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Biomedical subjects

G Jonsson

Publications and source records attributed to G Jonsson.

At least 145 records · Page 8Linked to original sources
PubMed1978

Developmental plasticity of central serotonin neurons after 5,7-dihydroxytryptamine treatment.

Systemic administration of 5,7-HT to newborn rats produces an altered development of the 5-HT neurons in the central nervous system, with marked regional differences. 5,7-Hydroxytryptamine can enter the brain and elicit its neurotoxic actions after systemic administration in the neonatal stage due to an incompletely developed blood-brain barrier, which for 5,7-HT is elaborated between postnatal Days 5 and 7. Treatment with 5,7-HT at birth produces marked and permanent 5-HT denervation in the cerebral cortex and spinal cord, whereas hyperinnervation occurs in the 5-HT cell body-near regions (mesencephalon-pons-medulla). The latter effect is seen within the first week postnatally. Treatment with 5,7-HT also affects NA neurons in a similar manner, although the action is exerted preferentially on 5-HT neurons. A selective effect on 5-HT neurons can be achieved by DMI pretreatment, after which both NA and DA neurons develop normally. No signs of any interaction among growing 5-HT, NA, and DA neurons can be observed. Studies of the postsynaptic 5-HT receptor in vitro with [3H]-5-HT and [3H]LSD binding indicate that this receptor develops independently of presynaptic 5-HT nerve terminals. Neither 5-HT denervation nor 5-HT hyperinnervation was accompanied by any change in receptor-binding characteristics or receptor density. The results available are compatible with the view that the consequences for 5-HT neurons that occur after neonatal 5,7-HT administration are mainly due to a "pruning effect." The developing 5-HT neurons seem to be programmed to produce a certain quantity of nerve terminal arborizations, which they try to conserve after 5-HT-induced injury, leading to the observed rearrangement of 5-HT nerve terminals.

5,7-Dihydroxytryptamine↗
PubMed1978

Milk fever prevention.

Milk fever is a disease of increasing importance. In dairy herds its incidence has doubled since 1950; today about 8 per cent of parturitions in Swedish dairy cattle are complicated by milk fever. At the same time, the clinical picture has changed and the effectiveness of calcium therapy has been markedly reduced. Thirty to 40 per cent of cows with milk fever need more than one treatment. These trends are obvious in Sweden and Norway and have been reported from many other parts of the world. However, there are also geographical and breed differences so that these figures might not be applicable under British conditions.

Animal Feed↗
PubMed1978

Serotonin and substance P coexist i, neurons of the rat's central nervous system.

5-Hydroxytryptamine (serotonin)-containing neurons in the rat's medullary raphe and interfascicularis hypoglossi cell groups were identified by means of autoradiography following prolonged intraventricular administration of 5-hydroxy[(3)H]tryptamine, fluorescence histochemistry for the demonstration of endogenous 5-hydroxytryptamine, and microspectrofluorimetric analysis of excitation and emission spectra. Immunocytochemical methods (the unlabeled primary antibody-peroxidase antiperoxidase and indirect immunofluorescence methods) were applied with antisera to substance P in order to localize immunoreactivity in these medullary neurons. It was demonstrated that the raphe nuclei and the interfascicularis hypoglossi nucleus are heterogeneous cell groups that contain: (i) Neurons that display both an uptake-storage capacity for 5-hydroxy[(3)H]tryptamine and a formaldehyde-induced fluorescence with spectral characteristics identical to those of the 5-hydroxytryptamine fluorophor. These cells exhibit high to low fluorescence intensities without detectable substance P-like immunoreactivity. (ii) Neurons with various 5-hydroxytryptamine fluorescence intensities and intense to low degrees of substance P-like immunoreactivity. (iii) Neurons with various degrees of substance P-like immunoreactivity without detectable 5-hydroxytryptamine fluorescence or 5-hydroxy[(3)H]tryptamine uptake and storage capacity. These results indicate that some neurons contain high or low levels of only 5-hydroxytryptamine or substance P, whereas other neurons contain both 5-hydroxytryptamine and substance P in various proportions. The present findings demonstrate the presence of two putative transmitters, a biogenic amine and a polypeptide, within the same neuron in the mammalian central nervous system.

Animals↗
PubMed1978

Myoglobin.

Explore the source record for details and available documents.

Evaluation Studies as Topic↗
PubMed1978

Maxillary growth after palatal surgery. An experimental study on dogs.

Maxillary growth after unilateral closure of surgically induced defects in the hard palate in 6- to 8-week old Beagle puppies was studied. The hard palate except for a 4 mm wide strip of bone in the midline and with its overlaying oral mucoperiosteum was removed. On one side the nasal mucoperiosteum was covered with an autogenous full-thickness skin graft (side SGS) and, on the other side the raw surface (side RS) was left for secondary epithelialization. The animals were killed at 47 to 52 weeks of age. Measurements on the dried skulls of the experimental dogs showed no difference in total maxillary length between the two sides of the maxilla. However, the posterior half of the maxilla was longer in 8 dogs on side SGS and the anterior half of the maxilla was in 7 dogs long on side RS. The palatine suture was displaced towards side RS on all dogs, and the height of the nose was in all dogs greater on side SGS. There was a small consistent tendency that the overall growth was more pronounced on the side with the full-thickness skin graft. It is concluded that reducing the amount of scar tissue by covering raw surfaces with an autogenous full-thickness skin graft is one way to reduce maxillary growth impairment after palatal surgery.

Animals↗
PubMed1976

Behavioral effects of 5, 7-dihydroxytryptamine lesions of ascending 5-hydroxytryptamine pathways.

In protriptyline (25 mg/kg) pretreated rats stereotactic 5,7-dihydroxytryptamine (5,7-DHT) lesions of the medial plus laternal 5-hydroxytryptamine (5-HE) bundles in the mesencephalon increased the 5-HT fluorescence in these bundles, and reduced the in vitro uptake of [3H] 5-HT in the hypothalamus to 16% of control values after 2 mug 5,7-DHT/4mul and 12% after 4 mug 5,7-DHT/4mul, and in the cortex cerebri to 35 and 34% of control values, respectively. Selective lesion of the medial 5-HT bundle reduced [3H] 5-HT uptake both in hypothalamus and in cortex cerebri to 45-48% of control values, while selective lesion of the lateral 5-HT bundles significantly reduced [3H] 5-HT uptake only in cortex (to 73-75%). No significant change was observed in [3H] noradreanaline uptake after any injection, or in [3H] 5-HT uptake after vehicle injections. Locomotor activity in an open field 3-10 days postoperatively was significantly reduced by lesions of the medial plus lateral 5-HT bundles. 5-Hdroxytryptophan (50 mg/kg) and a peripheral decarboxylase inhibitor (MK 486, 75 mg/kg) 17 days postoperatively induced a pronounced behavioral "5-HT syndrome" in these rats with medial plus lateral lesions but not in controls. Pain sensitivity, as measured by the hot plate test, was not changed by any lesion, even when tryptophan hydroxylase was partly inhibited with alpha-propyldopacetamide (100 mg/kg). Morphine analgesia and acquisition of a one-way avoidance response also were unchanged. Apomorphine (2 mg/kg)-induced locomotor activity and stereotyped behavior, as measured in an Animex activity meter, were not significantly different from control values in the 5,7-DHT groups. It was concluded that the medial 5-JT BUNDLE INNERVATES BOTH THE HYPOTHALAMUS AND THE CORTEX CEREBRI AND THE LATERAL 5-HT bundle mainly the cortex. These ascending 5-HT neurons are involved in maintaining open field ambulation. No wupport was obtained for the view that they are involved in pain mechanisms, in morphine-induced analgesia, in apomorphine-induced motor behavior, or in one-way avoidance learning.

Afferent Pathways↗
PubMed1976

Primary treatment of prostatic carcinoma with estramustine phosphate: preliminary report.

Estramustine phosphate has been used as primary treatment in 38 patients with advanced prostatic carcinoma. Of these 38 patients 36 responded objectively to treatment, regression occurring in 10 patients with soft tissue metastases, 3 with pulmonary metastases and 3 with bony metastases. Primary cytotoxic treatment in patients with far advanced prostatic carcinoma is advocated and a randomized clinical study is suggested.

Aged↗
PubMed1976

Microfluorimetric quantitation of catecholamine fluorescence in rat median eminence. I. Aspects on the distribution of dopamine and noradrenaline nerve terminals.

Using the fluorescence histochemical technique of Falck and Hillarp, a quantitative microfluorimetric study of the catecholamine fluorescence in the median eminence has been performed. On the basis of morphologic criteria, the median eminence was subdivided into various areas from which the microfluorimetric measurements were made; the subependymal layer, the medial and lateral palisade zone of the rostral and the central and caudal region of the median eminence (for definitions of the various areas and regions, see Anatomical Subdivision). The highest fluorescence intensities were recorded from the lateral palisade zone, indicating that this area has the most dense catecholamine innervation, whereas the lowest fluorescence intensities were recorded from the subependymal layer. Dopamine-beta-hydroxylase inhibition produced by FLA-63, fusaric acid or diethyldithiocarbamate resulted in all cases in a 50-70% reduction of the catecholamine fluorescence in the subependymal layer, whereas only minute effects were observed in the lateral palisade zone. In the medial palisade zone, these treatments generally led to a substantial reduction (30-50%) of the catecholamine fluorescence. Basal hypothalamic deafferentation according to Halasz, or lesioning of the ventral catecholamine bundle, produced an almost complete disappearance of the fluorescence in the subependymal layer, while both procedures were largely ineffective in affecting the catecholamine fluorescence in the lateral palisade zone. On basal hypothalamic deafferentation the catecholamine fluorescence in the medial palisade zone was markedly reduced (40-60%), while the ventral bundle lesions were less efficient in this respect. From the present results it is suggested that the subependymal layer is mainly innervated by noradrenaline nerve terminals and the lateral palisade zone is mainly innervated by dopamine nerve terminals, whereas the medial palisade zone receives a mixed innervation of dopamine and noradrenaline terminals, the dopamine proportion being in the order of 50-75% of total catecholamine content.

Animals↗
PubMed1976

Microfluorimetric quantitation of catecholamine fluorescence in rat median eminence. II. Turnover changes in hormonal states.

Catecholamine nerve terminals in the rat median eminence have been studied using the fluorescence histochemical technique of Falck and Hillarp in combination with quantitative microfluorimetry. The catecholamine fluorescence intensities recorded from various parts of the median eminence were all found to be within the linear part of the dopamine or noradrenaline concentration-fluorescence relationship as studied in an agar-albumin model system. The catecholamine fluorescence was also found to disappear with time in an exponential manner following tyrosine hydroxylase inhibition produced by alpha-methyl-p-tyrosine methylester (H44/68). Similar results were obtained when measuring the dopamine decline by mass fragmentography in the median eminence after H44/68 treatment. These results and analysis of fluorescence frequency histograms strongly indicate that the catecholamine fluorescence values recorded are proportional to the catecholamine concentration. It is concluded that the microfluorimetric technique used is a reliable method for catecholamine quantitation in discrete nerve terminal areas of the median eminence. The main advantages of the technique are that a high sensitivity and quantitative data on the transmitter content can be obtained in strict relation to the neuroanatomy. Measurement of the catecholamine fluorescence disappearance after H44/68 was used to evaluate catecholamine turnover during various endocrine states. The results showed that two dopamine systems with different transmitter turnover may be distinguished. Tuberinfundibular dopamine neurons projecting to the lateral palisade zone were thus shown to have a slower turnover than those projecting medially to the capillary loops. No definite changes in catecholamine turnover were observed after adrenalectomy and castration in the male, although there was a tendency toward increased noradrenaline turnover in both states. During pregnancy an increase in noradrenaline as well as dopamine turnover was noted. The present results therefore give further evidence for the view that catecholamine nerve terminals in the median eminence may participate in the regulation of gonadotrophin secretion.

Adrenalectomy↗
PubMed1976

Resistance of central phenylethanolamine-n-methyl transferase containing neurons to 6-hydroxydopamine.

The effects of the catecholamine neurotoxin 6-hydroxydopamine on phenylethanolamine-N-methyl transferase (PNMT) in rat brain has been investigated by biochemical and immunohistochemical analysis. 6-Hydroxydopamine was administerered either intracisternally to adult rats or systemically to newborn rats, treatments known to affect markedly central noradrenaline neurons. None of these treatments had any significant effect on the PNMT activity in the hypothalamus, pons-medulla and the spinal cord, as measured in vitro using a radiometric assay. The neonatal 6-hydroxydopamine treatment, which produced an almost complete noradrenaline denervation in the spinal cord, had no notable effect on the specific PNMT immunofluorescence localized in nerve terminals in the spinal cord. Transection of the spinal cord led to an almost complete disappearance of the PNMT activity and the specific immunofluorescence below the transection, pointing to the existence of a descending PNMT containing pathyway in the spinal cord. The present results show that the PNMT neurons are resistant to the neurotoxic action of 6-hydroxydopamine, possibly due to lack of catecholamine uptake mechanism or due to these neurons having an uptake mechanism with a low affinity for 6-OH-DA. Furthermore, the data support the view that the noradrenaline and PNMT containing neurons constitute separate neuron systems.

Adrenergic Fibers↗
PubMed1976

Studies on the mechanisms of 6-hydroxydopamine cytotoxicity.

The uptake-accumulation and binding of radioactivity in mouse heart after administration of the catecholamine neurotoxin [3H]6-hydroxydopamine (6-OH-DA, 1 or 3 mg/kg, i.v.) has been investigated. It was confirmed that a substantial portion (8--20%) of the radioactivity taken up and retained by the heart could not be extracted with perchloric acid, in all probability representing covalently bound oxidation products of 6-OH-DA to tissue proteins. Pharmacological analysis showed that a large part of this fraction was associated with the adrenergic nerves. The time-course of the perchloric acid resistant binding to the adrenergic nerves was found to parallel that of the neurotoxic action of 6-hydroxydopamine as evaluated by monitoring the change in [3H]noradrenaline uptake. Calculation of the intranelronal 6-hydroxydopamine concentration (average) needed to induce degeneration showed it to be in the order of 50 mM. The binding ratio for tritium deriving from [3H]6-OH-DA between the intraneuronal and extraneuronal compartments was found to be 10,000 to 30,000, pointing to a very high neuronal specificity for 6-hydroxydopamine. The 'covalent' binding of oxidation products of [3H]6-OH-DA was considerably reduced after desipramine or 1-phenyl-3(2-thiazolyl)-2-thiourea administration, treatments both known to protect the adrenergic nerves from undergoing degeneration. Conversely it was found that the binding increased during conditions known to potentiate the neurotoxic action of 6-hydroxydopamine, e.g., after monoamine oxidase inhibition with nialamide. Subcellular fractionation studies indicated that the predominant site of interaction between 6-hydroxydopamine oxidation products and neuronal proteins is the cytoplasm and the axonal membrane. Analysis of the effect in vivo administration of 6-hydroxydopamine on the field-stimulated induced release of [3H]noradrenaline previously taken up in the adrenergic nerves showed a 6-hydroxydopamine indiced reduction in [3H]noradrenaline release which was approximately proportional to the reduction in the number of nerve terminals. These findings further support the view that 6-hydroxydopamine acts largely in an "all-or-none' fashion with respect to the neurodegenerative action. Administration of [3H]dopamine also resulted in a fraction which was not extractable with perchloric acid, although this fraction was very small compared to that found after an equal dose of [3H]6-hydroxydopamine. These data may indicate that oxidation products of dopamine can interact with tissue proteins. From the present results it can be concluded that there is a close relationship between 'covalent' binding of 6-hydroxydopamine oxidation products to neuronal elements and the cytotoxic action of 6-hydroxydopamine, indicating that this binding may play an important role in the neurodegenerative action of 6-hydroxydopamine on catecholamine neurons.

Adrenergic Fibers↗