Search PubMed⌕ Search

Biomedical subjects

J Koenig

Publications and source records attributed to J Koenig.

At least 91 records · Page 5Linked to original sources
PubMed1982

[In vitro study of the action of isaxonine on the growth of rat spinal cord neurons (author's transl)].

Dissociated spinal cord cells were cultured in appropriate culture medium. In these conditions the cell bodies tended to emit neurites and to interconnect. Grown with isaxonine, spinal cord neurons form larger aggregates, neurites number is higher, connection between cellular groups is more larger, and branching of neurites is more distal. Future research will try to verify the assumption of an increase in neuromuscular contacts under the influence of isaxonine.

Animals↗
PubMed1982

The effects of neurotensin on anterior pituitary hormone secretion.

The present experiments were conducted to determine the effects of neurotensin on secretion of a variety of anterior pituitary hormones. Conscious rats with indwelling cannulae in the third ventricle and external jugular vein were used and the effects on plasma hormone levels measured by radioimmunoassay. Neurotensin was found to decrease plasma prolactin levels in ovariectomized females, normal males, and males in which prolactin levels had been elevated by ether or by a combination of fluoxetine and 5-hydroxytryptaphane. The prolactin-lowering effect was blocked by alpha-methyl-tyrosine to inhibit catecholamine synthesis and by the specific dopamine receptor blocker, spiroperidol. In ovariectomized females, neurotensin was also capable of suppressing LH and elevating growth hormone following its intraventricular injection. Intravenous injection of the peptide elevated prolactin but had no effect on the release of the other pituitary hormones. When hemipituitaries of ovariectomized rats were incubated in vitro, neurotensin elevated prolactin and TSH release into the medium. The minimal effective dose to elevate prolactin and TSH release was 50 ng/ml. Release of gonadotropins and growth hormone was unaffected. It is concluded that neurotensin inhibits prolactin release by a CNS, presumably hypothalamic action, to stimulate the tuberoinfundibular dopaminergic neurons. The dopamine released then inhibits prolactin release either by a direct action on the pituitary or by release of another prolactin-inhibiting factor. In addition, the peptide has a direct prolactin-releasing action on the pituitary. Neurotensin can inhibit LH and stimulate growth hormone presumably by a hypothalamic action since there was no effect on the release of these pituitary hormones by glands incubated in vitro. Although the peptide had no effect on TSH release following its intraventricular injection, it stimulated prolactin release by pituitaries incubated in vitro. The physiological significance of these results is not yet established; however, the presence of the peptide in regions concerned with pituitary control suggests that it may play a physiological role.

5-Hydroxytryptophan↗
PubMed1982

Establishment of neuromuscular contacts in cultures of rat embryonic cells: effect of tetrodotoxin on maturation of muscle fibers and on formation and maintenance of acetylcholinesterase and acetylcholine receptor clusters.

The part played by muscle activity was mainly studied in relation to the formation and persistence of cytochemically detectable spots of acetylcholinesterase (AChE) during synaptogenesis. A correlation was found between AChE spot evolution and that of two other morphological synapse markers, silver salt-impregnated nerve endings and clusters of acetylcholine receptors (AChR) exposed to 125I-alpha-bungarotoxin and revealed by radioautography. The formation and persistence of AChE spots were activity-dependent but in the case of neuronally induced synaptic nerve endings and AChR clusters, both morphological markers were independent of such activity. The final evolution and maturation of neuromuscular contacts were linked to the differentiation stage reached by the muscle fibers at the time when they established contact with nerve endings. The fibers acquired this differentiated state independently of tetrodotoxin-blocked muscle activity.

Acetylcholine↗
PubMed1981

Biochemical stability of the AChE molecular forms after cytochemical staining: postnatal focalization of the 16S AChE in rat muscle.

A biochemical analysis of rat muscle acetylcholinesterase (AChE) is possible after a cytochemical staining at pH7 (Koelle and Friedenwald method). The solubilization properties, the physicochemical characteristics (sedimentation coefficients) of the multiple molecular forms of AChE are similar before and after the cytochemical procedure without fixation and without ammonium sulfide treatment. This is in contrast to the partial inactivation obtained after conventional pH 5 cytochemical staining, which selectively inactivates 16S AChE. We found that pH 7 cytochemical staining in these same conditions afford a satisfying morphological visualization of the motor end-plate AChE. The combined cytochemical-biochemical techniques allow a very precise dissection of motor end-plate containing (neural) and free (aneural) regions. In rat muscle (sternomastoid), high levels of 16S AChE are present in the aneural region in the first stages of postnatal development. At the end of the 1st month after birth, the 16S AChE becomes restricted to the neural (motor end-plate) region.

Acetylcholinesterase↗
PubMed1980

Role of central nervous system neurotransmitters in mediating the effects of morphine on growth hormone- and prolactin-secretion in the rat.

Unanesthetized adult male rats with indwelling right atrial cannulae were used in the majority of experiments. Morphine (MOR, 3.0 mg/kg) caused a large but transient increase in both GH and PRL levels, which could be prevented with naloxone. Disruption of central noradrenergic function with diethyldithiocarbamate (400 mg/kg) or phenoxybenzamine (15 mg/kg) abolished the GH-releasing effect of MOR, without interfering with the PRL secretory response. Depletion of brain serotonin stores with p-chlorophenylalanine (300 mg/kg) or 5,7-dihydroxytryptamine or administration of serotonin receptor blocker, cyproheptadine (2.5 mg/kg), did not diminish the GH respnse to MOR but it inhibited, or in the case of 5,7-DHT treatment abolished the activation of PRL secretion. Additionally, metergoline (0.1 and 1.0 mg/kg), another serotonin receptor blocker, caused an inhibition of the GH-releasing action of MOR; however, this inhibition was reversed by pretreatment with spiroperidol (0.1 mg/kg). Metergoline also markedly diminished the MOR-induced elevation of PRL. Inhibition of catecholamine synthesis with alpha-methyl-p-tyrosine (alpha-MT, 250 mg/kg) blunted the effect of MOR on GH; however, dopamine receptor blockers, spiroperidol (0.01 and 0.1 mg/kg) or (+)butaclamol (0.3 and 1.3 mg/kg), were without any influence. alpha-MT or spiroperidol did not alter the effect of MOR on PRL secretion, but the higher dose of (+)butaclamol suppressed it. It is concluded that the GH-releasing action of MOR requires unimpaired functioning of the central noradrenergic system, while the serotonergic and dopaminergic systems appear to play no significant role in it. In contrast, serotonergic systems seem to be essential for the activation of PRL secretion, whereas the noradrenergic system is not involved. It remains uncertain whether morphine activtes PRL secretion also through inhibition of dopaminergic activity. We favor the view that the dopaminergic component participates in the PRL activation by MOR, but that its contribution to the overall effect is rather small.

Animals↗
PubMed1978

[Formation of the neuromuscular junction in cultures of rat embryonic cells].

The morphological evidence of the primary nerve muscle contacts are described. They consist of areas of cholinesterase activity (detected histochemically) localized on the myotube membranes and of mutiple clusters of ACh receptors whose 125I-alpha-bungarotoxin binding sites are revealed by radio-autography. After the stage of the primary nerve muscle contacts, some of which seem transient, characteristic neuromuscular junctions appear. These neuromuscular junctions which possess subneural infoldings are similar to the end-plates of the Rat in vivo.

Animals↗
PubMed1978

[Molecular forms of acetylcholinesterase in the slow muscle and the fast muscle of the chicken].

Five molecular forms of AChE are present in the slow (ALD) and twitch (PLD) muscles of the chick. These forms have 4 S, 7 S, 11 S, 15 S and 20 S sedimentation coefficient in sucrose gradient. The heaviest forms, the 20 S and 15 S of AChE are absent in uninnervated muscles and present in innervated muscles. In innervated muscles, the 20 S and 15 S AChE are present in both nerve-free segments and end-plates zones. The 20 S and 15 S which are not specifically associated with the end-plate zones in the chick could be considered as a biochemical "marker" of neuromuscular interactions.

Acetylcholinesterase↗
PubMed1976

[Influence of some nutritional factors on the canthaxanthine pigmentation of the rainbow trout].

The present investigation was made to approve nutritionnal factors which affect the utilisation of food canthaxanthin by hatchery trout. Rainbow trout were obtained from a commercial trout farm, kept in running water and feeding in experimental pellets for 4 to 8 weeks. Five diets were tested (1-standard [7.5 u.i/g], 2-low protein content, 3-High lipid content, 4-non supplemented with vitamin A, 5-High vitamin A content [23 U.I./g]). All diets containing 250 mg of canthaxanthin per kilo of food, the fish were fed at the rate of approximately 2.5 p. 100 of their body weight per day. The estimation of canthaxanthin from fish tissues was accomplished as follows: the tissues were gomogeneized and extracted with several volumes of solvents. The solution containing all the pigment was evaporated. The purification of the canthaxanthin was obtained by column silica gel chromatography. The pigment was eluated with ethyl-ether as solvent. Quantitative assay of total carotenoïd was effected by spectre photometric estimation of optical density at 480 nm of this fraction dissolved in benzene. The carotenoïd composition of this fraction was studied by silica-gel thin layer chromatography. In these conditions:--it was shown by spectral studies that the canthaxanthins present in the diet are essentially those deposed in the flesh of the trout fed;--a series of experiment were made to examine the effect of composition of artificially composed feeds for pigmentation of the rainbow trout. The pigment deposition was found to correlate with the amount of lipids present in these diet. In this condition, the pigment is more dispersed with lipids present and the pigment absorption may be facilitated and later be deposed. 8 weeks alimentation are needed to observe the effect of these nutritionnal factor;--when the diet is non supplemented with vitamin A, the same quantity of canthaxanthin mixed with this food gives trout redder flesh than the standard diet. On an other hand, an antagonist effect of diet with high vitamin A content is demonstrated on the amount of the pigment deposed in the flesh of trout;--no effect of protein content of the diet was found in these experiments;--no effect of ratio calorie/protein of the diets with the intensity of deposed pigment in the flesh rainbow trout;--a correlation between neutral lipids of the tissue and the pigment deposed in the flesh of the trout fed with canthaxanthin was confirmed.

Animal Nutritional Physiological Phenomena↗