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Biomedical subjects

G Skofitsch

Publications and source records attributed to G Skofitsch.

At least 55 records · Page 3Linked to original sources
PubMed1985

Distribution of atrial natriuretic factor-like immunoreactive neurons in the rat brain.

Using antisera generated in rabbits against rat atriopeptin III [alpha-rANP(5-28)] and human alpha-atrial natriuretic polypeptide we mapped the distribution of atrial natriuretic factor-like immunoreactivity throughout the rat central nervous system. Cell bodies were observed in the telencephalon (nucleus interstitialis striae terminalis and between the amygdala centralis and medialis), throughout the diencephalon in all nuclei of the "anteroventral third ventricle", the base of the hypothalamus, the subzona incerta area, the medial forebrain bundle and the medial habenula, in the mesencephalon (mamillary body, substantia nigra lateralis, dorsal and ventral parabrachial nuclei) and very sparse in the medulla oblongata along the fourth ventricle towards the vestibular nuclei, the nucleus tractus solitarii and nervi trigemini. Fibers were present wherever cell bodies were located. The highest relative densities were observed in the anteroventral third ventricle area and the medial habenula. Sparse fibers were also seen in the spinal cord (dorsal and ventral horn and around the central canal) and in the posterior pituitary. The predominance of the atrial natriuretic factor-like perikarya and fibers in the anteroventral third ventricle area suggests an involvement of this peptide in central blood pressure control.

Animals↗
PubMed1985

Binding sites for corticotropin releasing factor in sensory areas of the rat hindbrain and spinal cord.

Binding sites of 125I-Tyr-O-ovine corticotropin releasing factor have been demonstrated in sensory areas of the rat hindbrain and spinal cord mainly in the posterior part of the nucleus tractus solitarii, the substantia gelatinosa nervi trigemini and the superficial layers of the spinal cord (laminae I and II). Specific binding was inhibited in the presence of unlabeled synthetic ovine or rat/human CRF indicating that the receptors recognize both forms of CRF.

Animals↗
PubMed1985

Galanin-like immunoreactivity in capsaicin sensitive sensory neurons and ganglia.

In rats treated with capsaicin (CAP) as neonates, galanin-like (GA) immunoreactivity is markedly decreased in the trigeminal ganglion and the dorsal root ganglia as well as in the superficial layers of the dorsal spinal cord (laminae I and II), the substantia gelatinosa, the nucleus and tractus of the spinal trigeminal nerve and the nucleus commissuralis. Since CAP causes selective degeneration of primary sensory neurons of the C-fiber type and type B-cells of sensory ganglia, it is concluded that GA in CAP-sensitive primary sensory neurons represents a novel peptidergic system possibly involved in the transformation or modulation of peripheral nociceptive impulses. This system differs from the CAP-resistant GA-like neurons in other brain areas.

Animals↗
PubMed1985

Immunohistochemical localization of a melanin concentrating hormone-like peptide in the rat brain.

Using antisera generated in rabbits against salmon melanin concentrating hormone (MCH) coupled to human thyroglobulin, the distribution of MCH-like immunoreactivity was mapped throughout the rat central nervous system. The distribution of MCH-like immunoreactivity in rat brain is unique and different from the distribution of other neuropeptides. MCH-like immunoreactive perikarya and fibers are predominant in the posterior hypothalamic area, mostly in the medial forebrain bundle-lateral hypothalamic area subzona incerta and the perifornical area. Cell bodies are located mainly in the medial forebrain bundle and in proximity to well defined hypothalamic nuclei. Fibers are seen throughout the rat brain in all neocortical areas, the neostriatum and the amygdala, in the diencephalon in most hypothalamic nuclei, the habenula, the mamillary body and very dense in the medial forebrain bundle and just ventral to the zona incerta ("subzona incerta"). In the mesencephalon there are fibers in the central gray; in the pons-medulla fibers are contained in the dorsal and ventral parabrachial nuclei; in the tegmental area ventral to the fourth ventricle; in the spinal trigeminal area, the substantia gelatinosa and the reticular nuclei. In the spinal cord there are more fibers in the dorsal than in the ventral horn. The posterior pituitary also contained few MCH-like fibers. It is suggested that a peptide similar, but not identical, to salmon MCH is present in the rat central nervous system.

Animals↗
PubMed1985

Evidence for the existence of atrial natriuretic factor-containing neurons in the rat brain.

Immunoreactive atrial natriuretic factor- (ANF-)positive nerve fibers and cell bodies were observed in the preoptic area, hypothalamus, mesencephalon, and pons of rats. In colchicine-treated animals a large number of immunoreactive ANF-positive cell bodies were seen in the organum vasculosum of the lamina terminalis, in several hypothalamic nuclei (e.g. periventricular, arcuate, and ventral premammillary nuclei), and in the dorsolateral tegmental nuclei of the pons. Varicose nerve fibers containing ANF were generally observed in the vicinity of the cells. These findings indicate that a widespread network of ANF-containing neurons is present in the brain.

Animals↗
PubMed1984

Primate model of Parkinson's disease: alterations in multiple opioid systems in the basal ganglia.

A motor disorder similar to idiopathic Parkinson's Disease develops in rhesus monkeys after several daily repeated doses of N-methyl-4-phenyl, 1,2,3,6-tetrahydropyridine (MPTP). The concentrations of peptides derived from proenkephalin A, proenkephalin B, substance P and somatostatin were measured by specific radioimmunoassays in the basal ganglia of MPTP-treated monkeys. In MPTP-treated monkeys, dynorphin B concentration was reduced in the caudate. In the putamen, the concentrations of peptides derived from both proenkephalin A and proenkephalin B were decreased. In the globus pallidus, the concentrations of all opioid peptides tend to be increased, reaching significance only for alpha-neo-endorphin. In the substantia nigra, only Met-enkephalin concentration was reduced, while other peptides derived from either proenkephalin A or proenkephalin B were not changed. Substance P and somatostatin were not changed in any brain area examined. Some of the symptoms associated with Parkinson's Disease may be related to altered activity of endogenous opiates in basal ganglia.

Animals↗
PubMed1984

Inhibition of compound 48/80--induced vascular protein leakage by pretreatment with capsaicin and a substance P antagonist.

Intravenous injection of compound 48/80 (1 mg X kg-1) induced an acute increase in vascular permeability to plasma proteins in various organs of rats. The compound 48/80 response was partly inhibited by histamine H1 and H2 receptor blockade in the urinary bladder and in the duodenum, but not in the trachea, the oesophagus, the ureter and the paw skin. Blockade of 5-hydroxytryptamine receptors with methysergide led to a reduction of the permeability response in the oesophagus and in the urinary bladder, leaving responses in other organs unchanged. Pretreatment of neonatal rats with capsaicin almost abolished the 48/80 response in all organs except in the duodenum. Pretreatment of rats with [D-Arg1, D-Trp7,9, Leu11]-substance P, a substance P antagonist, also caused a partial inhibition of the permeability response to compound 48/80 in several organs. Topical administration of compound 48/80 (1 mg X ml-1) onto the tracheal mucosa induced local Evans blue extravasation. This response was resistant to pretreatment with histamine receptor antagonists, but was largely inhibited after neonatal capsaicin pretreatment. Topical administration of compound 48/80 (1 mg X ml-1 or 10 mg X ml-1) into the eye did not cause visible Evans blue extravasation in the conjunctiva, nor any signs of pain reaction as indicated by the absence of the wiping response, usually seen upon noxious chemical stimuli in the eye. In guinea-pigs, 10 mg X kg-1 compound 48/80 i.v. were required to induce vascular protein leakage in different organs. This response was blocked by pretreatment with H1 and H2 receptor antagonists, but only slightly reduced after systemic capsaicin pretreatment of guinea-pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Corticotropin releasing factor-like immunoreactive neurons in the rat retina.

Corticotropin releasing factor (CRF)-like immunoreactive neurons have been identified in the rat retina by immunohistochemical methods using antisera directed against ovine and rat CRF. CRF-like immunoreactivity was observed in both amacrine and ganglion cells which projected fine varicose processes to the inner plexiform layer of the retina. It is suggested that CRF may play a role in retinal function.

Animals↗
PubMed1984

Release of endogenous 5-hydroxytryptamine from the myenteric plexus of the guinea-pig isolated small intestine.

The presence of 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in, and the release of these substances from, the myenteric plexus-longitudinal muscle (MPLM) layer of the guinea-pig isolated small intestine were investigated. 5-HT and 5-HIAA were measured by high performance liquid chromatography and electrochemical detection. Freshly prepared MPLM contained measurable amounts of 5-HT and 5-HIAA. For the release experiments, the MPLM was incubated in a medium containing the 5-HT uptake inhibitor fluoxetine and the monoamine oxidase inhibitor nialamide; this led to a decrease in the 5-HIAA content of the MPLM whereas the 5-HT content remained unchanged. There was a spontaneous release of 5-HT and 5-HIAA from the MPLM. The release of 5-HT was so small that it was just detectable; it seemed equivalent to about 0.8% of the tissue stores released per min. Depolarization of the tissue by increasing the [K+] or by exposing it to veratridine enhanced the release of 5-HT in a Ca2+-dependent manner whereas the release of 5-HIAA was not increased. Tetrodotoxin inhibited the veratridine-evoked release of 5-HT but did not affect the K+-evoked release of 5-HT. The presence of 5-HT in myenteric neurones and the characteristics of the release of 5-HT from these neurones strongly support the hypothesis that 5-HT is an enteric neurotransmitter.

Animals↗
PubMed1984

Capsaicin depletes corticotropin-releasing factor-like immunoreactive neurons in the rat spinal cord and medulla oblongata.

Treatment of newborn rats with capsaicin was shown to cause a disappearance of corticotropin-releasing factor immunoreactive nerve fibers in the dorsal horn of the spinal cord (laminae I and II), the spinal trigeminal nucleus and tract, and the nucleus tractus solitarius, but not in the median eminence and the nucleus amygdaloideus centralis. Since it is well known that capsaicin acts selectively on primary sensory neurons of the C-fiber type, it is suggested that corticotropin-releasing factor is also located in peripheral sensory neurons, representing a novel peptidergic neuronal system, possibly involved in the modulation or transmission of peripheral nociceptive impulses, which is different from the capsaicin-resistant hypothalamoinfundibular corticotropin-releasing factor system.

Animals↗
PubMed1984

Comparison of nonivamide and capsaicin with regard to their pharmacokinetics and effects on sensory neurons.

Nonanoyl vanillylamide (nonivamide NVA) was compared with trans-8-methyl-N-vanillyl-nonenamide (capsaicin, CAP) with regard to their pharmacokinetic properties, their potency in stimulating primary afferent neurons and depleting them of substance P and somatostatin in rats. Following the injection of 50 mg kg-1 the time course of the presence of NVA in brain and blood was similar to that of CAP. The concentration of NVA in brain was higher than in blood; the reverse was true for CAP. The ability of NVA and CAP to stimulate afferent neurons was measured by the reflex depressor response following i.v. injection and by the number of wiping movements following instillation of the substances into the eye. In both tests, the potency of NVA was about half of that of CAP. Treatment of newborn rats by s.c. injections of 50 mg kg-1 NVA or CAP seemed to cause a larger depletion of substance P and somatostatin in the sciatic nerve and the spinal cord than treatment of adult rats. Depletion by CAP was generally larger than that by NVA although depletion experiments are hardly suitable for quantification. The depletion of substance P by CAP and NVA could be correlated with the extent to which ocular chemosensitivity and neurogenic plasma extravasations were attenuated. The methods used are discussed in view of their possible use in screening further capsaicin analogues.

Animals↗
PubMed1983

Phenyldiguanide and capsaicin stimulate functionally different populations of afferent C-fibers.

Effects of phenyldiguanide (PDG) and capsaicin (CAP) were compared. (1) The reflex fall in blood pressure following PDG i.v. was only partially but that following CAP i.v. completely inhibited in capsaicin-desensitized rats. (2) Bilateral vagotomy in rats abolished cardiovascular reflexes by PDG i.v., but not those by CAP i.v. (3) Instillation of PDG into the rat trachea did not cause neurogenic plasma extravasation whereas CAP does. (4) Bronchial tone of guinea-pigs remained unchanged after PDG i.v. whereas it was increased by CAP i.v. It is concluded that PDG activates vagal afferent fibers which are distinct from the substance P-containing afferent fibers stimulated by CAP.

Animals↗
PubMed1983

Vascular protein linkage in various tissue induced by substance P, capsaicin, bradykinin, serotonin, histamine and by antigen challenge.

Plasma extravasation was induced in rats or guinea-pigs by intravenous injections of (1) substance P (SP), (2) the C-terminal SP-hexapeptide SP(6--11), (3) serotonin (5-HT), (4) histamine, (5) bradykinin, (6) capsaicin and (7) by antigen challenge. Plasma extravasation induced by SP, SP(6--11), by 5-HT and by capsaicin was, with few exceptions, observed in the same tissues. The effect of SP was not blocked by H1 and H2 histamine receptor antagonists. The effect of i.v. capsaicin was absent in capsaicin desensitized animals. Plasma extravasation upon i.v. SP, SP(6--11), 5-HT and capsaicin was seen in the skin and in all organs containing mucous membranes except the intestinal mucosa. Plasma extravasation by histamine, bradykinin, and antigen challenge of sensitized guinea-pig was, in addition, also observed in the stomach and intestine. Plasma extravasation and bronchoconstriction by antigen challenge with 20 micrograms/kg ovalbumin was completely blocked by combined H1 and H2 histamine receptor blockade. Both responses were reduced to about the half capsaicin desensitized guinea-pigs, although the reduction of the permeability response was statistically not significant in all organs. In conclusion, several substances including anaphylaxis induce protein leakage in many tissues with differing selective distribution patterns. Anaphylactic histamine release leads to protein leakage partly via activation of sensory neurons. SP is a likely mediator of neurogenic protein leakage in many organs.

Animals↗
PubMed1983

Release of histamine by neuropeptides from the perfused rat hindquarter.

The release of histamine and serotonin by neuropeptides and capsaicin was measured in the isolated perfused rat hindquarter preparation. Substance P and two antagonistic peptides, [D-Pro2, D-Phe7, D-Trp9]-SP and [D-Pro2, D-Trp7,9)]-SP, release histamine, the SP(4-11) and SP(6-11) analogues did not. VIP and somatostatin released histamine and also serotonin. No amines were released by bombesin. Thus, all amine releasing peptides possessed at least two basic charges. However, the histamine releasing activity of the neuropeptides tested did not correlate with their reported ability to cause vasodilation and plasma extravasation. The SP(4-11) and SP(6-11) analogues which did not release histamine caused plasma extravasation. It is concluded that SP causes plasma extravasation by a direct action on blood vessels. Capsaicin released only serotonin but no histamine either in untreated rats and such desensitized with capsaicin as neonates. In rats desensitized with capsaicin 4 days prior to the experiment the substance P induced histamine release was as high as in untreated controls; it was, however, absent in rats desensitized with capsaicin as neonates. It is assumed that the sensitivity of mast cells to substance P is lost after degeneration of substance P containing primary sensory fibers.

Animals↗
PubMed1983

Serum levels of dimenhydrinate. Determination by HPLC with UV detection after intake of dimenhydrinate in a coated chewing gum dragee.

HPLC with UV detection allowed to separate dimenhydrinate and three major metabolites (diphenyl-methoxy-ethylamine, diphenyl-methoxy-acetic acid, diphenyl-methoxy-N-methyl-amine) in human serum without extraction procedure. Detection limit was 25 ng per 500 microliter injected sample, the recovery ranged from 70 to 95%. Serum levels of dimenhydrinate were measured in healthy volunteers 15, 30, 60 and 120 min after intake of two commercially available preparations, one of them a dimenhydrinate tablet, the other one a dimenhydrinate containing coated chewing gum dragee (Travel-Gum dragee). The rise of the serum concentration of dimenhydrinate up to 30 min was smaller after intake of the coated chewing gum preparation than after swallowing the tablet. The serum concentrations at 1 or 2 h after the intake of either a tablet or the chewing gum were comparable. The variability of the serum concentrations was considerable with both preparations and seemed to be influenced more by individual factors than by previous food intake.

Administration, Oral↗
PubMed1982

Visceral pain reflex after pretreatment with capsaicin and morphine.

1. Distension of the proximal jejunum by increasing the intraluminal pressure for short time periods causes a reflex response in blood pressure of anaesthetized rats which correlates with the magnitude of distension. The blood pressure response consists of a short initial rise followed by a marked decrease for the time of distension. 2. The absence of the depressor response in capsaicin desensitized rats indicates its mediation by C fibre afferents. These afferents are located within the periarterial mesenteric nerves. The depressor response was also elicited by stimulation of these nerves and abolished by local application of percain or capsaicin onto the mesenteric stalk. Vagal afferents were not involved in this depressor response as shown by bilateral vagotomy or by afferent vagus stimulation. 3. The depressor response is absent in spinal rats. Therefore, the location of the reflex centre is assumed to be supraspinal. Because it is augmented by naloxone and abolished by morphine in a naloxone reversible way it is regarded as a nociceptive reflex response. 4. The efferent side of the depressor response is unknown; cholinergic and alpha-adrenergic activation were excluded. 5. The initial pressor response to intestinal distension or to afferent periarterial mesenteric nerve stimulation persists in capsaicin desensitized rats excluding the involvement of C fibre afferents and in spinal rats indicating that the reflex centre is within the spinal cord. It is not diminished by morphine and therefore not a nociceptive response. Its inhibition by phentolamine suggests an alpha-adrenergic spinal response to intestinal distension. In control rats the pressor response is greatly overlapped by the much more pronounced depressor response.

Anesthetics, Local↗