{"title":"Long-term treatment with haloperidol or clozapine does not affect dopamine D4 receptors in rat frontal cortex.","authors":"I Kusumi, T Ishikane, S Matsubara, T Koyama","doi":"10.1007/BF01271560","DOIUrl":"https://doi.org/10.1007/BF01271560","url":null,"abstract":"<p><p>We examined the effects of long-term treatment with haloperidol and clozapine on dopamine D4 receptors in rat frontal cortex. Dopamine D4 receptor binding sites were indirectly determined from the displacement experiments of [3H]clozapine binding using nemonapride. Three-weeks administration of haloperidol (0.5 mg/kg) or clozapine (10 mg/kg) did not significantly affect the D4 receptors in the frontal cortex. The density of D2 receptors, determined by [3H]spiperone binding to striatum, was increased by long-term treatment with haloperidol, but it was not significantly changed by that with clozapine.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"231-5"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271560","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669637","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}
X M Li, L Ferraro, S Tanganelli, W T O'Connor, U Hasselrot, U Ungerstedt, K Fuxe
{"title":"Neurotensin peptides antagonistically regulate postsynaptic dopamine D2 receptors in rat nucleus accumbens: a receptor binding and microdialysis study.","authors":"X M Li, L Ferraro, S Tanganelli, W T O'Connor, U Hasselrot, U Ungerstedt, K Fuxe","doi":"10.1007/BF01276508","DOIUrl":"https://doi.org/10.1007/BF01276508","url":null,"abstract":"<p><p>An in vitro receptor binding and in vivo microdialysis study was performed to further investigate the modulation of dopamine (DA) D2 receptors by neurotensin (NT) peptides. Saturation experiments with the D2 agonist [3H]NPA (N-propylnorapomorphine) showed that 10 nM of NT, 10 nM of neuromedin N (NN) and 1 nM of the C-terminal NT-(8-13) fragment significantly increased the KD values by 125%, 181%, and 194%, respectively without significantly affecting the Bmax value of the [3H]NPA binding sites in coronal sections of rat ventral forebrain mainly containing the nucleus accumbens (Acb) and the olfactory tubercle. In line with the previous findings that NT can increase GABA release in the Acb and that NT receptors are not found on DA terminals in this brain region, the present in vivo microdialysis study demonstrated that local perfusion of NT (1 nM) counteracted the D2 agonist pergolide (2 mu M) induced inhibition of GABA, but not of DA release in the rat Acb. This result indicates that NT counteracts the D2 agonist induced inhibition of GABA release in the rat Acb, via an antagonistic postsynaptic NT/D2 receptor interaction as also suggested by the inhibitory regulation of D2 receptor affinity in the Acb by the NT peptides demonstrated in the present receptor binding experiments. Thus, the neuroleptic and potential antipsychotic profile of the NT peptides may involve an antagonistic NT/D2 receptor regulation in the ventral striatum.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 2","pages":"125-37"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276508","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19720928","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":"D1 receptor binding in rat striatum: modification by various D1 and D2 antagonists, but not by sibutramine hydrochloride, antidepressants or treatments which enhance central dopaminergic function.","authors":"S C Cheetham, C J Kettle, K F Martin, D J Heal","doi":"10.1007/BF01276563","DOIUrl":"https://doi.org/10.1007/BF01276563","url":null,"abstract":"<p><p>[3H]SCH 23390 is a selective high affinity ligand for D1 receptors in vitro. Using this ligand persistent blockade of D1 receptors by SCH 23390 and cis-flupenthixol was shown to significantly increase the number of D1 receptor binding sites in rat striatum. In contrast, repeated administration of the D2-selective antagonist, clebopride, resulted in a small, but significant, reduction in number. No differences in binding affinity were observed and a single dose of these compounds was without effect. The D2-selective antagonist, haloperidol, the non-selective D1/D2 receptor antagonist, chlorpromazine, the dopamine reuptake inhibitors, bupropion, GBR 12909 and nomifensine, and the dopamine releasing agent, d-amphetamine, had no effect on D1 receptors. The antidepressant treatments, desipramine, zimeldine, amitriptyline, tranylcypromine, mianserin and ECS and the monoamine reuptake inhibitor, sibutramine, similarly did not alter striatal D1 sites. Thus, of the treatments investigated only chronic receptor blockade by high affinity antagonists altered D1 receptor binding in rat striatum.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"35-46"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276563","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19757410","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":"Effects of localized histamine microinjections into the hippocampal formation on the retrieval of a one-way active avoidance response in rats.","authors":"E O Alvarez, A M Banzan","doi":"10.1007/BF01271557","DOIUrl":"https://doi.org/10.1007/BF01271557","url":null,"abstract":"<p><p>The possible role of histamine (HA) locally applied into the hippocampus on memory mechanisms of the rats was studied. The acquisition of a one-way active avoidance response to an ultrasonic 40 kHz sinus-wave tone anticipating an electric shock was used as experimental model. Learning sessions consisted in placing animals into a two compartment cage were they learnt to escape to the safe compartment after an ultrasonic tone anticipating an electric feet shock. After acquiring the conditioned avoidance response, animals were implanted with microinjection cannulae and injected with 1 microliter of saline, or increasing doses of histamine (9, 22.5, 45, and 90 nmol) into the hippocampus. In the experimental sessions, 4 trials before (PRE) and 4 trials afterward treatment (POST), the percentage of conditioned avoidance responses (% CAR) and the latency time to escape (LT) were measured. Results showed that HA increased significantly the LT and this effect was grossly dose-dependent. % CAR was also affected and the score was significantly inhibited by the imidazolamine administration. Results suggest that HA may be involved in memory retrieval processes in the hippocampus.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"201-11"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271557","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669634","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":"Drug-induced oral dyskinesias in rats after traditional and new neuroleptics.","authors":"T Kakigi, X M Gao, C A Tamminga","doi":"10.1007/BF01271544","DOIUrl":"https://doi.org/10.1007/BF01271544","url":null,"abstract":"<p><p>Tardive dyskinesia (TD) is a serious human side effect of neuroleptic treatment in psychotic disorders. Although the etiology is clear (i.e. chronic neuroleptic drugs), its pathophysiology has not yet been satisfactorily explained. This is important not only theoretically but also to inform drug development, allowing the introduction of antipsychotic compounds without TD liability. The development of an animal condition which putatively models these delayed onset dyskinesias, has provided a technique to differentiate between neuroleptic drug effect and dyskinesia correlates. We report here the development of oral dyskinesias in rats in response to a number of different neuroleptics, which have a range of neurochemical and clinical characteristics. Traditional neuroleptics (e.g. haloperidol) produced rat oral dyskinesias, in an open-cage environment. Clozapine, while it produced an increased rate of oral movements, showed a significantly decreased potency in this model. SCH23390 (D1 antagonist) neither produced the oral movements nor modified their onset by coadministration with raclopride. These data replicate and extend other similar studies in the literature. They suggest that clozapine differs from traditional neuroleptics with respect to motor side effects.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"41-9"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271544","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669640","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":"Effects of pineal indoles on ovarian response to gonadotropin-induced ovulation in mice.","authors":"W Y Chan, T B Ng","doi":"10.1007/BF01276461","DOIUrl":"https://doi.org/10.1007/BF01276461","url":null,"abstract":"<p><p>Ovulation was induced in immature mice by injections of pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (HCG) spaced 48 hours apart. The mice were divided into six groups: one group received intraperitoneal injections of normal saline, another group received alcoholic saline which was used as the vehicle of pineal indoles, and the remaining groups received respectively hydroxyindoleacetic acid (HIAA), melatonin (MEL), methoxytryptamine (MTA) and methoxytryptophol (MTP). The pineal indoles were administered 24 hours before, on the same day as, 24 hours after and 48 hours after the PMSG injection. The mice were sacrificed 24 hours after the HCG injection. The numbers of growing primary follicles, multilaminar primary follicles, Graafian follicles, preovulatory follicles and corpora lutea in the ovary were not altered by treatment with pineal indoles. However, there was an increased incidence of follicular atresia in the groups treated with MEL, MTA and MTP. The pineal indoles did not affect the number of ovulated oocytes, but there was a large number of degenerated and fragmented ovulated oocytes in the MTA- and MTP-treated groups. Treatment with MEL, MTA and MTP also resulted in lower plasma levels of estradiol-17 beta and progesterone.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 3","pages":"239-46"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276461","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721553","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":"The neurotrophic effects of ebiratide, an analog of ACTH4-9, on cultured septal cells and aged rats.","authors":"T Matsumoto, S Tsuda, S Nakamura","doi":"10.1007/BF01276861","DOIUrl":"https://doi.org/10.1007/BF01276861","url":null,"abstract":"<p><p>The neurotrophic effects of ebiratide, an ACTH4-9 analog, have been examined using both fetal rat septal cultures and aged rats. The 5-day treatment with ebiratide (10-100 pmol/ml) partially prevented neuronal degeneration that occurred in the cultures in which cells were sparsely plated. Ebiratide (10 pmol/ ml) increased choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities up to 1.5 and 1.2 times the respective control values in the sub-confluent cultures. AChE cytochemistry of the cultures has shown that ebiratide increased the stained area per cell. Ebiratide subcutaneously administered by constant infusion (10 nmol/body/hr) for 4 weeks elevated ChAT activities in the septum (35% over control), neocortex (79%) and hippocampus (89%) of aged rats. Thus, the present study indicates that ebiratide shares neurotrophic properties which may prove beneficial in the therapy for CNS degenerative disorders, especially Alzheimer's disease.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 1","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276861","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721616","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 effects of adenosine locally applied into ventral hippocampus of adult male rats.","authors":"S L Salas, F A Redmond, E O Alvarez","doi":"10.1007/BF01276866","DOIUrl":"https://doi.org/10.1007/BF01276866","url":null,"abstract":"<p><p>The possible effects of Adenosine (AD), locally applied into the ventral Hippocampus (HPCv) on the expression of general motor activity and some stereotyped behaviours were studied in adult male rats. Locomotion display was recorded in a hole-board equipped with automatic infrared animal activity detectors. Stereotyped behaviours were measured by direct inspection by two observers. Animals were implanted with microinjection cannulae into the HPCv and 72 h later they were injected with saline, or increasing doses of AD. In one experiment rats were microinjected once with saline or Adenosine and general motor activity and exploration were examined. In other experiment, rats were injected into the HPCv twice with saline, the AD-receptors antagonist 1,3-dipropil-methyl-xanthine (DMX) or AD and only stereotyped behaviours were examined. Results of Experiment 1 showed that the 40 nMol dose of AD was significantly effective to inhibit by about 30% several motor activities such as vertical, horizontal and ambulatory behaviours. Results of Experiment 2, showed that grooming was not modified by AD but the dose of 10 nMol increased the time of immobility by about 3 times over controls. DMX was able to block completely the AD effects on immobility. The present results suggest that in the rat AD might modulate the hippocampal-mediated expression of some motor and stereotyped behaviours induced by unknown environments.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 1","pages":"63-72"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721621","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":"Does bright light suppress nocturnal melatonin secretion more in women than men?","authors":"P Monteleone, G Esposito, A La Rocca, M Maj","doi":"10.1007/BF01276567","DOIUrl":"https://doi.org/10.1007/BF01276567","url":null,"abstract":"<p><p>Sex differences in the sensitivity of the human pineal gland to the suppressant effect of bright light on melatonin synthesis were studied in 6 healthy men and women. Blood samples were collected in two randomly ordered sessions: in one, subjects rested supine in bed, in the dark, from 21.00 to 7.00 h; in the other session, they were exposed to bright light (2,000 lux) from 2.00 to 4.00 h. In the dark condition, no significant differences were observed between men and women in either the timing or the absolute values of melatonin plasma levels, whereas after bright light exposure, the suppression of plasma melatonin was a 40% greater in women than in men. These findings suggest that, in humans, there is a sex difference in the nocturnal sensitivity of the pineal to light.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"75-80"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276567","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756683","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":"Correlation between cognitive brain function and electrical brain activity in dementia of Alzheimer type.","authors":"T Dierks, L Frölich, R Ihl, K Maurer","doi":"10.1007/BF01271469","DOIUrl":"https://doi.org/10.1007/BF01271469","url":null,"abstract":"<p><p>Psychometric tests which assess cognitive brain function in dementia disorders are partly prone to artifacts, e.g., the experience of the investigator and the cooperation of the patient influences the results. An objective way to assess the degree of cognitive disturbance could be to measure neuronal activity represented by the electrical brain activity. The aim of the present study was to investigate how well cognitive function in dementia assessed by psychometric tests correlates with electrical brain activity (EEG). Multichannel EEG data was reduced into 3-D intracerebral equivalent dipole EEG generators allowing a more convenient statistical data management and valid physiological data interpretation. 35 patients suffering from dementia of Alzheimer type were investigated. An increase of dipole strength in the slow frequency bands, a more anterior equivalent dipole of alpha- and beta-activity, and a slowing of the EEG with increasing cognitive deterioration could be demonstrated. The results support the hypothesis that the amount of disturbance of cognitive function in dementia can be assessed by measuring the electrical activity of the brain.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"55-62"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271469","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559287","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}