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116 results on '"Fuxe K."'

10. Interactions among adenosine deaminase, adenosine A1 receptors and dopamine D1 receptors in stably cotransfected fibroblast cells and neurons

Author

Torvinen, M, primary, Ginés, S, additional, Hillion, J, additional, Latini, S, additional, Canals, M, additional, Ciruela, F, additional, Bordoni, F, additional, Staines, W, additional, Pedata, F, additional, Agnati, L.F, additional, Lluis, C, additional, Franco, R, additional, Ferré, S, additional, and Fuxe, K, additional

Published
2002
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36. On the distribution patterns of D1, D2, tyrosine hydroxylase and dopamine transporter immunoreactivities in the ventral striatum of the rat

Author

Jansson, A., Goldstein, M., Tinner, B., Zoli, M., Meador-Woodruff, J.H., Lew, J.Y., Levey, A.I., Watson, S., Agnati, L.F., and Fuxe, K.

Abstract

The distribution of dopamine D1 and D2 receptor immunoreactivities in the nucleus accumbens and the olfactory tubercle of adult and postnatal male rats were compared with the distribution of tyrosine hydroxylase and dopamine transporter immunoreactivities. An overall co-distribution of D1 and D2 receptor immunoreactivities with tyrosine hydroxylase immunoreactivity was found in the nucleus accumbens and the olfactory tubercle. However, the major finding in this study was, following a more detailed analysis in coronal sections of the shell part of the nucleus accumbens, the existence of nerve cell patches of strong D1 receptor immunoreactivity associated with low D2 receptor, dopamine transporter and tyrosine hydroxylase immunoreactivities. These patches were mainly surrounded by areas of strong D2 receptor, tyrosine hydroxylase and dopamine transporter immunoreactivities and could be found also in the olfactory tubercle. Similar observations were made in postnatal rats. Serial reconstructions of the patches of strong D1 receptor immunoreactivity in the rostrocaudal direction were made. The patches formed a continuous tubular nerve cell system in the shell part of the nucleus accumbens. Since this nerve cell system was found to be surrounded by a high density of dopamine terminals, it may represent a compartment where dopamine transmission mainly acts on D1 receptors via local diffusion (i.e. via volume transmission). However, it must be noted that the D1 receptor rich patches constitute only a small fraction of the nucleus accumbens and the overall density of tyrosine hydroxylase immunoreactive terminals correlates with the density of both D1 and D2 receptors in the nucleus accumbens.

Published
1998
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38. Increased potency of neuropeptide y to antagonize α2-adrenoceptor function in the nucleus tractus solitarii of the spontaneously hypertensive rat

Author

Yang, S.-N, Fior, D.R, Hansson, A.C, Cintra, A, Castellano, M, Ganten, U, Ganten, D, Agnati, L.F, and Fuxe, K

Abstract

The regulation by neuropeptide Y of α2-adrenoceptors in the nucleus tractus solitarii was evaluated in the adult normotensive Wistar Kyoto rat and the adult spontaneously hypertensive rat. The microinjection of a submaximal dose of l-noradrenaline (800pmol in 50nl) alone into the nucleus tractus solitarii produced a significant reduction in the mean arterial blood pressure in either strain. The threshold dose (1pmol in 50nl) of neuropeptide Y(1–36) for the vasodepressor response in the Wistar Kyoto rat was five times higher than that (0.2pmol in 50nl) in the spontaneously hypertensive rat. Furthermore, neuropeptide Y(1–36) at 0.2pmol in 50nl could significantly counteract the vasodepressor response to l-noradrenaline (800pmol in 50nl) in the spontaneously hypertensive rat, but not in the Wistar Kyoto rat, in which 1pmol in 50nl of neuropeptide Y(1–36) must be employed to counteract the vasodepressor response to l-noradrenaline (800pmol in 50nl), although the vasodepressor responses are of a similar magnitude. The in situhybridization and quantitative receptor autoradiographical experiments showed that the α2A-adrenoceptor messenger RNA levels and the Bmaxvalue of the α2-adrenoceptor agonist [3H]p-aminoclonidine binding sites measured in the nucleus tractus solitarii of the spontaneously hypertensive rat were substantially lower than those in the Wistar Kyoto rat. The quantitative receptor autoradiographical results were consistent with the cardiovascular results and showed that in the spontaneously hypertensive rat, neuropeptide Y(1–36) at 1nM led to a significant increase in the Kdvalue of [3H]p-aminoclonidine binding sites. In the Wistar Kyoto rat, neuropeptide Y(1–36) produced this effect only at 10nM. The present study provides evidence for an increase of the potency of neuropeptide Y(1–36) to antagonistically modulate α2-adrenoceptors in the nucleus tractus solitarii of the spontaneously hypertensive rat. This enhanced antagonistic action may partly be related to a reduction in the number of α2A-adrenoceptors in the nucleus tractus solitarii of the spontaneously hypertensive rat, since a decrease has been observed in the α2A-adrenoceptor messenger RNA levels and the α2-adrenoceptor binding sites in the spontaneously hypertensive rat.

Published
1997
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41. Morphometrical and microdensitometrical studies on phenylethanolamine-N-methyltransferase- and neuropeptide Y-immunoreactive nerve terminals and on glucocorticoid receptor-immunoreactive nerve cell nuclei in the paraventricular hypothalamic nucleus in adult and old male rats

Author

Zoli, M., primary, Agnati, L.F., additional, Fuxe, K., additional, Zini, I., additional, Pich, E. Merlo, additional, Grimaldi, R., additional, Härfstrand, A., additional, Goldstein, M., additional, Wikström, A.C., additional, and Gustafsson, J.-Å., additional

Published
1988
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44. Morphometrical evidence for a complex organization of tyrosine hydroxylase-,enkephalin- and darpp-32-like immunoreactive patches and their codistribution at three rostrocaudal levels in the rat neostriatum

Author

Agnati, L.F., primary, Fuxe, K., additional, Zoli, M., additional, Ferraguti, F., additional, Benfenati, F., additional, Ouimet, C.C., additional, Walaas, S.I., additional, Hemmings, H.C., additional, Goldstein, M., additional, and Greengard, P., additional

Published
1988
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46. Distribution of dopamine D2-like receptors in the rat amygdala and their role in the modulation of unconditioned fear and anxiety

Author

de la Mora, M. Perez, Gallegos-Cari, A., Crespo-Ramirez, M., Marcellino, D., Hansson, A.C., and Fuxe, K.

Subjects
*DOPAMINE receptors, *AMYGDALOID body, *LABORATORY rats, *FEAR, *CONDITIONED response, *ANXIETY
Abstract

Abstract: Amygdaloid dopamine D2 receptors play an important role in the modulation of fear/anxiety. Their topographical distribution within the amygdala is however unclear, and their role in unconditioned fear/anxiety remains largely unknown. The aim of this paper was to study the intra-amygdaloid distribution of D2 receptors and to ascertain their role in unconditioned anxiety. Chemical anatomical studies in the rat, using D2 and D3 in situ hybridization, quantitative receptor autoradiography with either [3H]raclopride or [125I]sulpiride, and D2-like immunocytochemistry showed that the highest density of dopamine D2 receptors is present in the central amygdaloid nucleus, particularly within its latero-capsular division, in which a D2 but not a D3 mRNA signal was observed. However, although at considerably reduced densities dopamine D2 receptors were also found in other locations within the amygdala, including the basolateral nucleus. Behaviorally, the infusion of raclopride (0.75–4 μg/side) in the area of the central amygdaloid nucleus resulted at low doses in the appearance of anxiogenic-like effects in the Shock-Probe Burying test, whereas no effects of raclopride treatment were found at any dose in the Elevated Plus-Maze and the Open-Field test. Our results indicate that amygdaloid dopamine D2-like receptors have a topographically differentiated distribution within the rat amygdala, the major location being in the central amygdaloid nucleus. D2-like receptors play a role in the modulation of anxiety responses involving a potential differential function of D2-like receptors in the central amygdaloid nucleus versus the basolateral amygdaloid nucleus. [Copyright &y& Elsevier]

Published
2012
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47. Cellular localization and distribution of dopamine D4 receptors in the rat cerebral cortex and their relationship with the cortical dopaminergic and noradrenergic nerve terminal networks

Author

Rivera, A., Peñafiel, A., Megías, M., Agnati, L.F., López-Téllez, J.F., Gago, B., Gutiérrez, A., de la Calle, A., and Fuxe, K.

Subjects
*NEUROTRANSMITTERS, *CEREBRAL cortex, *AMINO acids, *NUCLEAR physics
Abstract

Abstract: The role of the dopamine D4 receptor in cognitive processes and its association with several neuropsychiatric disorders have been related to its preferential localization in the cerebral cortex. In the present work we have studied in detail the regional and cellular localization of the dopamine D4 receptor immunoreactivity (IR) in the rat cerebral cortex and its relationship to the dopaminergic and noradrenergic nerve terminal networks, since both dopamine and noradrenaline have a high affinity for this receptor. High levels of D4 IR were found in motor, somatosensory, visual, auditory, temporal association, cingulate, retrosplenial and granular insular cortices, whereas agranular insular, piriform, perirhinal and entorhinal cortices showed low levels. D4 IR was present in both pyramidal and non-pyramidal like neurons, with the receptor being mainly concentrated to layers II/III. Layer I was observed to be exclusively enriched in D4 IR branches of apical dendrites. Finally, mismatches were observed between D4 IR and tyrosine hydroxylase and dopamine β-hydroxylase IR nerve terminal plexuses, indicating that these receptors may be activated at least in part by dopamine and noradrenaline operating as volume transmission signals. The present findings support a major role of the dopamine D4 receptor in mediating the transmission of cortical dopamine and noradrenaline nerve terminal plexuses. [Copyright &y& Elsevier]

Published
2008
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48. Interactions among adenosine deaminase, adenosine A1 receptors and dopamine D1 receptors in stably cotransfected fibroblast cells and neurons

Author

Torvinen, M., Ginés, S., Hillion, J., Latini, S., Canals, M., Ciruela, F., Bordoni, F., Staines, W., Pedata, F., Agnati, L.F., Lluis, C., Franco, R., Ferré, S., and Fuxe, K.

Subjects
*ADENOSINE deaminase, *DOPAMINE receptors, *FIBROBLASTS
Abstract

The role of adenosine deaminase in the interactions between adenosine A1 and dopamine D1 receptors was studied in a mouse fibroblast cell line stably cotransfected with human D1 receptor and A1 receptor cDNAs (A1D1 cells). Confocal laser microscopy analysis showed a high degree of adenosine deaminase immunoreactivity on the membrane of the A1D1 cells but not of the D1 cells (only cotransfected with human D1 receptor cDNAs). In double immunolabelling experiments in A1D1 cells and cortical neurons a marked overlap in the distribution of the A1 receptor and adenosine deaminase immunoreactivities and of the D1 receptor and adenosine deaminase immunoreactivities was found. Quantitative analysis of A1D1 cells showed that adenosine deaminase immunoreactivity to a large extent colocalizes with A1 and D1 receptor immunoreactivity, respectively. The A1 receptor agonist caused in A1D1 cells and in cortical neurons coaggregation of A1 receptors and adenosine deaminase, and of D1 receptors and adenosine deaminase. The A1 receptor agonist-induced aggregation was blocked by R-deoxycoformycin, an irreversible adenosine deaminase inhibitor. The competitive binding experiments with the D1 receptor antagonist [3H]SCH-23390 showed that the D1 receptors had a better fit for two binding sites for dopamine, and treatment with the A1 receptor agonist produced a disappearance of the high-affinity site for dopamine at the D1 receptor. R-Deoxycoformycin treatment, which has previously been shown to block the interaction between adenosine deaminase and A1 receptors, and which is crucial for the high-affinity state of the A1 receptor, also blocked the A1 receptor agonist-induced loss of high-affinity D1 receptor binding.The conclusion of the present studies is that the high-affinity state of the A1 receptor is essential for the A1 receptor-mediated antagonistic modulation of D1 receptors and for the A1 receptor-induced coaggregates of A1 and adenosine deaminase, and of D1 and adenosine deaminase. Thus, the confocal experiments indicate that both A1 and D1 receptors form agonist-regulated clusters with adenosine deaminase, where the presence of a structurally intact adenosine deaminase bound to A1 receptors is important for the A1–D1 receptor–receptor interaction at the level of the D1 receptor recognition. [Copyright &y& Elsevier]

Published
2002
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49. Transcription factor gene expression profiling after acute intermittent nicotine treatment in the rat cerebral cortex

Author

Kjell Fuxe, Giuseppe Amato, Giuseppa Mudò, Wolfgang H. Sommer, P.-A. Olsson, Natale Belluardo, BELLUARDO N, OLSSON PA, MUDO' G, SOMMER WH, AMATO G, and FUXE K

Subjects
Male, Nicotine, Gene Expression, Biology, Neuroprotection, Cerebral Cortex/drug effect, Neurotrophic factors, medicine, Animals, Nicotinic Agonists, Rats, Wistar, In Situ Hybridization, Oligonucleotide Array Sequence Analysis, Cerebral Cortex, Microarray analysis techniques, Gene Expression Profiling, General Neuroscience, Rats, Gene expression profiling, Nicotinic agonist, Nicotine/pharmacology Nicotinic Agonists, biology.protein, Gene Expression/drug effect, Immediate early gene, Neuroscience, Transcription Factors, medicine.drug, Neurotrophin
Abstract

Several studies in different in vitro and in vivo models have demonstrated neuroprotective effects of nicotinic receptor agonists and indirect trophic actions of nicotine on brain are suggested from observations describing nicotine as a cognitive enhancer by increasing vigilance and improving learning and memory. While an increasing number of studies have given evidence of neuroprotective and neurotrophic effects of nicotine treatment, the molecular mechanism mediating the neurotrophic effects of nicotine are not fully understood. Previously in an analysis of several neurotrophic factors as possible mediators of nicotine-induced neuroprotection and/or neurotrophic effects we could reveal that an acute intermittent nicotine treatment increases fibroblast growth factor-2 mRNA and protein in several brain regions of rat brain. Even if other studies have demonstrated in different paradigms that nicotine administration modulates expression level of a variety of genes, there is still a lack of indication which candidate genes, involved in neuroprotective responses are modulated by nicotine. In the present work we have used a microarray assay to further find and characterize new genes responsive to acute intermittent nicotine treatment and linked to neuroprotection. Therefore, we used Rat Genome U34A Affymetrix GeneChip arrays containing about 8800 probe sets to characterize transcriptional responses in the rat parietal cortex after acute intermittent nicotine treatment. We focused our attention to expression of transcription factors and several of them were up- or down-regulated by nicotine, among these Nr4a1 (Nurr77), Egr-1 and Egr-2. In situ hybridization was used to corroborate the microarray data and to reveal further spatial and temporal patterns of these nicotine induced genes. Taken together the present results identified several novel candidate genes modified by acute intermittent nicotine exposure and as such potentially involved in neuroprotective-neurotrophic actions.

Published
2005

50. Evidence for a differential cholecystokinin-B and -A receptor regulation of gaba release in the rat nucleus accumbens mediated via dopaminergic and cholinergic mechanisms

Author

Luca Ferraro, U Ungerstedt, X. M. Li, Sergio Tanganelli, Kjell Fuxe, Roberto Rimondini, Lorenzo Beani, William T. O'Connor, Ferraro L., O'Connor W.T., Li X.-M., Rimondini R., Beani L., Ungerstedt U., Fuxe K., and Tanganelli S.

Subjects
Male, medicine.medical_specialty, receptor binding, Dopamine, Microdialysis, anaesthetized rat, Striatum, Nucleus accumbens, Cholecystokinin receptor, Nucleus Accumbens, microdialysi, Rats, Sprague-Dawley, Dopamine receptor D1, Parasympathetic Nervous System, Internal medicine, Dopamine receptor D2, medicine, Animals, receptor-receptor interaction, gamma-Aminobutyric Acid, Cholecystokinin, Chemistry, General Neuroscience, digestive, oral, and skin physiology, Receptor, Cholecystokinin B, cholecystokinin, Rats, Receptor, Cholecystokinin A, Endocrinology, Dopamine receptor, microdialysis, Cholecystokinin B receptor, Receptors, Cholecystokinin, hormones, hormone substitutes, and hormone antagonists
Abstract

In the present study we characterized the cholecystokinin receptor regulation of (i) the dopamine D2 agonist binding sites in striatal sections including the nucleus accumbens and (ii) GABA and dopamine release in the central part of the rat nucleus accumbens, by combining the in vitro filter wipe-off and the in vivo microdialysis techniques. In the binding study we demonstrate that sulphated cholecystokinin octapeptide (1 nM) increased (219 +/- 30%) the KD value of the D2 agonist [3H]N-propylnorapomorphine binding sites in sections from the striatum including the accumbens. This effect was counteracted by the cholecystokinin-B antagonist PD134308 (50 nM). In a parallel study using microdialysis in the central nucleus accumbens, we found that local perfusion with sulphated cholecystokinin octapeptide (1 microM) induced an increase in GABA (135 +/- 7%) and dopamine (146 +/- 8%) release which was unaffected by the cholecystokinin-A antagonist L-364,718 (10 nM). In contrast, when the cholecystokinin-B antagonist PD134308 (10 nM) was co-perfused with the peptide it prevented the increase in dopamine and decreased GABA release (-24 +/- 2%). This reduction was counteracted by the addition to the perfusate medium of the cholecystokinin-A antagonist or the cholinergic muscarinic M2 receptor antagonist AF-DX 116 (0.1 microM). Taken together, these data demonstrate that the facilitation by sulphated cholecystokinin octapeptide of GABA and dopamine release in the central accumbens probably reflects an inhibitory effect of the peptide on both pre- and postsynaptic D2 receptors, mediated via cholecystokinin-B receptor activation. In addition, for the first time we provide evidence for a differential cholecystokinin-A and -B receptor-mediated regulation of GABA transmission in the central accumbens, where the cholecystokinin-B receptor exerts a dominant excitatory influence while the cholecystokinin-A receptor mediates an inhibition of GABA release via a local muscarinic M2 receptor.

Published
1996

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