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Biomedical subjects

G von Euler

Publications and source records attributed to G von Euler.

68 records · Page 4Linked to original sources
PubMed1989

Pertussis toxin treatment counteracts the cardiovascular effects of neuropeptide Y and clonidine in the awake unrestrained rat.

The role of G-proteins in the mediation of the cardiovascular effects of neuropeptide Y and the alpha 2-adrenoceptor agonist clonidine was investigated by injections of pertussis toxin (10 micrograms/30 microliters, i.v.t., 24 h) in the awake unrestrained male rat. Treatment with pertussis toxin was found to inhibit the hypotensive and bradycardic actions of neuropeptide Y (1250 pmol) and the hypotensive actions of clonidine (1875 pmol). Control experiments showed that treatment with pertussis toxin caused an approximately 50% reduction in the back-ADP-ribosylation of GTP-binding proteins. These results suggest that G-proteins mediate the central cardiovascular actions of neuropeptide Y and clonidine.

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

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↗
PubMed1988

Effects of toluene treatment in vivo and in vitro on the binding characteristics of [3H]neurotensin in rat striatal membranes.

The effects of treatment with toluene in vivo (80 ppm, 3 days, 6 h/day) and in vitro (19 mumol/ml) were analyzed on the binding characteristics of [3H]neurotensin in rat striatal membranes. Exposure to toluene in vivo did not produce any significant effects on the binding characteristics of [3H]neurotensin. However, the addition of toluene in vitro caused a trend for a decreased Bmax value and produced a significantly reduced KD value of [3H]neurotensin binding. The absence of effects at 80 ppm indicates that the neurotensin receptor is relatively insensitive to toluene exposure, in contrast to, e.g. the dopamine agonist binding sites. Furthermore, the toluene response of the neurotensin receptor, as seen after treatment in vitro, is different from the responses seen in many monoamine receptors, which show decreased affinities following toluene exposure. It is possible that toluene is mediating its effects on the neurotensin receptor by changing the lipid micro-environment in which the receptor is situated. Another explanation would be that toluene selectively acts on the monoamine receptors, e.g. the more sensitive dopamine receptors, which through receptor-receptor interactions would cause the response seen in the neurotensin receptor. However, it cannot be excluded that the suggested receptor-receptor interaction itself is affected by toluene.

Administration, Inhalation↗
PubMed1988

Toluene induces changes in the morphology of astroglia and neurons in striatal primary cell cultures.

Toluene (4.7-150) mumol per ml) was added for 30 or 60 min to astroglial and neuronal primary cell cultures from rat striatum and changes in cell morphology were analyzed by light microscopy. After 60 min incubation in 40 mumol toluene/ml, the cell bodies of the astrocytes appeared contracted, and their processes and nuclei were clearly visible. At higher doses of toluene the astrocytes seemed to be flattened and major cell damage was visualized by the uptake of vital dyes. The neurons, however, became affected and judged by morphological criteria only at the higher toluene doses. In conclusion, toluene induced morphological changes in primary astrocyte cultures and also in primary neuronal cultures at higher toluene concentrations.

Animals↗
PubMed1988

Effects of acute haloperidol treatment on regional catecholamine levels and utilization in rats exposed to toluene.

The aim of the present investigation was to evaluate whether the responses of central catecholamine (CA) neurons to CA receptor blockade by haloperidol are altered upon toluene exposure. Male rats were exposed to air or toluene (80 ppm) for 5 and 4 days, 6 h day-1. CA levels and utilization were determined in discrete regions of the forebrain and hypothalamus as well as in the substantia nigra (SN) and anteromedial frontal cortex (AMFC). Serum levels of corticosterone, thyroid stimulating hormone, luteinizing hormone and prolactin were determined by radioimmunoassay procedures. Toluene exposure led to increased dopamine (DA) utilization in the AMFC and increased CA utilization in the paraventricular hypothalamic nuclei. In air-exposed rats haloperidol (1 mg kg-1, i.p., 2 h before killing) increased DA utilization in the marginal part of the nucleus caudatus putamen (CAUD). In toluene-exposed rats, haloperidol induced significant depletions of DA stores in the SN and in the medial and central parts of the CAUD. In the posterior nucleus accumbens (ACC) DA utilization was significantly increased. Combined haloperidol and toluene treatment selectively decreased DA levels in the ACC and SN, and significantly increased DA utilization in the CAUD, as compared with the air-exposed control group. Furthermore, after combined treatment, there was a specific increase in noradrenaline (NA) utilization in the SN and in CA utilization in the medial palisade zone of the median eminence. Serum prolactin levels were substantially raised in both the air and toluene groups after the haloperidol treatment. In conclusion, acute haloperidol treatment preferentially reduces DA levels and increases DA and NA utilization in the SN and in discrete tel- and diencephalic areas in rats exposed to toluene.

Animals↗
PubMed1988

Pre- and postsynaptic features of the central angiotensin systems. Indications for a role of angiotensin peptides in volume transmission and for interactions with central monoamine neurons.

The transmitter receptor matches and mismatches in the angiotensin (ANG) immunoreactive (IR) neuronal systems of the rat CNS have been characterized in various regions by means of ANG II immunocytochemistry and 125I-angiotensin II receptor autoradiography. By means of in situ hybridization the distribution of angiotensinogen mRNA has been mapped out and related to the distribution of ANG IR. In some areas, high densities of ANG IR nerve terminals and ANG II receptors (e.g. paraventricular hypothalamic nucleus, locus coeruleus and nucleus tractus solitarius) or high densities of ANG II receptors alone (e.g. medial geniculate body, subthalamic nucleus and superficial layer of the superior collicle) were often associated with high levels of angiotensinogen mRNA, suggesting the existence of an extracellular formation of ANG II, mediating biological responses. These results underline a role of ANG peptides in volume transmission in addition to transmitter function. Other areas, such as nuc. n. hypoglossi, practically lacking ANG IR terminals, pericarya and receptors, also contained high levels of angiotensinogen mRNA, suggesting a different role of angiotensinogen in these areas. Evidence for presynaptic (turnover changes) and post-synaptic (receptor-receptor crosstalk) interactions with CA neuronal systems has been obtained especially in cardiovascular centers. Thus, ANG II reduces in a concentration related way the affinity of 3H-paraminoclonidine binding sites in the dorsomedial medulla without influencing the Bmax value. These results indicate the existence of intramembrane interactions between ANG II and alpha 2 adrenergic receptors. Finally paraventricular but not perifornical ANG immunoreactive nerve cells costore nuclear glucocorticoid receptor IR, suggesting that some ANG neurons may be directly regulated by glucocorticoids.

Angiotensin II↗
PubMed1987

Ganglioside GM1 treatment prevents the effects of subacute exposure to toluene on N-[3H]propylnorapomorphine binding characteristics in rat striatal membranes.

The effects of ganglioside GM1 treatment (10 mg/kg, i.p., 3 days, once daily) were analyzed on N-[3H]propylnorapomorphine ([3H]NPA) binding characteristics in striatal membrane preparations from air or toluene (80 ppm, 3 days, 6 h/day) exposed adult male rats. It was found that toluene exposure induced increased Kd and Bmax values for [3H]NPA binding. These changes could be blocked by GM1 treatment, which by itself had no significant effects on the binding characteristics of [3H]NPA. The addition of toluene (9.3 mumol/ml) in vitro had similar effects on [3H]NPA binding characteristics as toluene exposure in vivo. These results indicate that the effects of toluene exposure on dopamine receptors are due to an alteration of membrane fluidity which is prevented by GM1 treatment.

Animals↗
PubMed1987

Chronic imipramine treatment reduces (+)2-[125I]iodolysergic acid, diethylamide but not 125I-neuropeptide Y binding in layer IV of rat cerebral cortex.

The effects of chronic oral (2 X 10 mumol/kg, twice daily for 14 days) imipramine treatment on (+)2-[125I]-iodolysergic acid, diethylamide (125I-LSD) and 125I-neuropeptide Y (125I-NPY) receptor binding were examined in rat cerebral cortex by quantitative receptor autoradiography. A 35% reduction of 125I-LSD binding was observed in layer IV, both in the frontal and occipital cortex, while there was no significant change in 125I-NPY binding. The observed decrease in 125I-LSD binding is probably due to a reduction in the density of 5-hydroxytryptamine (5-HT) receptors of the 5-HT2 type. This reduction may represent a disturbance in the 5-HT synapses, regulating the transmission of the specific afferents innervating layer IV of the cerebral cortex.

Animals↗
PubMed1987

Effects of subacute treatment with toluene on cerebrocortical alpha- and beta-adrenergic receptors in the rat. Evidence for an increased number and a reduced affinity of beta-adrenergic receptors.

Subacute treatment with toluene (80-1500 p.p.m.) produces a dose-dependent reduction of affinity and increase in density of the beta-adrenergic antagonist [3H]dihydroalprenolol binding sites in the frontoparietal cortex of the male rat, while the binding characteristics of alpha 1-adrenergic ([3H]WB 4101) and alpha 2-adrenergic ([3H]p-aminoclonidine) binding sites in the same region is unaffected by this treatment as evaluated in vitro. Therefore, it is suggested that the cortical beta-adrenergic receptors are particularly vulnerable to the action of toluene in vivo. It is speculated that as a result cortical beta-adrenergic neurotransmission may be altered following exposure to low concentrations of toluene, possibly related to the physico-chemical properties of toluene, leading to changes in membrane fluidity.

Animals↗