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J Ichikawa

Publications and source records attributed to J Ichikawa.

At least 37 records · Page 2Linked to original sources
PubMed1998

Comparison of the expression of two immediate early gene proteins, FosB and Fos in the rat preoptic area, hypothalamus and brainstem during pregnancy, parturition and lactation.

Medial preoptic area (MPA), supraoptic nucleus (SON), magnocellular (MaPVN) and parvocellular (PaPVN) paraventricular hypothalamic nuclei, and mesencephalic lateral tegmentum (MLT) are involved in maternal behavior, parturition and lactation. This study investigated the FosB and Fos immunoreactivity in these regions of virgin, pregnant, parturient, lactating, and lactating-arrested rats. The patterns of FosB and Fos expression were compared between the sections taken from the same animals. Quantitative immunohistochemistry revealed a significant increase in the numbers of FosB-positive neurons in the MPA, SON, MaPVN, and MLT of parturient and lactating females as compared with pregnant or virgin animals. In lactating rats, the numbers of FosB-positive neurons in the MPA, PaPVN, and MLT were increased, but the numbers in the SON and MaPVN were decreased as compared with parturient females. Many Fos-positive neurons were also seen in parturient and lactating rats, and the patterns of Fos expression in each region were quite similar to those of FosB. Moreover, double-labeling immunohistochemistry revealed that: (1) many FosB-positive nuclei were observed in oxytocin and vasopressin neurons of the SON and PVN in parturient rats; (2) within FosB-positive neurons, 89.5% in the MPA, 86.8% in the MLT of parturient rats, and 92% in the MPA and 90.8% in the MLT of lactating animals were also Fos-positive. Only a small number of FosB and Fos-positive neurons were seen in females that were killed in the early stage of parturition. Removal of the litters immediately after parturition completely eliminated FosB and Fos expression in each region in the dams. Taken together, the present results suggest that FosB expression is co-involved with Fos in the neural activation during parturition and lactation in rats.

Animals↗
PubMed1998

Localization of cytoplasmic free calcium ions in PC12 cells with varicose fibers.

Differentiated PC12 cells with varicose fibers were used as a model of sympathetic neurons to demonstrate the intracellular localization of cytoplasmic free calcium ions. Changes in the concentration of cytoplasmic free calcium ions were analyzed at individual varicosities upon stimulation with acetylcholine by laser scanning confocal microscopy. Transient increases in cytoplasmic free calcium ion concentration were localized in the varicosities and recognized in both the absence and presence of extracellular Ca2+. Immunocytochemical analysis of intracellular calcium channels, 1, 4, 5-trisphosphate receptors and ryanodine receptors, by electron microscopy demonstrated that immunoreactive sites were mainly localized in large dense core vesicles in the varicosities and neurites. These results suggest that the exocytosis of large dense core vesicles is regulated by an increase in cytoplasmic free calcium ion concentration from an intracellular Ca2+ store.

Acetylcholine↗
PubMed1997

The effect of streptozotocin-induced diabetes on dopamine2, serotonin1A and serotonin2A receptors in the rat brain.

The effect of streptozotocin (STZ)-induced diabetes and a combination of chronic treatment with haloperidol (HPD) on dopamine (DA)D2, serotonin (5-HT) 5-HT1A and 5-HT2A receptors was investigated in rat brain. Rats were randomly assigned to one of four groups: vehicle-vehicle, STZ-vehicle, vehicle-HPD, and STZ-HPD groups. Four weeks after single administration of STZ (65 mg/kg IV) or vehicle (citrate buffer), rats received depot HPD (4 mg/kg IM) or vehicle (sesame oil) once a week for 4 weeks. Sixteen days after the last injection of HPD or vehicle, rats were sacrificed, and the density of binding sites was determined using [3H]spiperone as ligand in the striatum (D2),[3H]8-hydroxy-2-(di-n-propyl)-aminotetraline in the hippocampus (5-HT1A), and [3H]ketanserin in the frontal cortex (5-HT2A). The density of D2 receptors was significantly increased in the vehicle-HPD compared to vehicle-vehicle controls. However, striatal D2 receptor density of the STZ-HPD and the STZ-vehicle were not significantly different from the vehicle-vehicle group. A significant increase in cortical 5-HT2A receptor density was observed only in the group of STZ-vehicle. Treatment with STZ, HPD, or the combination thereof, did not affect the density of 5-HT1A receptors. The affinity constants for D2, 5-HT1A, and 5-HT2A receptors were not affected by any treatment. These results suggest that diabetic state may affect brain serotonergic activity via an increase in the density of 5-HT2A receptors. This may indicate an increased vulnerability to major depression in patients with diabetes. The lack of an effect of the combined chronic treatment with STZ and HPD on the D2 receptor density may correspond to the increased risk to develop tardive dyskinesia in patients with diabetes.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

R(+)-8-OH-DPAT, a 5-HT1A receptor agonist, inhibits amphetamine-induced serotonin and dopamine release in rat medial prefrontal cortex.

Pretreatment with R(+)-8-OH-DPAT, a selective serotonin (5-HT)1A receptor agonist (50 micrograms/kg, s.c.), inhibited D-amphetamine sulfate (1.0 mg/kg, s.c.)-induced increases in extracellular levels of both 5-HT and dopamine (DA) in rat medial prefrontal cortex, as determined by in vivo microdialysis. The inhibitory effect of R(+)-8-OH-DPAT was completely reversed by the selective 5-HT1A receptor antagonist WAY 100,635 (100 micrograms/kg s.c.) administered 5 min prior to R(+)-8-OH-DPAT. These results suggest that stimulation of 5-HT1A receptors may inhibit amphetamine-induced release of 5-HT and DA in the medial prefrontal cortex.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

R(+)-8-OH-DPAT, a 5-HT1A receptor agonist, inhibits amphetamine-induced dopamine release in rat striatum and nucleus accumbens.

Systemic administration of R(+)-8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin), a selective serotonin (5-hydroxy-tryptamine, 5-HT)1A receptor agonist (25, 50, and 100 mu g/kg s.c.), administered 30 min prior to d-amphetamine, significantly inhibited the d-amphetamine sulfate (1.0 mg/kg s.c.)-induced increase in extracellular dopamine levels in the striatum and nucleus accumbens of freely moving rats, as determined by in vivo microdialysis. The ability of R(+)-8-OH-DPAT (50 mu g/kg s.c.) to inhibit d-amphetamine sulfate (1.0 mg/kg s.c.)-induced increase in extracellular dopamine levels was abolished by WAY 100,635 (n-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-n-(2-pyridinyl) cyclohexanecarboxamide trihydrochloride), a selective 5-HT1A receptor antagonist (100 mu g/kg s.c.), administered 5 min prior to R(+)-8-OH-DPAT in both regions. These results indicate that the 5-HT1A receptor may exert an inhibitory effect on amphetamine-induced dopamine release.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

DOI, a 5-HT2A/2C receptor agonist, potentiates amphetamine-induced dopamine release in rat striatum.

The effects of (+-)-DOI (1-(2,5-dimethoxy-4-iodophenyl)-aminopropane) hydrochloride, a mixed 5-HT2A/2C receptor agonist, on the release of dopamine (DA) following D-amphetamine sulfate (AMP) or a DA D2 autoreceptor selective dose of (-)-apomorphine hydrochloride (APO), were investigated in rat striatum (STR) and nucleus accumbens (NAC), using in vivo microdialysis. AMP (1.0 mg/kg, s.c.) produced marked increases in extracellular DA levels in both the STR and the NAC whereas DOI (2.5 mg/kg, i.p.) alone had no significant effect on extracellular DA levels in either region. Pretreatment with DOI 30 min prior to AMP, further enhanced the AMP-induced increase in striatal extracellular DA levels. On the other hand, DOI pretreatment attenuated the APO (50 micrograms/kg, s.c.)-induced decrease in extracellular DA levels in the STR. Pretreatment with DOI did not affect the ability of either AMP or APO to modulate extracellular DA levels in the NAC. These results provide further evidence that 5-HT2A/2C receptors modulate the release mechanisms of DA in the STR. Possible mechanisms are discussed.

Amphetamine↗
PubMed1995

Effect of antidepressants on striatal and accumbens extracellular dopamine levels.

The effect of the selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitor, fluoxetine (10 mg/kg s.c.), two tricyclic antidepressants, clomipramine (10 mg/kg s.c.) and imipramine (10 mg/kg s.c.), and vehicle on extracellular dopamine levels was studied in rat nucleus accumbens and striatum by in vivo microdialysis. Fluoxetine produced significant decreases in extracellular dopamine levels in both the nucleus accumbens and striatum (mean maximum percentage decrease: 58% and 57% of pre-drug baseline, respectively). In contrast, imipramine and clomipramine significantly increased extracellular dopamine in the striatum (148% and 150%, respectively) compared to the effect of vehicle alone (118%). These results suggest that the selective serotonin reuptake inhibitor, fluoxetine, and the tricyclic antidepressants, clomipramine and imipramine, affect dopaminergic activity in diverse ways and in a region-specific manner. Thus, the antidepressant effect of these drugs is unlikely to be related to their acute effects on dopaminergic neurotransmission. The differential effects of the selective serotonin reuptake inhibitor and tricyclic antidepressants on extracellular dopamine could account for other differences in their clinical and side effect profiles. Further studies of the chronic effects of the selective serotonin reuptake inhibitor and the tricyclic antidepressants on dopaminergic activity are required to elucidate the role of dopamine in the antidepressant effect.

Animals↗
PubMed1995

Influence of alterations in the oral environment on speech production.

We examined the influence on temporal aspects of three consonants, /k/, /c/ and /s/, of alterations in the oral environment produced by either palatal augmentation or by an increase in the vertical dimension of occlusion. Voice onset time (V.O.T.) for /k/ and /c/ was influenced more than aspiration time by the palatal augmentation. Consonant duration for /s/ was also influenced by palatal augmentation. Significant influence of an increase in vertical dimension on the timing was not recognized. Speech disorder caused by the malformation of palate seems to be more frequent than that caused by vertical dimension. Adaptation to prostheses would seem to be definitely concerned with orosensory feedback.

Adaptation, Physiological↗
PubMed1995

[A case of pancreatic cancer surviving for 7 years 11 months following intra-arterial and portal infusion chemotherapy].

A case of unresectable pancreatic cancer in a 76-year-old female was reported, in which a tumor had liver involvement. She was treated with infusion chemotherapy of mitomycin C (MMC) from gastroduodenal artery and portal vein after palliative operation. A drug was administered via an extracorporeal infusion catheter. MMC was given totally 47 mg from artery and 27 mg from portal vein for 9 months. Then, the serum CA 19-9 level gradually decreased, the metastatic liver tumor disappeared and the pancreatic tumor became smaller. After that, the tumor did not grow. The patient survived for 7 years 11 months until she died from other causes. Thus, it seems that infusion chemotherapy might be tried in some cases of pancreatic cancer.

Adenocarcinoma↗
PubMed1992

The effect of chronic atypical antipsychotic drugs and haloperidol on amphetamine-induced dopamine release in vivo.

The effect of chronic administration of antipsychotic drugs (21 days in drinking water followed by 3 days drug washout) on the D-amphetamine (1.0 mg/kg, s.c.)-induced increase in dopamine (DA) release in the striatum and the nucleus accumbens of awake, freely-moving rats was investigated with microdialysis. Chronic administration of haloperidol, a typical antipsychotic, (0.5 mg/kg/day), decreased basal extracellular DA release in the striatum and the nucleus accumbens but did not affect D-amphetamine-induced DA release in either region. In marked contrast, chronic administration of three atypical antipsychotic drugs: amperozide (2 mg/kg/day), clozapine (10 mg/kg/day) and melperone (2 mg/kg/day) increased basal extracellular DA and enhanced D-amphetamine-induced DA release in the striatum. In the nucleus accumbens, basal extracellular DA was decreased by chronic amperozide, unchanged by chronic clozapine and increased by chronic melperone. Most significantly, D-amphetamine-induced DA release was inhibited by chronic amperozide or clozapine, but unaffected by chronic melperone in this region. These results suggest that atypical antipsychotic drugs can alter DA release in a region specific manner. In particular, attenuation of amphetamine-like stimulation of DA release with reduced basal DA release in the nucleus accumbens could contribute to the antipsychotic action of amperozide which has a very weak affinity for D2 DA receptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Amperozide, a novel antipsychotic drug, inhibits the ability of d-amphetamine to increase dopamine release in vivo in rat striatum and nucleus accumbens.

The in vivo effects of amperozide, a novel atypical antipsychotic drug, on the release of dopamine (DA) and the output of its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), were investigated in the striatum and the nucleus accumbens of awake, freely moving rats using microdialysis. Amperozide (2-10 mg/kg, s.c.) significantly increased extracellular levels of DA in both the striatum and nucleus accumbens in a dose-dependent manner. It had a similar but lesser effect on extracellular DOPAC levels in both regions. d-Amphetamine (2 mg/kg, s.c.) alone produced a very large (43-fold) increase in DA release, together with a 70% decrease in DOPAC levels in both the striatum and the nucleus accumbens. Amperozide (1-5 mg/kg, s.c.) 30 min before d-amphetamine (2 mg/kg) dose-dependently attenuated d-amphetamine-induced DA release but had no effect on the d-amphetamine-induced decrease in extracellular DOPAC levels in both regions. The effect of amperozide on d-amphetamine-induced DA release in the nucleus accumbens may explain the inhibitory effect of amperozide on amphetamine-induced locomotor activity. However, the failure of amperozide to block amphetamine-induced stereotypy, despite marked inhibition of striatal DA release, suggests the need to reexamine the importance of striatal DA for amphetamine-induced stereotypy.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Differential effects of repeated treatment with haloperidol and clozapine on dopamine release and metabolism in the striatum and the nucleus accumbens.

The differential effects of haloperidol (HAL) and clozapine (CLOZ) on dopamine (DA) release and metabolism (dihydroxyphenylacetic acid levels) in striatum and nucleus accumbens (accumbens) of freely moving rats were investigated using microdialysis. Chronic HAL (2 mg/kg/day x 21 days in drinking water) decreased basal DA release and metabolism in both regions, and produced tolerance to HAL-induced increase in DA metabolism in striatum. No modification of HAL-induced increases in DA release and metabolism were observed in accumbens. Together with D2 receptor blockade, this may produce decreased dopaminergic neurotransmission in both regions during chronic treatment. Chronic HAL (0.5 mg/kg/day x 21 days in drinking water) also decreased basal DA release and metabolism in both regions which were not reversed by 25 micrograms/kg of (-)-apomorphine, s.c. In marked contrast, chronic CLOZ (20 mg/kg/day x 21 days in drinking water) had no effect on basal DA release and metabolism in either region, whereas it produced tolerance to CLOZ-induced increase in DA release and metabolism in accumbens. Together with weak D2 receptor blockade, this may lead to slightly decreased dopaminergic neurotransmission in accumbens and slightly increased dopaminergic neurotransmission in striatum during chronic CLOZ treatment. These differences may contribute to the clinical differences between the two agents.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

The effect of chronic clozapine and haloperidol on basal dopamine release and metabolism in rat striatum and nucleus accumbens studied by in vivo microdialysis.

The effects of chronic treatment with clozapine and haloperidol on basal dopamine release and metabolism were studied in the striatum and the nucleus accumbens of awake, freely moving rats using in vivo microdialysis. Chronic haloperidol (2 mg/kg X 21 days) but not chronic clozapine (20 mg/kg X 21 days) decreased basal dopamine release and metabolism in both the striatum and the nucleus accumbens. These results differ significantly from those previously reported with in vivo voltammetry. Possible explanations are discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Apomorphine does not reverse reduced basal dopamine release in rat striatum and nucleus accumbens after chronic haloperidol treatment.

Chronic administration of haloperidol (2 mg/kg x 21 days) in drinking water decreased basal dopamine (DA) release and metabolism in rat striatum and nucleus accumbens in awake, freely moving rats. In contrast with previous in vivo voltammetric studies in chloral hydrate-anesthetized rats, DA release and metabolism decreased in both regions following administration of (-)apomorphine (50 micrograms/kg, i.v.). These results demonstrate that stimulation of pre- or postsynaptic DA receptors by apomorphine in rats chronically treated with haloperidol further diminishes the release of DA and decreases DA metabolism. These results are difficult to reconcile with current concepts of neuroleptic-induced depolarization inactivation which predict increased release of DA following DA agonist administration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

[Changes in behavior and central monoaminergic systems in the rat after repeated methamphetamine pretreatment: presynaptic regulatory mechanism].

We used various methods, including intracerebral dialysis, to investigate behavioral sensitization to methamphetamine (MAP) and neurochemical alterations of monoaminergic systems in rat striatum after repeated intermittent pretreatment with increased doses of MAP (2.5, 5, 7.5, 10 mg/kg sc x 2, every other day for a week) as an experimental model of MAP psychosis. MAP-pretreated rats showed an enhancement in MAP-stimulated striatal dopamine (DA) efflux from the neuron terminals into the synaptic cleft. The MAP-induced behavioral changes correlated significantly with the amount of DA efflux. The number of D2 receptors was not changed after the repeated MAP pretreatment. Therefore, as the possible explanations for the enhanced DA release. mechanism, it was suggested that the repeated exposure to abnormally high concentrations of DA produced by repeated MAP administration changed the presynaptic regulation mechanism as follows. (1) DA autoreceptor became subsensitive because low doses of (+/- ) apomorphine (25-50 micrograms/kg sc), a selective DA agonist, decreased striatal DA efflux below the predrug basal level in controls, but not in MAP-pretreated rats. It is recognized that low doses of apomorphine inhibit DA release via DA autoreceptor. (2) "Releasable DA pool" at the neuron terminals increased as shown by the enhanced DOPA accumulation 30 min after NSD1015 (100 mg/kg ip), an aromatic 1-amino acid decarboxylase inhibitor. (3) DA uptake decreased for the significantly more decreased DOPAC and HVA efflux after MAP challenge in MAP-pretreated rats. Serotonergic alteration was also indicated in MAP-pretreated rats, because of the significant decrease of 5-HIAA efflux after MAP challenge.

Animals↗