{"title":"Striatal dopaminergic D1 and D2 receptors after intracerebroventricular application of alloxan and streptozocin in rat.","authors":"M Salković, I Sabolić, Z Lacković","doi":"10.1007/BF01271536","DOIUrl":"https://doi.org/10.1007/BF01271536","url":null,"abstract":"<p><p>Intracerebroventricular application of low, nondiabetogenic doses (500 micrograms kg-1) of alloxan and streptozocin is followed by alterations of the dopaminergic system in rat striatum. In this brain region the dopamine content significantly increased, while the density of dopaminergic D1 receptors significantly decreased seven days after the intracerebroventricular application of betacytotoxics, as compared with the control group. The density of dopaminergic D2 receptors in striatum remained unchanged. Dopaminergic D1 and D2 receptors operate through signalling mechanism of G proteins, but no changes of Gs and Gi proteins content have been found in rat striatum after the intracerebroventricular application of betacytotoxics. As intracerebroventricular, nondiabetogenic administration of betacytotoxics produces changes of the striatal dopamine content and D1 receptor density similar to that produced by peripheral, diabetogenic administration of these drugs, the effect might be related not solely to pancreatic beta cells damage, but to alterations of the brain insulin system, as well.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 2","pages":"137-45"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271536","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19924824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K Kobayashi, O Inoue, Y Watanabe, H Onoe, B Långström
{"title":"Difference in response of D2 receptor binding between 11C-N-methylspiperone and 11C-raclopride against anesthetics in rhesus monkey brain.","authors":"K Kobayashi, O Inoue, Y Watanabe, H Onoe, B Långström","doi":"10.1007/BF01271537","DOIUrl":"https://doi.org/10.1007/BF01271537","url":null,"abstract":"<p><p>The effects of anesthesia on dopamine D2 receptor binding in the rhesus monkey brain were examined using positron emission tomography. The bindings of 11C-N-methylspiperone (NMSP) and 11C-raclopride (RAC) were measured under controlled ketamine or isoflurane anesthesia. The binding of 11C-NMSP was significantly lower in the striatum anesthetized with isoflurane than with ketamine. There was a smaller change in the binding of 11C-RAC than of 11C-NMSP. These findings suggest that changes in 11C-NMSP or 11C-RAC binding induced by anesthetics were not due solely to changes in the competition of endogenous dopamine.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 2","pages":"147-51"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271537","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19924825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S Murai, H Saito, E Abe, Y Masuda, J Odashima, T Itoh
{"title":"MKC-231, a choline uptake enhancer, ameliorates working memory deficits and decreased hippocampal acetylcholine induced by ethylcholine aziridinium ion in mice.","authors":"S Murai, H Saito, E Abe, Y Masuda, J Odashima, T Itoh","doi":"10.1007/BF01277590","DOIUrl":"https://doi.org/10.1007/BF01277590","url":null,"abstract":"<p><p>The effects of acute and chronic administration of MKC-231, a new choline uptake enhancer, and two other nootropic agents, linopiridine (Dup 996) and tetrahydroaminoacridine (THA) on working memory deficits and decreased hippocampal acetylcholine (ACh) content were studied in a delayed non-matching to sample task, using a T-maze, in ethylcholine aziridinium ion (AF64A)-treated mice. Treatment with AF64A (3.5 nmol, i.c.v.) produced memory deficits and decreased hippocampal ACh content. In acute behavioral experiments, MKC-231 and THA had no significant effect on AF64A-induced memory deficits at any doses tested (0.3, 1.0 and 3.0 mg/kg), whereas Dup 996, at a dose of 1.0 mg/kg, significantly improved memory deficits. In chronic experiments, MKC-231 improved memory deficit at all doses tested (0.3, 1.0, or 3.0 mg/kg p.o., once daily for 11 days) and Dup 996 did so only at a dose of 3.0 mg/kg, whereas THA did not improve memory deficit at any doses tested. In acute neurochemical experiments, MKC-231 and THA did not reverse the AF64A-induced hippocampal ACh depletion. Dup 996, however, further decreased hippocampal ACh content compared to that in the AF64A-treated group. In chronic experiments, MKC-231 significantly reversed hippocampal ACh depletion at doses of 0.3 and 1.0 mg/kg, whereas neither Dup 996 nor THA reversed hippocampal ACh depletion at any doses tested. These results indicate that MKC-231 improved the AF64A-induced working memory deficit and hippocampal ACh depletion, probably by recovering reduced high-affinity choline uptake and ACh release.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"98 1","pages":"1-13"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01277590","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18713469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of pertussis toxin on the response of rat medial prefrontal cortex cells to the iontophoresis of serotonin receptor agonists.","authors":"J Y Zhang, C R Ashby, R Y Wang","doi":"10.1007/BF01271563","DOIUrl":"https://doi.org/10.1007/BF01271563","url":null,"abstract":"<p><p>In this study, we examined the response of spontaneously active as well as quiescent cells (L-glutamate-activated) in the rat medial prefrontal cortex (mPFc) to the iontophoresis of 2-methylserotonin (2-Me-5-HT, 5-HT3 receptor agonist), (+/-)-2,5-dimethoxy-(4-iodo-phenyl)-2-aminopropane (DOI, 5-HT2A,2C receptor agonist), 8-hydroxy-N,N-di-propylamino tetralin (8-OH-DPAT, 5-HT1A receptor agonist) and gamma-aminobutyric acid (GABA, a non-selective GABA receptor agonist) after the intracerebral administration of pertussis toxin, an inactivator of the Gi/o protein. This was accomplished using the techniques of extracellular single cell recording and iontophoresis. The administration of pertussis toxin (0.5 microgram, 24 hours before the experiment) into the mPFc did not alter the response of mPFc cells to the iontophoresis of DOI, 2-Me-5HT or GABA compared to saline treated controls. However, the response of mPFc cells to the iontophoresis of 8-OH-DPAT was significantly attenuated in the animals pretreated with pertussis toxin compared to controls. These results suggest that the 5-HT1A but not 5-HT2A,2C or 5-HT3 receptor is coupled to the Gi/o protein.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"95 3","pages":"165-72"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271563","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18866009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N Waters, L Löfberg, S Haadsma-Svensson, K Svensson, C Sonesson, A Carlsson
{"title":"Differential effects of dopamine D2 and D3 receptor antagonists in regard to dopamine release, in vivo receptor displacement and behaviour.","authors":"N Waters, L Löfberg, S Haadsma-Svensson, K Svensson, C Sonesson, A Carlsson","doi":"10.1007/BF01277593","DOIUrl":"https://doi.org/10.1007/BF01277593","url":null,"abstract":"<p><p>To establish possible functional differences between the dopamine D2 and D3 receptor we investigated the relation between the ability, for a set of nine mixed dopamine D2 and D3 receptor antagonists, to displace N, N-dipropyl-2-amino-5,6-dihydroxy tetralin (DP-5,6-ADTN) from striatal binding sites and the subsequent behavioural consequences in vivo. Dopamine D2 receptor preferring antagonists are powerful displacers of DP-5,6-ADTN from the striatum. Maximal displacement is followed by strong hypomotility. Displacement of the agonist by the D3 preferring antagonist U99194A is only partial and results in synergistic increases in locomotor activity. Superimposing haloperidol upon GBR12909 leads to a synergistic increase in striatal dialysate dopamine concentrations. This effect is absent when combining GBR12909 with the putative D3 antagonist U99194A. These data give support for the hypothesis that the dopamine D3 receptor is functionally relevant at the postsynaptic level. Here, in contrast to the D2 receptor, it is proposed to exert an inhibitory influence on psychomotor functions.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"98 1","pages":"39-55"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01277593","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18713470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T Takahashi, Y Deng, W Maruyama, P Dostert, M Kawai, M Naoi
{"title":"Uptake of a neurotoxin-candidate, (R)-1,2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline into human dopaminergic neuroblastoma SH-SY5Y cells by dopamine transport system.","authors":"T Takahashi, Y Deng, W Maruyama, P Dostert, M Kawai, M Naoi","doi":"10.1007/BF01277014","DOIUrl":"https://doi.org/10.1007/BF01277014","url":null,"abstract":"<p><p>Uptake of catechol isoquinolines to dopamine cells was studied using human dopaminergic neuroblastoma SH-SY5Y cells. Only (R)-1,2-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline [(R)-1,2-DiMeDHTIQ] was transported by dopamine uptake system, while (S)-1,2-DiMeDHTIQ, (R)- and (S)-1-methyl-6,7-dihydroxy-tetrahydroisoquinoline, and 1,2-dimethyl-6,7-dihydroxyisoquinolinum ion were not. Kinetical study showed that the uptake of (R)-1,2-DiMeDHTIQ followed the Michaelis-Menten equation, and the values of the Michaelis constant and the maximal velocity were obtained to be 102.6 +/- 36.9 microM and 66.0 +/- 2.8 pmol/min/mg protein. Dopamine was found to inhibit (R)-1,2-DiMeDHTIQ uptake competitively. These results suggest that the selective uptake by dopamine transporter may account for the specific neurotoxicity of (R)-1,2-DiMeDHTIQ to dopamine neurons.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"98 2","pages":"107-18"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01277014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18735930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"GABA binding sites: their density, their affinity to muscimol and their behaviour against neuroactive steroids in human gliomas of different degrees of malignancy.","authors":"A Jussofie, V Reinhardt, R Kalff","doi":"10.1007/BF01294790","DOIUrl":"https://doi.org/10.1007/BF01294790","url":null,"abstract":"<p><p>The aim of the present investigation was to answer the question if there exists a relation between the equipment of human gliomas with GABA binding sites and the degree of malignancy of these tumours diagnostically characterized according to WHO classification. The following parameters were assessed: the density, the affinity and the sensitivity to the modulating steroids 3 alpha-hydroxy-5 alpha-pregnane-20-one (3 alpha OH-DHP) and 3 alpha,21 dihydroxy-5 alpha-pregnane-20-one (THDOC). Scatchard analysis and non linear computerization revealed that the occurrence of GABA sites was directly related to the degree of tumour malignancy: GABA sites were only detectable in lower malignant gliomas of WHO grade II but not in the very malignant glioblastomas. However, irrespective of the individual density to be detected all glioma GABA sites were sensitive to 3 alpha-hydroxy-5 alpha-pregnane-20-one (3 alpha OH-DHP) and 3 alpha,21 dihydroxy-5 alpha-pregnane-20-one (THDOC) without exception. The effects of THDOC were due to increases in the number of binding sites whereas in the presence of 3 alpha OH-DHP a decrease in affinity was noted, additionally. These findings support the view of a normal functional integrity of GABA receptors in gliomas.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"96 3","pages":"233-41"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01294790","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18825147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Similar effects of glycine, zinc and an oxidizing agent on [3H]dizocilpine binding to the N-methyl-D-aspartate receptor in neocortical tissue from suicide victims and controls.","authors":"A M Palmer, M A Burns, V Arango, J J Mann","doi":"10.1007/BF01277923","DOIUrl":"https://doi.org/10.1007/BF01277923","url":null,"abstract":"<p><p>This study used [3H]dizocilpine (MK-801) binding to the N-methyl-D-aspartate (NMDA) receptor to examine glycine, redox and zinc modulatory sites in membranes derived from the frontal and parietal cortex of control subjects (n = 8) and suicide victims (n = 6). [3H]dizocilpine binding in the presence of glutamate and glutamate plus glycine was similar in control and suicide subjects. The sulphydryl redox site was assessed using the oxidizing agent 5,5'-dithio-bis (2-nitrobenzoic acid), which inhibited binding in a dose-dependent fashion. Both redox and zinc sites were unaffected in the frontal and parietal cortex of suicide victims. These data indicate that the NMDA receptor and its glycine, redox and zinc subsites are preserved in the neocortex of suicide victims.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"96 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01277923","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18537801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Behavioural actions of prolactin locally applied into the hippocampus of adult female rats.","authors":"E O Alvarez, A M Banzan","doi":"10.1007/BF01283027","DOIUrl":"https://doi.org/10.1007/BF01283027","url":null,"abstract":"<p><p>The probable behavioural effects of rat prolactin (rPRL) locally applied into the ventral hippocampus (HPC) were studied in cycling female rats. Three experiments were performed examining the behavioural responses of rats subjected to three different situations: (i) Exploratory activity in an enriched holeboard (ii) exploratory activity under conflicting situation and (iii) escape behaviours in a forced swimming test. Behavioural parameters studied were: underground and object-directed exploration and locomotion (Experiment 1); latency time and exploration behaviours (Experiment 2); swimming time and escape behaviours (Experiment 3). In Experiment 1 results showed that rPRL decreased the underground exploration and also locomotion but increased the object-directed exploration and had no effect on non-ambulatory activity. In Experiment 2 results showed that treatment of rPRL increased the latency time but did not modify the exploratory activity. In Experiment 3 results showed that rPRL augmented the swimming time and one of two parameters (frequency of immersions intents) of the escape behaviour. Results are interpreted as local actions of PRL on hippocampal neuron affecting expression of behaviours of rats depending on the stressful conditions of the environment.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"95 1","pages":"17-28"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01283027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18856351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N G Cascella, F Macciardi, C Cavallini, E Smeraldi
{"title":"d-cycloserine adjuvant therapy to conventional neuroleptic treatment in schizophrenia: an open-label study.","authors":"N G Cascella, F Macciardi, C Cavallini, E Smeraldi","doi":"10.1007/BF01276429","DOIUrl":"https://doi.org/10.1007/BF01276429","url":null,"abstract":"<p><p>D-cycloserine, a partial agonist at the strychnine-insensitive glycine site of the NMDA receptor complex, was tested as adjuvant treatment to conventional neuroleptics in chronic schizophrenic volunteers. The drug was administered, o.a.d., at the daily dose of 250 mg for six weeks. Mental status outcome measures were completed at the end of each week of treatment. The major finding was a deterioration of the patients' clinical condition, specifically of their psychotic symptoms. These preliminary results are discussed among others in view of d-cycloserine pharmacologic properties and recent findings on the interaction between NMDA agonists and dopamine system. This study, finally, suggests the need for a controlled dose-finding trial to establish the activity and a therapeutic \"window\" of this drug in schizophrenia.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"95 2","pages":"105-11"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276429","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18862692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}