Biomedical subjects

T Kameyama

Publications and source records attributed to T Kameyama.

At least 19 recordsLinked to original sources

PubMed1992

Effect of naftidrofuryl oxalate on 5-HT2 receptors in mouse brain: evaluation based on quantitative autoradiography and head-twitch response.

The effects of naftidrofuryl oxalate (LS-121) on 5-HT2 receptors in the brain were assessed in mice on the basis of quantitative autoradiography and head-twitch responses. LS-121 inhibited [3H]ketanserin (2 nM) binding in all brain areas assayed in which there were 5-HT2 receptors, such as the frontal cortex, cingulate cortex, parietal cortex, occipital cortex, temporal cortex, nucleus accumbens, caudate-putamen, olfactory tubercle and hippocampus. In the frontal cortex, which has the highest density of 5-HT2 receptors, the Ki value of LS-121 was 6.08 x 10(-8) M. The inhibitory potencies of methysergide and ritanserin for 5-HT2 receptors were about 16- and 60-fold stronger, respectively, than that of LS-121. Moreover, in behavioral studies, LS-121 (12.5-50 mg/kg i.p.) produced dose-dependent and significant inhibitory effects on head twitches induced by 5-hydroxytryptophan (5-HTP) plus pargyline, which is a 5-HT2 receptor-dependent behavior in mice. These results suggest that LS-121 inhibits 5-HTP plus pargyline-induced head twitches by blocking 5-HT2 receptors.

5-Hydroxytryptophan↗

PubMed1992

Multidimensional behavioral analyses show dynorphin A-(1-13) modulation of methamphetamine-induced behaviors in mice.

The effects of intracerebroventricular (i.c.v.) injection of dynorphin A-(1-13) on methamphetamine-induced behavioral alterations in mice were determined by using multidimensional behavioral analyses. Methamphetamine (0.3, 1.0 and 3.0 mg/kg s.c.) produced a marked increase in linear locomotion, circling, rearing and/or grooming behaviors. The behavioral effects of methamphetamine (1.0 mg/kg s.c.) were almost completely antagonized by pretreatment with the dopamine D2 receptor antagonist, S(-)-sulpiride (3.0 and/or 10.0 mg/kg i.p.), but not with the dopamine D1 receptor antagonist, SCH 23390 (0.01 or 0.03 mg/kg i.p.). Although dynorphin A-(1-13) (3.0 or 12.5 micrograms i.c.v.) alone did not produce any significant effects on behavior, the methamphetamine (1.0 mg/kg s.c.)-induced increase in circling ipsilateral to the injection side was markedly enhanced by dynorphin A-(1-13) (12.5 micrograms i.c.v.). In contrast, the peptide (12.5 micrograms i.c.v.) inhibited the methamphetamine (1.0 mg/kg s.c.)-induced increase in rearing, whilst the increase in grooming remained unchanged. The effects of dynorphin A-(1-13) (12.5 micrograms i.c.v.) were fully reversed by the opioid antagonist, Mr 2266 (5.6 mg/kg s.c.). These results suggest that the unilateral administration (i.c.v.) of dynorphin A-(1-13) inhibits the activity of dopamine-elicited neurotransmission, resulting in an increase in ipsilateral circling and in a decrease in rearing.

Animals↗

PubMed1992

Denervation of dopaminergic neurons with 6-hydroxydopamine increases nerve growth factor content in rat brain.

Denervation of dopaminergic neurons by intra nigral injection of 6-hydroxydopamine (6-OHDA) increased nerve growth factor (NGF) content in the cortex and hippocampus, both of which are innervated by cholinergic neurons. The increase continued during an observation period of 0.5-28 days after the lesion. The time course of changes in NGF content was quite different from that of cholinergic neuron denervation. The decreased dopamine content produced in the striatum by 6-OHDA injection was not recovered during the observation period. These results suggest that dopaminergic neuron damage may affect NGF synthesis.

Animals↗

PubMed1992

Involvement of the cholinergic system in the effects of nefiracetam (DM-9384) on carbon monoxide (CO)-induced acute and delayed amnesia.

The effects of N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)-acetamide (DM-9384, nefiracetam), a cyclic derivative of GABA, were investigated in the carbon monoxide (CO)-induced amnesia model in mice using the passive avoidance task. Memory deficiency occurred when mice were exposed to CO before memory was completely consolidated after training (acute amnesia), at 7 days before training and 7 days after training (delayed amnesia). DM-9384 prolonged the step-down latency in mice with CO-induced amnesia. Scopolamine blocked the anti-amnesic effect of DM-9384 on delayed amnesia that had been induced by pre- or post-training exposure to CO. Bicuculline had a tendency to antagonize the anti-amnesic effect of DM-9384, but this tendency was not significant. Under these conditions, no significant change in the activity of choline acetyltransferase and glutamic acid decarboxylase was observed in the frontal cortex, striatum and hippocampus. These results suggest that DM-9384 potentiates cholinergic neuronal function and that it may modify acquisition and/or consolidation of memory.

Amnesia↗

PubMed1992

Effects of NIK-247 on CO-induced impairment of passive avoidance in mice.

The effect of NIK-247 on carbon monoxide (CO)-induced amnesia were investigated. A step-down type passive avoidance task with mice was used to compare the effects of NIK-247 with those of tacrine. Two types of CO-induced amnesia model, acute and delayed models, were used. The acute amnesia model was developed using mice exposed to CO before memory consolidation, just after training, and a retention test carried out 24 h after training. The delayed amnesia model was prepared 7 days after CO exposure even when the animals were exposed to CO 4 h after training, after memory had consolidated. NIK-247 administered post-training at 0.03-0.3 and 3 mg/kg or pre-retention test (24 h after training) at 0.3 and 10 mg/kg attenuated the acute amnesia. In addition, NIK-247 (0.03, 0.1, 1 and 10 mg/kg) and tacrine (0.03, 0.1 and 1 mg/kg) administered before the retention test (7 days after CO exposure) improved retrieval in the delayed amnesia model. Tacrine (0.01-0.3 and 3 mg/kg), administered post-training, attenuated the acute amnesia but pre-retention test administration did not. The dose-response curves for NIK-247 and tacrine were biphasic bell-shaped. These results indicated that NIK-247 has an improving effect on hypoxia-induced acute and delayed cognitive dysfunction, and suggest that NIK-247 has promise as a nootropic drug for therapy of memory deficits in patients with cerebrovascular-type dementing disorders.

Aminoquinolines↗

PubMed1992

Effects of dopamine receptor agonists on passive avoidance learning in mice: interaction of dopamine D1 and D2 receptors.

The present study examined the effects of dopamine D1 and D2 receptor agonists on the acquisition stage of passive avoidance learning and on locomotor activity in mice. The D2 agonist, RU 24213 (1-10 mg/kg s.c.), and the non-selective agonist, apomorphine (0.3-3 mg/kg s.c.), but not the D1 agonist, SKF 38393 (1-10 mg/kg s.c.), impaired learning and activated locomotion. RU 24213 (1 mg/kg s.c.) was more effective in impairing learning than in activating locomotion. The concurrent administration of SKF 38393 (10 mg/kg i.p.) and RU 24213 (1 and 3 mg/kg s.c.) produced a synergistic effect in both behavioral situations. The D1 antagonist, SCH 23390 (0.025 mg/kg i.p.), slightly inhibited the effects of apomorphine and of the combination of SKF 38393 and RU 24213 on learning but not on locomotion. The D2 antagonist, (-)-sulpiride (40 mg/kg i.p.), completely blocked these effects in both situations. These results suggest that dopamine receptor agonists impair passive avoidance learning through the D2 receptor, and that D1 and D2 receptors act synergistically in this impairment, as they do in their effects on locomotion. The involvement of D1 and D2 receptors is qualitatively similar in each of these behaviors, although some small differences may exist.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1992

Combination of a delta opioid receptor agonist but not a mu opioid receptor agonist with the D1-selective dopamine receptor agonist SKF 38393 markedly potentiates different behaviors in mice.

The effects of intracerebroventricular injections of opioid peptides selective for mu or delta opioid receptors on behaviors induced by the D1 dopamine agonist SKF 38393 were investigated by using multi-dimensional behavioral analyses. A 10.0 mg/kg dose of SKF 38393 produced a marked increase in grooming behavior. The SKF 38393 (10.0 mg/kg)-induced increase in grooming behavior was clearly antagonized by SCH 23390 (0.03 mg/kg), a D1 dopamine antagonist, but not by S(-)-sulpiride (10.0 mg/kg), a D2 dopamine antagonist. [D-Ala2,MePhe4,Gly5-ol]enkephalin (DAMGO) (0.003 and 0.01 microgram), a mu-selective agonist, or [D-Pen2,L-Pen5]enkephalin (DPLPE) (0.3 or 1.0 microgram), a delta-selective agonist, failed to affect spontaneous behaviors. The combination of DPLPE (0.3 and 1.0 microgram) but not of DAMGO (0.003 and 0.01 microgram) with SKF 38393 (10.0 mg/kg) produced a marked increase in linear locomotion and circuling away from the side receiving the peptide, whereas grooming behavior was not affected. The effects induced by DPLPE (1.0 microgram) plus SKF 38393 (10.0 mg/kg) were fully reversed by the delta-selective opioid antagonist naltrindole (10.0 mg/kg), SCH 23390 (0.03 mg/kg) and S(-)-sulpiride (10.0 mg/kg). These findings suggest that delta but not mu opioid systems interact with D1 dopamine receptors, resulting in a marked increase in linear locomotion and contralateral circuling without causing marked changes in grooming behavior.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1992

Effects of nefiracetam, DM-9384 on amnesia and decrease in choline acetyltransferase activity induced by cycloheximide.

The effects of nefiracetam, [N-(2,6-dimethyl-phenyl)-2-(2-oxo-pyrrolidinyl)acetamide, DM-9384], a cyclic derivative of GABA, were investigated in the cycloheximide (CXM)-induced amnesia animal model using the passive avoidance task. Pre-training administration of DM-9384 attenuated the CXM-induced amnesia as indicated by prolongation of step-down latency. It protected against CXM-induced inhibition of choline acetyltransferase activity in the cerebral cortex. These results suggest that DM-9384 attenuates CXM-induced amnesia by interacting with AChergic neuronal system and enhancing protein synthesis in the brain.

Amnesia↗

PubMed1992

Stress-induced changes in brain Met-enkephalin, Leu-enkephalin and dynorphin concentrations.

Methionine-enkephalin (Met-enkephalin), leucine-enkephalin (Leu-enkephalin) and dynorphin A (1-17) (dynorphin A) concentrations in discrete brain areas were determined in the mice showing behavioral changes induced by stress using radioimmunoassay (RIA). In the present experiment, we used environment-induced conditioned suppression of motility and forced swimming-induced immobility. In the environment-induced conditioned suppression of motility, Met-enkephalin concentration in the striatum and hypothalamus significantly decreased. Leu-enkephalin concentration in the hypothalamus also decreased. Dynorphin A concentration in the striatum decreased, but significantly increased in the hypothalamus and pituitary. In the forced swimming-induced immobility, Met-enkephalin concentration in the striatum significantly decreased. Leu-enkephalin concentration in the hypothalamus and pituitary significantly decreased. Dynorphin A concentration in the pituitary decreased, but significantly increased in the hypothalamus. Our results indicated that the concentrations of Met-enkephalin, Leu-enkephalin and dynorphin A in the discrete brain areas changed in two different stressful situations. These findings suggested that these peptides might modulate the behavioral changes induced by stressors.

Animals↗

PubMed1992

Effects of vinconate on spatial learning impairments induced by medial septal lesion in rats.

We investigated the effects of vinconate, a novel vinca alkaloid, on spatial learning deficits induced by medial septal (MS) lesion in rats. MS lesion was produced by passing an anodal DC current. In vehicle-treated MS-lesioned rats impairment of spatial learning was observed, shown by a decrease in correct choices and an increase in total errors during training in a radial arm maze task. Vinconate (10 mg/kg) treatment alleviated the decrease in correct choices and the increase in total errors induced by MS lesion. Vinconate (5 and 10 mg/kg) treatment showed a tendency to reverse the decrease in choline acetyltransferase activity in the hippocampus caused by MS lesion. The present study suggests that vinconate has an anti-amnesic effect on MS lesion-induced amnesia by ameliorating the dysfunction in cholinergic (ACh) neurons.

Animals↗

PubMed1992

Systemic administration of dynorphin A(1-13) markedly inhibits different behavioural responses induced by cocaine in the mouse.

The effects of systemic administration (i.p.) of dynorphin A(1-13) on the cocaine-induced behavioural alterations in the mouse were determined by using multi-dimensional behavioural analyses, based upon a capacitance system. A 1.0 mg/kg dose of cocaine did not influence behaviour, while increasing doses to 3-30 mg/kg produced a significant increment in the frequency of behaviour, such as linear locomotion, circling, rearing and grooming. Although a 1.0 mg/kg dose of dynorphin A(1-13) alone produced a significant decrease in grooming behaviour, larger doses (3.0 and 10.0 mg/kg) of the peptide failed to affect different behaviour. The cocaine (3.0 mg/kg)-induced increases in linear locomotion, circling and rearing behaviour were significantly inhibited by dynorphin A(1-13) (10.0 mg/kg). The inhibitory effects of dynorphin A(1-13) (10.0 mg/kg) were antagonized by the opioid antagonist Mr 2266 (5.6 mg/kg). It is thus possible that the systemic administration of dynorphin A(1-13) inhibits different behavioural responses induced by cocaine through the blood-brain barrier, although the instability of amino acid bonds or the relatively large molecular weight of dynorphin A(1-13), may result in the failure to demonstrate opioid activity by the peptide after systemic administration.

Analgesics↗

PubMed1992

Dentigerous cyst associated with a deciduous tooth. A case report.

A case of a dentigerous cyst associated with a deciduous tooth in a 2-year-old boy is presented. Radiologic examination revealed a well-defined radiolucency in the right maxilla associated with the crown of a maxillary second deciduous molar. The cyst cavity was lined with nonkeratinized squamous epithelium, and odontogenic epithelial islands were seen in subepithelial connective tissue.

Child, Preschool↗

PubMed1992

Dynorphin A(1-13) preferentially inhibits behaviors induced by the D2 dopamine agonist RU 24213 but not by the D1 dopamine agonist SK&F 38393.

The effects of dynorphin A(1-13) on the D1 dopamine agonist SK&F 38393- and the D2 dopamine agonist RU 24213-induced behavioral alterations in the mouse were determined by using multidimensional behavioral analyses based upon a capacitance system. Although dynorphin A(1-13) (3.0 or 12.5 micrograms) alone did not produce any significant effects on behaviors, the peptide (12.5 micrograms) caused an inhibitory effect on the RU 24213 (3.0 mg/kg)-induced increase in behavioral patterns such as linear locomotion and circling except rearing and grooming behaviors. The antagonistic effects of dynorphin A(1-313) (12.5 micrograms) were fully reversed by the opioid antagonist M(r) 2266 (10.0 mg/kg). However, dynorphin A(1-13) (3.0 or 12.5 micrograms) failed to affect behaviors elicited by SK&F 38393 (10.0 mg/kg). These results suggest that dynorphin A(1-13) plays an inhibitory role in behaviors induced by the D2 dopamine agonist but not by the D1 dopamine agonist, possibly through the mediation of kappa-opioid receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1992

Effects of [D-Ala2, D-Leu5]enkephalin and [D-Pen2, L-Pen5]enkephalin on apomorphine-induced motor activity in the mouse.

The effects of intracerebroventricular injections of opioid peptides such as DADL [( D-Ala2, D-Leu5]enkephalin) and DPLPE [( D-Pen2, L-Pen5]enkephalin) with different degrees of selectivity for delta- over mu-receptor on apomorphine (0.1, 0.3, 1.0 and/or 3.0 mg/kg)-induced motor activity were investigated in the mouse using multi-dimensional behavioral analyses. Lower doses (0.1 and 0.3 mg/kg) of apomorphine failed to affect significantly motor activity, whilst higher doses (1.0 and 3.0 mg/kg) of the drug produced a marked increase in linear locomotion, circling, rearing, and/or grooming behaviors. DADL (0.03, 0.1 or 0.3 microgram) by itself did not influence behaviors, while the peptide (0.1 and 0.3 microgram) produced a marked inhibition on apomorphine (1.0 but not 3.0 mg/kg)-induced increase in rearing behaviors. Furthermore, the inhibitory effect of DADL (0.3 micrograms) on the apomorphine (1.0 mg/kg)-induced increase in rearing was reversed by treatment with the alkylating agent beta-FNA (beta-funaltrexamine) (5.0 micrograms). In contrast to the effects of DADL, the much more delta-selective opioid agonist DPLPE (0.3, 1.0 or 1.75 micrograms) had no marked effects on apomorphine (1.0 mg/kg)-induced behaviors. These results suggest that delta opioid receptors do not play a principal role in the apomorphine-induced increase in circling, rearing or grooming behaviors.

Analgesics↗

PubMed1992

Effects of vinconate, a novel vinca alkaloid, on spatial learning deficits induced by the basal forebrain lesion in rats.

We investigated the effects of vinconate, a novel vinca alkaloid, on spatial learning deficits induced by the basal forebrain (BF) lesion in rats. Bilateral BF lesions were produced by injecting ibotenic acid (6 micrograms/0.5 microliter/side). In BF-lesioned rats, impairment of spatial learning in escaping onto the platform during training and decrease in spatial bias during the spatial probe trial in Morris's water maze task were both observed. Vinconate (5 and 10 mg/kg) treatment shortened the increase of escape latency to the platform in BF-lesioned rats and significantly reversed the decrease in spatial bias induced by the BF lesion. Vinconate (10 mg/kg) attenuated the decrease in choline acetyltransferase activity in the frontoparietal cortex caused by the BF lesion. The present study suggests that vinconate has an antiamnesic effect on the BF-lesion-induced amnesia by ameliorating the dysfunction in cholinergic neurons.

Animals↗

PubMed1992

Ventriculoarterial coupling during exercise in normal human subjects.

To examine the relative roles of ventricular contractility and loading conditions for cardiovascular adjustment during exercise, 10 normal human subjects were studied using a framework of ventriculoarterial coupling. Anaerobic threshold was evaluated to determine the work rates of aerobic and anaerobic exercise. Ventricular contractile properties were quantified by the slope of the end-systolic pressure-volume relationship (ventricular elastance) and arterial system properties were expressed by the end-systolic pressure-stroke volume relationship (arterial elastance). During aerobic exercise, left ventricular end-diastolic volume and stroke volume were increased by 14 and 33%, with plasma norepinephrine levels being doubled. Arterial elastance was reduced by 30%, but ventricular elastance did not change significantly. During anaerobic exercise, ventricular end-diastolic volume returned to the resting value, while stroke volume remained increased by 31%. In contrast to aerobic exercise, ventricular elastance rose substantially by 89% in association with about a 10 times increase in plasma norepinephrine. Arterial elastance remained the same as in aerobic exercise. Thus, the increase in stroke volume was primarily mediated by changes in loading conditions during aerobic exercise and by enhanced contractility during anaerobic exercise.

Adult↗

PubMed1992

Distributions of the Nd and P300 in a normal sample.

To obtain objective criteria for assessing the attentional and cognitive functioning of psychiatric populations, we attempted to standardize values of two components in Event-Related Potentials (ERPs), namely the attention-related negative potential (Nd) and the P300, in normal populations. The study consisted of 100 healthy volunteers (50 females, 50 males) who were given the task of making dichotic syllable discriminations requiring key-press responses. Their ages ranged between 18 and 59 years (mean +/- S.D., 32.3 +/- 11.3 years). Nd was found to be maximum in the Fz region, P300 being maximum in the Pz region. The means and standard deviations of Nd and P300 areas in their maximum regions were 554.1 +/- 307.8 microV ms and 2148.5 +/- 1248.5 microV ms, respectively. The transformation plot for symmetry indicated the suitable power of transformation to be 1/2 for both Nd and P300 distributions. After being transformed into square-root values, the distribution patterns of Nd and P300 areas were examined. When the lower limit of normal values was tentatively assigned to mean -2 S.D. using square-root transformed data for both Nd and P300, 97% of the subjects were found to display values above the lower normal limit for Nd, and 98% for the P300. Neither, Nd nor P300 areas correlated with age, while P300 latencies displayed a weak positive correlation with age. Females displayed relatively larger values than males for Nd and P300 areas and P300-peak amplitudes. However, the differences between females and males were not statistically significant. Females and males showed nearly equal P300-peak latencies.

Adolescent↗

PubMed1992

Information dysregulation and event-related potentials in schizophrenia.

Clinical experiences indicate that schizophrenic cognitive disturbances may be partly due to the unsuccessful construction of their cognitive context. In this article, two experiments are introduced in which schizophrenic deficits in utilization of information for construction of effective cognitive context were examined through measurements of event-related potentials, particularly P300s. In a 3-tone discrimination task, schizophrenic subjects failed to elicit P300s to frequent nontarget tones that were as important as standard tones for performing the required task. In the second task, consisting of detecting two consecutive identical tones, unlike healthy controls, schizophrenic subjects failed to display P300s to nontarget tones at target position. These results are discussed in relation to ineffective context construction of schizophrenic subjects. Moreover, a single-trial analysis of relationships between P300s and reaction times in the 3-tone discrimination task disclosed a loose coupling between the stimulus set and response set in patients.

Adult↗