Journal of neural transmission. General section最新文献

{"title":"The selective 5-HT2A receptor antagonist MDL 100,907 counteracts the psychomotor stimulation ensuing manipulations with monoaminergic, glutamatergic or muscarinic neurotransmission in the mouse--implications for psychosis.","authors":"M L Carlsson","doi":"10.1007/BF01276460","DOIUrl":"https://doi.org/10.1007/BF01276460","url":null,"abstract":"<p><p>The present study has shown that a subthreshold dose of the uncompetitive N-methyl-D-aspartate (NMDA) antagonist MK-801, combined with a subthreshold dose of LSD, produces marked locomotor stimulation in monoamine-depleted mice. Likewise, MK-801, as well as the muscarine receptor antagonist atropine and the alpha-adrenoceptor agonist clonidine, were found to interact synergistically with the putative 5-HT2 receptor agonist UH-232 to produce locomotor activation in monoamine-depleted mice. All these responses were effectively blocked by the highly selective 5-HT2A receptor antagonist MDL 100,907. On the other hand, MDL 100,907 did not antagonize the hyperactivity response produced by clonidine given in combination with MK-801 or atropine in monoamine-depleted mice, nor the response produced by the mixed DA receptor agonist apomorphine, underlining the selectivity in the antagonistic action of MDL 100,907. Furthermore, MDL 100,907 attenuated the hyperactivity produced in intact mice by such disparate agents as MK-801, atropine or the DA uptake inhibitor GBR 12,909. A putative \"permissive\" role of the 5-HT2 receptor in the context of psychomotor activation is discussed, as well as its possible importance as target for antipsychotic therapy.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 3","pages":"225-37"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276460","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721552","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":"Delayed changes in neural visinin-like calcium-binding protein gene expression caused by acute phencyclidine administration.","authors":"Y Kajimoto,&nbsp;O Shirakawa,&nbsp;T Kuno,&nbsp;N Nishino,&nbsp;H Nakai","doi":"10.1007/BF01276463","DOIUrl":"https://doi.org/10.1007/BF01276463","url":null,"abstract":"<p><p>Phencyclidine (PCP) induces a psychotomimetic state that closely resembles schizophrenia, and PCP-treated animals can serve as a model for schizophrenia. The effects of PCP on the gene expression of NVP-1, a novel Ca(2+)-binding protein, were studied in rats. After 24 hours, the NVP-1 mRNA level in the nucleus accumbens showed a significant decrease of 42%. This result suggests that alterations in Ca(2+)-binding protein may be involved in the pathology of PCP-induced psychosis and, presumably, schizophrenia.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 3","pages":"257-62"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276463","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721555","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":"Cyclic AMP enhances acetylcholine (ACh)-induced ion fluxes and catecholamine release by inhibiting Na+, K(+)-ATPase and participates in the responses to ACh in cultured bovine adrenal medullary chromaffin cells.","authors":"K Morita,&nbsp;N Minami,&nbsp;T Suemitsu,&nbsp;T Miyasako,&nbsp;T Dohi","doi":"10.1007/BF01276862","DOIUrl":"https://doi.org/10.1007/BF01276862","url":null,"abstract":"<p><p>The effects of cyclic AMP (cAMP) on intracellular Na+ concentration ([Na+]i), membrane depolarization and intracellular Ca2+ concentration ([Ca2+]i) and the involvement of cAMP in acetylcholine (ACh)-induced such cellular events and catecholamine (CA) release were studied in cultured bovine adrenal medullary chromaffin cells. 8-Bromo-cyclic AMP (8Br-cAMP) and forskolin caused a rise in [Na+]i, membrane depolarization and a rise in [Ca2+]i and potentiated these responses and CA release to ACh. The effects of 8Br-cAMP or forskolin on ACh-induced changes of but not on basal level of [Na+]i, membrane potential and [Ca2+]i were blocked by tetrodotoxin (TTX, 1 microM). In Na+ deprivated medium, forskolin failed to produce an increase in basal [Ca2+]i level and to potentiate ACh-induced rise. The similar results as in 8Br-cAMP and forskolin were obtained using ouabain, and 8Br-cAMP or foskolin produced no further effects in the presence of ouabain. Inhibitors of cAMP-dependent protein kinase not only blocked the effects of 8Br-cAMP and forskolin on membrane depolarization, [Ca2+]i rise and CA release, but also reduced these responses to ACh. From the similarity between the effects of cAMP and those of ouabain on the cellular events and the counteraction of the effects of cAMP by ouabain, it may be suggested that cAMP produces its effects on ion fluxes and CA release probably via an inhibition of Na+, K(+)-ATPase in intact chromaffin and cAMP may participate in the responses to ACh.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"100 1","pages":"17-26"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276862","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19721617","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":"An investigation of the activities of 3-hydroxykynureninase and kynurenine aminotransferase in the brain in Huntington's disease.","authors":"S J Pearson,&nbsp;A Meldrum,&nbsp;G P Reynolds","doi":"10.1007/BF01276566","DOIUrl":"https://doi.org/10.1007/BF01276566","url":null,"abstract":"<p><p>Previous reports have indicated abnormalities in the concentrations of metabolites of the tryptophan/kynurenine pathway in the brain in Huntington's disease. These have included an increase in 3-hydroxykynurenine and both increases and decreases in kynurenic acid. The activities of two enzymes involved in the metabolism of these compounds, 3-hydroxykynureninase and kynurenine aminotransferase, have been determined in post mortem brain tissue taken from Huntington's disease patients and control subjects.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 1","pages":"67-73"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276566","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756682","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":"Intracerebroventricular galanin and N-terminal galanin fragment enhance the morphine-induced analgesia in the rat.","authors":"B Przewłocka,&nbsp;H Machelska,&nbsp;P Rekowski,&nbsp;G Kupryszewski,&nbsp;R Przewłocki","doi":"10.1007/BF01281157","DOIUrl":"https://doi.org/10.1007/BF01281157","url":null,"abstract":"<p><p>Behavioral effect of galanin and its fragments, galanin1-15 and galanin16-29 (200 ng, 1 and 5 micrograms), after intracerebroventricular (i.c.v.) administration was studied in rats. The number of crossings and pippings and the time of locomotion (an open field test) showed a similar sedative action of galanin and galanin16-29, with no significant effect of galanin1-15. Galanin and its fragments, injected in doses of 200 ng, 1 and 5 micrograms, did not affect nociception, as measured by a tail-flick and paw pressure test. Galanin and galanin1-15, but not galanin16-29 (5 micrograms i.c.v.), injected together with morphine (2.5 micrograms i.c.v.), significantly potentiated the analgetic effect of morphine assessed by a paw pressure test; a similar tendency was also observed in a tail-flick test. Galanin and its two fragments injected in doses of 200 ng, 1 and 5 micrograms, did not change the effect of morphine given in a dose of 1 microgram. These data suggest that galanin, having no effect when given alone, potentiate the analgetic effect of morphine. The fact that the N-terminal fragment of galanin acts like a natural peptide suggests a receptor mediated action. In conclusion, the analgesic effect of morphine was potentiated by galanin and its N-terminal fragment galanin1-15. On the other hand, behavioral study showed a similar sedative action of galanin and C-terminal fragment galanin16-29. This suggests that the N- and C-terminal fragments of galanin are differentially involved in behavioral effects of the peptide.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 3","pages":"229-35"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01281157","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19758957","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":"Some methodological issues in neuroradiological research in psychiatry.","authors":"T Becker,&nbsp;W Retz,&nbsp;E Hofmann,&nbsp;G Becker,&nbsp;E Teichmann,&nbsp;W Gsell","doi":"10.1007/BF01271468","DOIUrl":"https://doi.org/10.1007/BF01271468","url":null,"abstract":"<p><p>An outline is given of some of the methodological issues discussed in neuroradiological research on psychiatric illness. Strengths and shortcomings of magnetic resonance imaging (MRI) in depicting and quantifying brain structures are described. Temporal lobe anatomy and pathology are easily accessible to MRI, whereas limits on anatomical delineation hamper approaches to frontal lobe study. White matter hyperintense lesions are sensitively depicted by MRI, but specificity is limited. Distinction of vascular and primary degenerative dementia is considerably improved by CT and MRI analysis. Computed tomography (CT) and MRI have enhanced the understanding of treatable organic psychiatric disorders, e.g., normal pressure hydrocephalus. Subcortical and white matter pathology has been replicated in CT and MRI studies of late-onset psychiatric disorders, clinical overlap with cerebrovascular disease or neurodegeneration may be of import. Transcranial sonography findings of brainstem structural change specific to unipolar depression may contribute to the understanding of affective psychoses. Magnetic resonance spectroscopy and functional MRI are likely to stimulate psychiatric research in the future.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"99 1-3","pages":"7-54"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271468","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19559293","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":"Crucial role of the accumbens nucleus in the neurotransmitter interactions regulating motor control in mice.","authors":"A Svensson,&nbsp;M L Carlsson,&nbsp;A Carlsson","doi":"10.1007/BF01271551","DOIUrl":"https://doi.org/10.1007/BF01271551","url":null,"abstract":"<p><p>Previous work, based on systemic drug administration, has shown that neurotransmitter interactions between dopaminergic, adrenergic, glutamatergic and cholinergic systems are involved in locomotor control in mice. In an attempt to identify the target sites in the brain of these interactions, we have started a series of experiments, where the drugs are administered intracerebrally in mice. The locomotor threshold doses of the competitive NMDA antagonist AP-5 and the noncompetitive NMDA antagonist MK-801 were investigated by means of local application in the accumbens nucleus of monoamine-depleted and monoaminergically intact mice, respectively. The threshold dose of AP-5 was lower in depleted than in intact animals, whereas the threshold dose of MK-801 was lower in monoaminergically intact than monoamine-depleted mice. The locomotor effects of AP-5 and the AMPA-kainate receptor antagonist CNQX were registered in monamine-depleted mice after local application in the accumbens or entopeduncular nucleus (= medial pallidum). Both AP-5 and CNQX stimulated locomotor activity in the accumbens, but had no effects in the entopeduncular nucleus. We have previously shown synergistic interactions with regard to locomotor stimulation in monoamine-depleted mice, between an NMDA antagonist and an alpha 2-adrenoceptor agonist or a dopamine D1 agonist (all drugs given systemically). In the present study the alpha 2-adrenoceptor agonist alpha-methylnoradrenaline was applied intracerebrally in combination with a subthreshold dose of MK-801 given intraperitoneally: Locomotor stimulation was produced after alpha-methyl-noradrenaline injection into the accumbens nucleus, but not after injection into the dorsal striatum, prefrontal cortex or thalamus. Likewise, local application of the D1 agonist SKF 38393, in combination with a subthreshold dose of MK-801 given intraperitoneally, point to an important role of the accumbens nucleus in motor control. Previous experiments based on systemic drug administration have also shown a synergistic interaction between a muscarine antagonist and an alpha 2-adrenoceptor agonist in monoamine-depleted mice. Local application of the muscarine antagonist methscopolamine, in combination with the alpha 2-adrenoceptor agonist clonidine given intraperitoneally, showed that the striatum, in this case both the ventral and dorsal parts of the striatum, is an important target for the muscarine antagonist. Unilateral injection of AP-5 into the accumbens nucleus of mice induces rotational behaviour: Previous findings have shown that the rotation is ipsilateral in monoaminergically intact animals, whereas monoamine-depleted animals rotate contralaterally. In addition, these findings have shown that dopamine D2 receptor stimulation seems to determine whether AP-5 will induce ipsilateral or contralateral rotation. In the present study we report further evidence for a crucial role of the D2 receptor in this respect. Finally, the rotational effec","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"127-48"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271551","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669006","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":"Cortical stimulation and reflex excitability of spinal cord neurones in man.","authors":"M Sabatino,&nbsp;P Sardo,&nbsp;L Iurato,&nbsp;V La Grutta","doi":"10.1007/BF01271553","DOIUrl":"https://doi.org/10.1007/BF01271553","url":null,"abstract":"<p><p>The H reflex technique was used to evaluate the influence exerted by cortical conditioning on the excitability of the alpha-motoneurone pool and on IA interneuronal activity (reciprocal inhibition). In ten subjects at absolute rest electrical and magnetic stimulation of the motor cortex was transcranially applied during flexor carpi radialis H reflex eliciting and in conditions of reciprocal inhibition induced by radial nerve stimulation. The time courses showed that at intensities below motor threshold, electrical brain conditioning induced an increase in the amplitude of the test reflex when the cortical shock was given 4 ms after the test H reflex. On the contrary, reciprocal inhibition was reduced by electrical cortical conditioning when the scalp stimulation was applied 2-3 ms after the test stimulus. Magnetic transcranial stimulation induced an increase of H reflex amplitude when the test shock was administered 5 and 2 ms prior to the scalp shock; it did not modify the degree of reciprocal inhibition. The experimental findings could be considered the electrophysiological manifestation of a differential cortico-spinal control on the pathway alpha-motoneurone/IA interneurone. Considerations on the delay allow the hypothesis of a further synapse between the cortico-spinal ending and the IA interneurone. Discrepancies with magnetic conditioning might be ascribed to a preferential transsynaptic action of magnetic mode of neural activation.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"159-68"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271553","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19669009","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":"SPECT imaging of dopamine receptors with [123I]epidepride: characterization of uptake in the human brain.","authors":"J Kornhuber,&nbsp;T Brücke,&nbsp;P Angelberger,&nbsp;S Asenbaum,&nbsp;I Podreka","doi":"10.1007/BF01271548","DOIUrl":"https://doi.org/10.1007/BF01271548","url":null,"abstract":"<p><p>[123I]Epidepride is a new ligand for single photon emission computerized tomography (SPECT) that specifically labels D2-like dopamine receptors with very high affinity. Here, we report on the regional kinetic uptake of [123I]epidepride in the brain of 4 normal volunteers and 3 patients with choreatic movement disorders. In healthy subjects striatal activity peaked at 2.5 hours after injection of the tracer and decreased slowly thereafter. There were no significant differences between left and right brain hemispheres. Activity above background was also measurable in areas corresponding to the thalamus, temporal cortex and frontal cortex. The striatal to cerebellar ratio was about 14 after 2.5 hours and this ratio steadily increased with time. The striatal to cerebellar ratio was clearly reduced in all 3 patients with choreatic movement disorders (from about 14 in control subjects after 2.5 hours to about 7 in choreatic patients). [123I]Epidepride may be a useful SPECT ligand for studying D2 receptors in the living human brain because of its high target to background ratio, its high affinity and the possibility to investigate extrastriatal D2 receptors.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"101 1-3","pages":"95-103"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01271548","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19670335","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":"Phencyclidine-induced increases in striatal neuron firing in behaving rats: reversal by haloperidol and clozapine.","authors":"I M White,&nbsp;G S Flory,&nbsp;K C Hooper,&nbsp;J Speciale,&nbsp;D A Banks,&nbsp;G V Rebec","doi":"10.1007/BF01276506","DOIUrl":"https://doi.org/10.1007/BF01276506","url":null,"abstract":"<p><p>Amphetamine and related drugs of abuse facilitate dopamine transmission in the striatum. This action is believed to underlie the increase in firing of striatal motor-related neurons after amphetamine administration in behaving rats. The present study extended this electrophysiological investigation to phencyclidine (PCP), a nonamphetamine psychomotor stimulant that acts primarily as a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) glutamate receptors. Like amphetamine, PCP (1.0, 2.5, or 5.0 mg/kg) increased the activity of striatal motor-related neurons concomitant with behavioral activation. These effects were blocked by subsequent administration of either 1.0 mg/kg haloperidol or 20.0 mg/kg clozapine, typical and atypical neuroleptics, respectively. Dizocilpine (MK- 801), another noncompetitive NMDA antagonist, mimicked the effect of PCP. Collectively, these results indicate that amphetamine and NMDA antagonists exert comparable effects on striatal motor-related neurons, suggesting that the response of these cells to psychomotor stimulants is regulated by a dopaminergic-glutamatergic influence.</p>","PeriodicalId":77215,"journal":{"name":"Journal of neural transmission. General section","volume":"102 2","pages":"99-112"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01276506","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19720926","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}