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Biomedical subjects

K Fuxe

Publications and source records attributed to K Fuxe.

At least 397 records · Page 22Linked to original sources
PubMed1989

Some aspects of the communicational and computational organization of the brain.

Some features of the morphofunctional organization of the CNS have been analysed. Different types of hierarchical organization have been recognized, each of which could deeply affect the circulation (communicational aspect) and elaboration (computational aspect) of information. These two aspects have been discussed on the basis of the existence of two types of electrochemical transmission in the CNS: wiring and volume transmission. By evaluating the CNS operations at different levels of analysis a 'computational hierarchical organization' has been delineated. This concept is very relevant to the understanding of the 'computational power' of the brain (Agnati & Fuxe 1984, Conrad 1985a). In fact, it leads to the distinction between horizontal and vertical elaboration of information. The hypothesis is introduced that in the vertical elaboration of information a central role may be played by the neuronal membrane. In fact, this structure can not only be influenced by the extra- and intracellular signals, but also effectively interconvert the electrical coding into the chemical coding of information. These aspects are discussed in the frame of the possible organization of the membrane into 'domains', each domain being a patch of membrane in which pre-selected molecular movements are possible, resulting in molecular interactions. The movement of a molecule outside its domain is considered energetically unfavourable. The possible formal treatment of this hypothesis is mentioned in Conrad's work (1985b).

Animals↗
PubMed1989

Neurotensin modulates the binding characteristics of dopamine D2 receptors in rat striatal membranes also following treatment with toluene.

The effects of neurotensin in vitro (1-100 nM) on the binding characteristics of [3H]N-propylnorapomorphine ([3H]NPA) were analysed in striatal membrane preparations of the adult male rat. Subsequently, it was investigated whether the modulatory effects of 10 nM neurotensin on [3H]NPA binding were altered by treatment with toluene in vivo (80 p.p.m., 3 days, 6 h day-1) and in vitro (19 mumol ml-1). Displacement of [3H]NPA binding by raclopride (IC50 about 15 nM) and SCH 23390 (without effect) indicated that [3H]NPA labelled only D2 dopamine receptors in the present study. Neurotensin was found to reduce the affinity of D2 receptors with a maximum response at 10 nM. At this concentration the KD value was increased by 30-40% without any consistent changes in the number of binding sites. The modulatory effect of neurotensin remained intact also following toluene treatment in vivo and in vitro, although at a higher KD range, since toluene alone increased the KD value of [3H]NPA binding by 40-50%. Thus, the mechanisms mediating the effects of neurotensin and toluene on the D2 receptor are likely to be different. When neurotensin and toluene treatments were combined, the KD values of [3H]NPA binding were about twice as high as in non-treated controls. These additive effects may lead to a severely decreased efficiency of dopamine D2-mediated neurotransmission in vivo.

Animals↗
PubMed1988

Effects of chronic toluene exposure on central monoamine and peptide receptors and their interactions in the adult male rat.

The effects of chronic toluene exposure (CTE) (80 ppm, 6 h/day, 5 days/week, 3 months) were studied on neuropeptide and 5-hydroxytryptamine receptors, on protein phosphorylation levels and on catecholamine levels in various brain regions in the 15-month-old male rat. Behavioral parameters and serum levels of hypophyseal hormones and corticosterone were also analyzed. CTE selectively reduced [3H]neurotensin [( 3H]NT) binding in the basal layers of the orbital cortex. Instead, CTE increased the binding of [3H]etorphine in the nucleus accumbens and of [125I]vasoactive intestinal polypeptide [( 125I]VIP) in the area postrema and hypoglossal nucleus. Acute treatment with the irreversible monoamine receptor antagonist N-ethoxycarboxyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) increased the binding of [3H]NT in the orbital cortex in toluene exposed rats as compared with the reduced [3H]NT binding obtained in air exposed rats treated with EEDQ. Furthermore, the EEDQ induced increase in [125I]VIP binding in the area postrema and the hypoglossal nucleus was replaced by a reduced binding of [125I]VIP in EEDQ-treated CTE rats. CTE produced an overall increase in calcium-induced back phosphorylation and an overall decrease in cyclic adenosine monophosphate-induced back phosphorylation in the frontoparietal cortex. Noradrenaline stores tended to be reduced within various hypothalamic subnuclei and the serum prolactin levels were increased following CTE. However, no marked effects of CTE were seen on the behavioral parameters. In conclusion, the regional selectivity of CTE in disturbing [3H]NT and [125I]VIP binding may be due to the demonstrated vulnerability of monoamine-neuropeptide interactions to toluene.

Animals↗
PubMed1988

Survival of adenohypophyseal homologous transplants in the rat striatum associated with prolactin-like immunoreactivity in the surrounding neuropil of the striatum.

By means of Cresyl violet stainings and immunocytochemical studies on prolactin-, luteinizing hormone (LH)-, and adrenocorticotropin (ACTH)-like immunoreactivities evidence has been obtained that homologous adenohypophyseal transplants survive for many weeks in the rat neostriatum. Gland cells maintain their endocrine properties and appear to secrete prolactin but not ACTH and LH into the surrounding neuropil of the rat neostriatum, since it contains a strong diffuse prolactin-like immunoreactivity. The diffuse zone of prolactin-like immunoreactivity disappears following inhibition of prolactin secretion by the dopamine agonist bromocriptine. The results support the existence of volume transmission in brain and offer a model for its analysis.

Animals↗
PubMed1988

Chronic nicotine treatment counteracts the disappearance of tyrosine-hydroxylase-immunoreactive nerve cell bodies, dendrites and terminals in the mesostriatal dopamine system of the male rat after partial hemitransection.

Male Sprague-Dawley rats were partially hemitransected at the mesodiencephalic junction and treated with nicotine (nicotine hydrogen (+)-tartrate) using Alzet minipumps implanted subcutaneously. Nicotine was delivered for 2 weeks in a dose of 0.125 mg/kg/h resulting in a serum nicotine level of 50.0 +/- 5.1 ng/ml. Three other groups of rats were analyzed: hemitransected rats receiving saline treatment and sham-operated animals receiving nicotine and saline, respectively. The effects of hemitransection and nicotine rostrally as well as caudally to the lesion were evaluated with image analysis of tyrosine hydroxylase (TH)-immunoreactive (IR) nerve cell body and dendrite profiles in the rostral and caudal substantia nigra and of TH-IR nerve terminal profiles in the striatum. Adjacent sections were taken to Nissl staining. [3H]Nicotine binding in the midbrain and forebrain was studied by means of receptor autoradiography on partially hemitransected rats receiving no treatment. Catecholamine (CA) levels in the frontal cortex were measured using high-performance liquid chromatography (HPLC). Striatal dopamine (DA) function was analyzed studying apomorphine-induced (1.0 mg/kg) ipsilateral rotational behavior. The spontaneous behavior of the rats was evaluated with a hole board. Furthermore, body temperature and body weight were measured. The results demonstrated a lesion-induced disappearance of TH-IR cell body and dendrite profiles in the substantia nigra and of TH-IR nerve terminal profiles in the striatum. Similar findings were seen after Nissl staining. A significant counteraction of this disappearance was found in the nicotine-treated animals. On the lesioned animals a marked reduction of [3H]nicotine binding in the striatum and the substantia nigra was found. In the functional experiments an enhancement of the apomorphine-induced ipsilateral rotational behavior was demonstrated. The degree of rotation was positively correlated with the serum nicotine level. The study on spontaneous activity in the hole board showed a slower restoration of total activity in the hemitransected nicotine-treated rats. All these results are compatible with the hypothesis that the protective action of nicotine on the mesostriatal DA system may be due to a desensitization of excitatory nicotine cholinoceptors located on the nigral DA nerve cells, leading to a reduction of firing rate and reduced energy demands. Such an action of nicotine could be of importance for a possible anti-parkinsonian effect.

Animals↗
PubMed1988

D1- and D2-receptor antagonists induce catalepsy via different efferent striatal pathways [corrected].

The D1- and D2-receptor antagonists SCH 23390 and raclopride produced a dose-dependent catalepsy as studied by a vertical grid test in the male rat. The benzodiazepine antagonist Ro 15-1788 antagonized catalepsy induced by the D2-receptor antagonist raclopride while it failed to block the action of SCH 23390. The antimuscarinic drug scopolamine reduced and the gamma-aminobutyric acid (GABA) agonist muscimol enhanced catalepsy induced by both SCH 23390 and raclopride. The results suggest that D2-antagonist-induced catalepsy is mainly mediated via activation of the strio-pallidal GABA pathways whereas D1-receptor antagonist induced catalepsy is mainly mediated via increased activity in the nigrothalamic GABA pathways.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Galanin selectively modulates 5-hydroxytryptamine 1A receptors in the rat ventral limbic cortex.

The effects of galanin (10 nM) in vitro were analyzed on the binding characteristics of 5-hydroxytryptamine (5-HT) receptor subtypes in the ventral limbic cortex of the rat. It was found that galanin markedly decreased the Kd value of 5-HT1A binding, while there were no effects on the binding characteristics of the 5-HT1B or 5-HT2 radioligands. These results indicate that the existence of a selective intramembrane interaction between galanin receptors and 5-HT1A receptors in the rat ventral limbic cortex.

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