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Biomedical subjects

K Fuxe

Publications and source records attributed to K Fuxe.

At least 541 records · Page 30Linked to original sources
PubMed1983

Effects of chronic sino-aortic denervation in male rats on regional catecholamine levels and turnover and on neuroendocrine function.

A four week sino-aortic denervation produces an increase of adrenaline (A) turnover in the anterior but not the posterior hypothalamus and a selective reduction of dopamine stores in the anterior hypothalamus. Furthermore, the mean arterial blood pressure and heart rate are unchanged in conscious animals, and a selective increase in LH secretion is observed. The activation of a compensatory vasodepressor adrenergic mechanism in the anterior hypothalamus may in part be responsible for the maintenance of a normal mean arterial blood pressure after chronic sino-aortic denervation. The neurochemical changes in the hypothalamic area may also be related to the increase in LH secretion found after chronic sino-aortic denervation.

Animals↗
PubMed1983

Subcortical limbic 3H-N-propylnorapomorphine binding sites are markedly modulated by cholecystokinin-8 in vitro.

By means of the dopamine (DA) agonist radio ligand 3H-N-propylnorapomorphine (3H-NPA) the effects of cholecystokinin-8 (CCK-8) have been evaluated in vitro on the binding characteristics of the DA agonist sites in membrane preparations from the subcortical limbic forebrain containing mainly nucleus accumbens and tuberculum olfactorium. It was shown that CCK-8 (10(-8) M) can produce a 40% increase in the KD value of the 3H-NPA binding sites and a significant 10% increase in the Bmax values of these sites. It is therefore suggested that there exist marked receptor-receptor interactions between the CCK-8 binding sites and DA agonist binding sites in the limbic forebrain. On the basis of these findings and in view of the fact that CCK peptides are comodulators in certain types of mesolimbic DNA neurons but cannot modulate DA release in these DNA synapses, the hypothesis is introduced that the presence of DA comodulators such as CCK-8 in the DA synapses makes possible a heterostatic regulation of the synapse. Thus, by means of receptor-receptor interactions, peptide comodulators may change the set point of the main transmission line without inducing homeostatic feedback responses on synthesis and release of the main transmitter, opening up a new way to modulate chemical transmission in general.

Animals↗
PubMed1983

Chronic antidepressant treatment and central 5-HT synapses.

The present studies have shown that chronic antidepressant treatment with desipramine, imipramine, zimelidine and alaproclate led to adaptive changes in both pre- and postsynaptic 5-hydroxytryptamine (5-HT) receptor mechanisms which appear to result in 5-HT sub- or supersensitivity development depending upon the 5-HT nerve terminal systems analyzed. The results underline the heterogeneity of the central 5-HT neurone systems in their responses to chronic antidepressant treatment. An involvement of 5-HT comodulators is postulated in the actions of antidepressants on central 5-HT synapses. Finally, the results point to the importance of 5-HT neurone systems as targets for the action for antidepressant drugs and they may mediate at least some of the therapeutic activity of antidepressant drugs.

Animals↗
PubMed1983

Effects of subacute treatment with toluene on central monoamine receptors in the rat. Reduced affinity in [3H]5-hydroxytryptamine binding sites and in [3H]spiperone binding sites linked to dopamine receptors.

Subacute treatment with toluene leads to a dose-related reduction of affinity in the [3H]spiperone binding sites labeling striatal dopamine (DA) receptors of the D2 type and cortical [3H]5-hydroxytryptamine (5-HT)-binding sites. It is suggested that these results represent a down regulation of activity at striatal DA and cortical 5-HT synapses, since they now may operate at higher concentrations of transmitters. The reduced affinity may be caused by the physicochemical properties of toluene leading to changes in membrane fluidity and thus in the regulation of DA and 5-HT receptors in the local circuits of the striatum and the dorsal cerebral cortex.

Animals↗
PubMed1983

Quantitative autoradiographic localization of [3H]imipramine binding sites in the brain of the rat: relationship to ascending 5-hydroxytryptamine neuron systems.

Quantitative autoradiography shows that there is a close relationship between [3H]imipramine binding sites and the distribution of 5-hydroxytryptamine (5-HT) neurons in the rat brain. High labeling is observed in the midbrain raphe nuclei, the areas of the dopamine cell groups of the substantia nigra and of the ventral tegmental area of Tsai, the ventral amygdaloid nucleus, the midline thalamic area, and parts of the hypothalmus. Thus, antidepressant drugs that have high affinity for [3H]imipramine binding sites can exert an influence at the 5-HT cell body as well as at the 5-HT nerve terminal level. The present results underline the possibility that the 5-HT and dopamine hypotheses for the mechanism of action of antidepressant drugs are not mutually exclusive, because both 5-HT and dopamine neurons can be regulated by large numbers of [3H]imipramine binding sites.

Animals↗
PubMed1983

Immobilization stress-induced changes in discrete hypothalamic catecholamine levels and turnover, their modulation by nicotine and relationship to neuroendocrine function.

Immobilization stress (1 h) induced discrete reductions in noradrenaline (NA) levels in the posterior periventricular hypothalamic region and in the paraventricular hypothalamic nucleus, and a decrease in dopamine (DA) turnover in the medial palisade zone (MPZ) of the median eminence, but failed to induce regional increases of hypothalamic NA turnover. Stress also stimulated the secretion of ACTH, corticosterone and prolactin, while vasopressin, LH and FSH serum levels were unaffected. The stress induced reduction of DA turnover in MPZ may mediate the stress induced increase of prolactin secretion. Nicotine (0.3 mg/kg, s.c., 1 h) did not by itself significantly influence catecholamine (CA) turnover in the various CA nerve terminal systems analyzed in the hypothalamus, but reduced NA levels in the subependymal layer (SEL) of the median eminence. Nicotine administration did not affect the serum levels of any of the hormones evaluated. Nicotine counteracted to a minor degree the immobilization stress-induced reduction in NA levels, and also the stress-induced secretion of ACTH, but not of prolactin suggesting the involvement of noradrenergic mechanisms possibly in the paraventricular nucleus in the nicotine modulation of stress induced increases of ACTH secretion. The nicotine-induced reduction of NA levels in SEL was blocked by stress as well as the tendency for nicotine induced increases of dopamine (DA) turnover in the medial and lateral palisade zones of the median eminence indicating opposing influences of immobilization stress and nicotine on at least some hypothalamic CA systems.

Adrenocorticotropic Hormone↗
PubMed1983

Chronic treatment with 1-dopa plus carbidopa in hemitransected rats: preferential effects at intact dopamine synapses leading to behavioural signs of dopamine receptor supersensitivity.

Chronic i.p. treatment with 1-dopa-carbidopa for 3 weeks in hemitransected male rats leads on one hand to tolerance to 1-dopa induced turning behaviour and on the other hand to behavioural and biochemical signs of dopamine (DA receptor supersensitivity on the intact side. Thus, the apomorphine induced ipsilateral turning behaviour is enhanced and the KD values of the 3H-spiperone binding sites linked to DA receptors of the D2 type on the intact, but not on the denervated side are reduced by 40%. However, the number of 3H-spiperone binding sites is reduced by 20% in striatal membranes on the intact side after this type of treatment. Therefore, chronic treatment with a catecholamine (CA) precursor leads to selective adaptive changes at intact striatal DA synapses with certain signs of the expected development of DA receptor subsensitivity, but above all with signs of paradoxical development of DA receptor supersensitivity. A hypothesis is introduced to explain these results.

Animals↗
PubMed1983

Intravenous injections of nicotine induce very rapid and discrete reductions of hypothalamic catecholamine levels associated with increases of ACTH, vasopressin and prolactin secretion.

The present findings show that nicotine given i.v. can within minutes induce increases of ACTH, vasopressin and prolactin secretion in the male rat, giving further evidence for the existence of nicotine-like cholinergic receptors involved in the regulation of these hormones. These changes were associated with rapid reductions of NA levels in the subependymal layer of the median eminence, in the nuc, dorsomedialis hypothalami and in the anterior and posterior periventricular hypothalamic area as revealed by quantitative microfluorimetrical measurements of CA fluorescence. Intraindividual correlations indicate the involvement of an inhibitory noradrenergic mechanism in the subependymal layer of the median eminence in the regulation of ACTH secretion, the involvement of noradrenergic mechanisms in the posterior periventricular area in the regulation of prolactin secretion and the involvement of dopaminergic mechanisms in the medial palisade zone of the median eminence in the regulation of prolactin secretion. A rapid rise of prolactin secretion seems to be associated mainly with a reduction of NA levels in the posterior periventricular area indicating the existence of a possible facilitatory noradrenergic mechanism in this region regulating prolactin secretion.

Adrenocorticotropic Hormone↗
PubMed1983

Gangliosides increase the survival of lesioned nigral dopamine neurons and favour the recovery of dopaminergic synaptic function in striatum of rats by collateral sprouting.

The effects of chronic ganglioside treatment GM-1 (10 mg/kg, i.p., once daily for 56 days) have been evaluated on the degenerative and regenerative features of nigrostriatal dopamine (DA) neurons following a partial lesion by tyrosine hydroxylase immunocytochemistry in combination with morphometrical analysis and by quantitative DA receptor autoradiography. Chronic GM-1 treatment resulted in the maintenance in the number of DA cell bodies, terminals and striatal area on the lesioned side and also increased dendrite length of the DA nerve cells in the zona reticulata on that side. The lesion induced DA receptor supersensitivity was counteracted by chronic treatment with GM-1 and the apomorphine induced rotational behaviour was significantly reduced. The hypothesis is introduced that following ganglioside treatment some lesioned DA nerve cells do not degenerate, but elongate their dendrites to give increased trophic support to DA cell bodies with intact DA axons. These increased dendro-dendritic interactions may enable the unlesioned DA cells to increase the density of their striatal nerve terminal networks via collateral sprouting leading to recovery of dopaminergic synaptic function as evidenced in the receptor autoradiographical and behavioural analysis. Gangliosides may therefore possibly represent a new type of drug in the treatment of Parkinson's disease and aging processes in DA systems.

Animals↗