg of p-CPA and the percentage of decrease in the slow wave sleep stage was much larger with 400 mg/kg of p-CPA than with 200 mg/kg and 400 mg/kg of p-CPA. In the O.B. lesioned rats, the insomnia produced by 200 mg/kg and 400 mg/kg of p-CPA disappeared with 5-HTP (5 mg/kg). On the other hand, the insomnia produced by 200 mg/kg of p-CPA did not recur with 5-HTP in the sham lesioned rats, but with 400 mg/kg there was a recurrence. These results suggest that the enhanced effect of p-CPA and 5-HTP followed by p-CPA in the O.B. lesioned rats is due to changes in the sensitivity of the serotonergic system in the brain.

Animals↗
PubMed1977

Pharmacological actions of intracerebrally administered polyamines in mice.

Pharmacological actions of spermidine (SPD) and spermine (SPM) in mice given these polyamines by intracerebral injection (i.c.) were investigated. The spontaneous motor activity (SMA) assessed by the photocell counter method did not change immediately following injection of 80 mug SPD, but was enhanced 24 hours after the injection of 40 or 80 mug. A significant decrease of SMA was not immediately evident after the administration of 40 mug SPM but was demonstrated 24 hours later. Mice given single doses of 20 mug SPD exhibited increase in weight gain and those given 40 mug showed no significant difference, whereas a conspicuous decrease in weight occurred in mice given 80 mug of SPD. The body weights of mice given single doses of 10 mug SPM remained much the same, while significant weight losses occurred in both the SPM 20 mug and 40 mug dosed groups. There was a significant prolongation of pentobarbital induced sleep 6 days after the injection of high doses of SPD or SPM. Similar prolongation of sleeping time was also evident 30 minutes after the injection of SPM. A maximal hypothermic response with a fall by about 1 degree C was observed immediately following injection of 80 mug of SPD and 24 hours after the injection of 40 mug SPM, respectively.

Animals↗
PubMed1977

[Analgesic effect of pentazocine and its action on nociceptive afferent pathway].

Nociceptive stimulus was applied to the skin of adult cats by pinching with a serrated forceps or by radiant heat with Pain meter. This stimulation caused motor or emotional responses such as movements of the head and trunk, vocalization, escape and attack. After the administration of pentazocine, these responses disappeared and the animals behaved normally. Analgesic action appeared approximately 15 min after the administration and lasted more than 90 min. Effects of pentazocine on pain-afferent pathways were studied and the evoked potential was recorded by tibial nerve stimulation. Though pentazocine did not influence the evoked potential recorded from somatic sensory area I and mesencephalic central gray, the evoked potential in pre-central association area, nucleus centralis lateralis, nucleus suprageniculatus-limitans and reticularis pontis caudalis was reduced by pentazocine.

Afferent Pathways↗
PubMed1977

[Central effects of beta-phenylethylamines. (8). Increase in spontaneous motor activities of mice caused by intracerebrally administered metaramino].

Metaraminol (MA) (40, 80 and 160 microng) was injected i.c. into mice and spontaneous motor activity (SMA) measured by photo-cell counters method was found to increase 30 min after the injection. Ninety min after, the SMA was restored to the saline treated control. MA (80 microng i.c.) was also injected into isocarboxazide (Iso) pretreated mice and the SMA markdly increased as compared with the Iso+saline treated group or tween+MA treated group. When MA was injected i.c. into alpha-methyl-p-tyrosine (alpha-MT) pretreated mice, the SMA significantly increased as compared with that of the alpha-MT+saline treated group, but there was a decrease as compared with that of the tween+saline or tween+MA treated group. In alpha-MT treated mice. L-Dopa restored the hyper-motor activity of animals treated with MA. Diethyldithiocarbamate (700mg/kg i.p.) had no influence, whereas haloperidol markedly blocked the hyper-motor activity induced by MA. The hyper-motor activity induced by MA in mice raised the question of a possible role of noradrenaline and dopamine in the mediation of this action.

Animals↗
PubMed1977

[Central action of beta-phenylethylamine derivatives (10). Effect of L-Dopa on metaraminol induced motor activity (author's transl)].

The present experiments were undertaken in investigate the effects of Ro4-4602 plus L-Dopa on biphasic action induced by metaraminol (MA) in mice. The following results were obtained: Spontaneous motor activity (SMA) suppressed by MA was recovered by pretreatment of Ro4-4602 plus L-Dopa and increased by more than 100 mg/kg of L-Dopa. However, SMA was increased by more than 400 mg/kg of L-Dopa in saline pretreated mice. In MA pretreated mice, SMA by L-Dopa markedly increased in proportion to the doses of MA. The peak time of SMA by L-Dopa in MA pretreated mice was observed to be faster than that in saline pretreated mice. When L-Dopa was injected into MA and saline pretreated mice, there was no significant difference of brain dopamine content between the two groups. From the above results, it is considered that the enhanced effect of L-Dopa in MA pretreated mice may be due to production of a supersensitivity to catecholamines in the central nervous system. MA induced hyper-motor activity was enhanced by pretreatment of Ro4-4602 plus L-Dopa which have no influence on SMA.

Animals↗
PubMed1977

[Central action of beta-phenylethylamine derivatives (9). Effects of intracerebral administration of metaraminol on brain monoamine in mice (author's transl)].

Effects of intracerebral (i.c.) administration of metaraminol (MA) on brain monoamine in mice were studied. The results were as follows: MA, dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) were separated with phosphate buffer using a phosphorylated cellulose column (1X11 cm, 9 ml, Lot No. 2809). When MA was i.c. injected into mice, fluorescence of MA at 275/305 nm decreased in proportion to the time course and remained even at 12 hr after injection. Thirty min after MA in doses of either 40 or 80 microgram, a significant decrease of DA as compared with that of saline-treated group occurred and MA, in doses of 40, 80 and 160 microgram produced a significant decrease of NA and 5-HT. Thirty min after 160 microgram of MA, there was no significant difference in DA. Three hr after MA, DA levels significantly decreased, and 168 hr after were restored to the levels of the saline-treated group. Thirty min after MA, NA and 5-HT signficantly decreased compared with those of the saline-treated group and recovery took place 48 hr and 168 hr after respectively. It was concluded that MA depletes not only NA but also DA and 5-HT in the mouse brain.

Animals↗
PubMed1976

[Effects of MS4101, a new benzodiazepine compound, on evoked potentials induced by noxious stimulation of hind legs in cats].

The effects of 10-chloro-11b-(2'-fluorophenyl)-2,3,5,6,7,11b-hexahydro-7-(2''-hydroxyethyl)benzo[6,7]-1,4-diazepino [5,4-b]oxazol-6-one (MS4101), a new benzodiazepine compound, on evoked potential in cats were examined and compared with diazepam. Though evoked potential in somatic cortex I, motor cortex I and posterior groups induced by tibial nerve stimulation were unaffected by a small dose of MS4101 (1 mg/kg) which did not influence on limbic system, the amplitude of evoked potential in midbrain reticular formation was reduced. The amplitude of evoked potential in amygdala and hippocampus induced by cutaneous nerve stimulation was reduced by MS4101 and diazepam. These two drugs had the same effect on amygdala and difference in the degree of action between these drugs was not observed. Sham rage response following head shake, circling and whine behaviour was observed by electrical stimulation of the hypothalamus. The threshold of sham rage response by raised by MS4101 and diazepam.

Animals↗
PubMed1976

[Effects of a benzodiazepine derivative, MS4101, on emotional behaviour of untamed cats].

Effects of MS4101 on emotional behaviour in untamed cats were studied and compared with those of diazepam. Offensive behaviour, i.e., whine response to a rod presented in front of the snout and blowing air on back hair was markedly observed, and whine, attacking and biting responses to tapping with a rod on the back in these cats were marked. Defensive behaviour, i.e., hissing, crouching body, ear flattening to blowing air on back hair, a rod presented and tapping was markedly observed. From 30 min after MS4101 and diazepam in doses of 2 approximately 4 mg/kg i.p., offensive behaviour in untamed cats was depressed. ID50 (50% of inhibition dose) of offensive behaviour for MS4101 and diazepam was 2.40 (1.95 approximately 2.95) mg/kg i.p. and 0.96 (0.69 approximately 1.34) mg/kg i.p., respectively. MS4101 and diazepam in doses of 2 approximately 4 mg/kg i.p. decreased the offensive behaviour. ID50 of defensive behaviour for MS4101 and diazepam was 3.00 (2.46 approximately 3.66) mg/kg i.p. and 1.45 (1.14 approximately 1.84) mg/kg i.p., respectively. Both MS4101 and diazepam exhibited muscle relaxant effects. Here, diazepam was more effective than MS4101. ED50 of muscle relaxant activity for MS4101 and diazepam was 4.30 (3.03 approximately 6.11) mg/kg i.p., 7.40 (5.04 approximately 10.66) mg/kg i.p., respectively. A single administration of MS4101 and of diazepam in doses 2 mg/kg i.p. enhanced food intake.

Agonistic Behavior↗