Über die cerebrale Ödemkrankheit des frühen Kindesalters

Zusammenfassung Es wird über einen Fall von cerebraler ödemkrankheit bei einem 5 Monate alt gewordenen Säugling aus klinischer und neuropathologischer Sicht berichtet. Der Fall stimmt in allen wesentlichen Punkten mit den wenigen bisher mitgeteilten Beobachtungen überein. Der pathogenetische Mechanismus des Leidens wird eingehend diskutiert.

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Summary Report of a case of spongy degeneration of the central nervous system in infancy. The patient was a suckling who died in an age of five months.The clinical picture of the disease which is familial in nature and prefers the Jewish race is characterized by convulsions, opisthotonos, spasticity, nystagmus, fever and vomiting or by a slow beginning marked by a failure of mental and motor development. Autopsy findings are a macrocephaly. Microscopically an intense vacuolation of the deep layers of the cortex, the subjacent white matter, the basal ganglia and the cortex cerebelli is seen besides a hyperplasia of the protoplasmic astrocytes. On the basis of clinical and pathological features this disorder was separated from other forms of leukodystrophy in infancy by van Bogaert and Bertrand.The clinical and pathological features of the case reported are in accordance with the few observations published until now. The etiologic and pathogenic mechanism of the disorder, which probably is caused by an autosomal-recessive inherited error of metabolism, is discussed.

     

The sensitivity of hippocampal pyramidal neurons to serotoninin vitro: Effect of prolonged treatment with clorgyline or clomipramine

Summary The sensitivity of hippocampal pyramidal neurons to the depressant action of serotonin was studied in hippocampal slices obtained from rats treated repetitively with clomipramine (10 mg/kg i.p.; 10 days or 4 weeks), with clorgyline (0.3 mg/kg s.c.; 10 days) or with the vehicle. Whereas clorgyline produced a very pronounced subsensitivity to serotonin, a moderate, non-significant reduction in sensitivity was observed with clomipramine. These electrophysiological findings are consistent with previous biochemical studies.     

Reduced sensitivity of neurons to noradrenamine after chronic treatment with antidepressant drugs

The sensitivity of cingulate cortical neurons to microiontophoretically administered noradrenaline (NE) and GABA was investigated in groups of rats treated either chronically or acutely with various antidepressant drugs or with the tricyclic antiepileptic carbamazepine. The chronically treated animals received one daily intraperitoneal injection of either desipramine (10 mg/kg), clomipramine (10 mg/kg), maprotiline (25 mg/kg), tranylcypromine (1 mg/kg) or carbamazepine (30 mg/kg p.o) for 4 weeks. The acutely treated rats received one daily injection of the vehicle for 4 weeks, followed by one single injection of one of the five drugs 24 h before the experiment. NE and γ-aminobutyric acid (GABA) were administered microiontophoretically during periods of 60 sec with various ejection currents. In chronically treated rats a statistically significant reduction in the sensitivity of cortical cells to NE was observed with all four antidepressants. However, in rats treated chronically with carbamazepine, no desensitisation was observed.Desensitization to NE following chronic treatment with desipramine developed within the first 10 days of treatment. Following a ten-day treatment, there was a 33 percent and by the end of the fourth week a 43 percent reduction in sensitivity to NE. The sensitivity of these cingulate neurons to GABA was unchanged after chronic treatment with the antidepressant drugs. In conclusion, the present study demonstrates that chronic treatment with antidepressant drugs leads to a postsynaptic subsensitivity of cortical neurons to NE.     

Neuronal sensitivity to substance P is increased after repeated treatment with tranylcypromine, carbamazepine or oxaprotaline, but decreased after repeated electroconvulsive shock

The responsiveness of neurones in the cingulate cortex of the rat to the excitatory effects of iontophoretically applied substance P (SP) was determined after chronic administration of several drugs known to possess antidepressant actions. The agents tested were tranylcypromine, carbamazepine and oxaprotiline [(+) and (-)isomers]. Twenty-four to 36 hr after the last of 14 consecutive daily treatments there was an increase in neuronal sensitivity to substance P with all three drugs. The two isomers of oxaprotaline were equally active in inducing this change in sensitivity. None of the agents significantly altered responses to substance P after a single acute treatment. Responsiveness to substance P was also tested one day after the last of 14 daily treatments with electroconvulsive shock. In this case there was a marked reduction of the sensitivity of cingulate neurones to substance P with no apparent change in responsiveness to acetylcholine. A single shock treatment did not detectably alter responses to substance P.     

Tachykinin responses in the rat cingulate cortex: a comparison of the effects of iontophoretically applied substance P and neurokinin A

The effects of substance P and neurokinin A were compared on spontaneously active cells in the anterior cingulate cortex of the rat. Most neurones were strongly excited by the iontophoretic applications of both peptides. However, many of the superficially located cells were clearly depressed by substance P but unaffected by the application of neurokinin A or even weakly excited. The results indicate that neuronal responses to tachykinins in this brain area may be mediated, at least in part, by separate receptors.     

Central actions of somatostatin

Somatostatin (SRIF) was applied microiontophoretically to neurons in the frontal and parietal neocortex, the hippocampus and the striatum of rats anaesthetized with either urethane or chloral hydrate. Qualitatively identical results were obtained under both anaesthetic conditions. In urethane-treated rats SRIF elicited a dose-dependent increase of the firing rate of 74% of the neurons studied in the frontal cortex and of 46% of the neurons studied in the parietal cortex. All cortical cells identified as pyramidal cells were excited. In the hippocampus SRIF provoked excitatory responses in two thirds of all neurons. Six out of the nine cells identified as pyramidal cells were excited by SRIF. In the striatum 80% of all neurons were excited. Following repeated exposure of central neurons to SRIF, the magnitude of the excitatory response gradually diminished, indicating desensitisation. SRIF in concentrations ranging from 10(-8) to 10(-4) M did not interfere with the binding of (3H)-muscimol to GABA receptor sites. The release of GABA from synapses preloaded with (3H-GABA) was not influenced by SRIF in the concentration range from 10(-6) to 10(-4) M. These results indicated that SRIF does not evoke the excitatory responses through attenuation of GABA-mediated inhibition. In conclusion, the findings support the hypothesis that somatostatin may function as a neurotransmitter in the central nervous system.     

Altered sensitivity of forebrain neurones to iontophoretically applied noradrenaline in aging rats

Responses of unidentified neurones in the rostral cerebral cortex to iontophoretically applied noradrenaline and GABA were compared in young (3-4 months old) and old (22-24 months old) albino rats. Depressant responses to noradrenaline were smaller in the older animals and this was manifested particularly as a decrease in response duration. Depressant responses to GABA did not differ significantly in the two groups. The results indicate that neurones in the cerebral cortex, as in the cerebellum, exhibit a decrease in postsynaptic responsiveness to noradrenaline with advancing age.     

The effects of arotinoids on rat mammary carcinogenesis

Summary The influence of two retinoids, Ro 13–6298, an arotinoid ethyl ester, and Ro 15–1570, an arotinoid ethyl sulfone, on rat mammary carcinogenesis was investigated. Mammary carcinomas were induced by oral administration of 15 mg dimethylbenz(a)anthracene (DMBA) to 50-day-old female Sprague-Dawley rats. Oral administration of the two retinoids significantly inhibited the development of tumors. The number and volume of mammary neoplasms were influenced in a dose-dependent manner.     

Sialografie im Kindesalter

Zusammenfassung Die Speicheldrüsenkontrastdarstellung oder Sialografie wird auf Grund eigener Untersuchungen in ihrer Durchführung beim Kinde beschrieben. Die Fragen des Instrumentariums, der verschiedenen Hilfsmittel und aller methodischen Einzelheiten werden erörtert, bei Kontrastölfüllungen gesunder und kranker Speicheldrüsen von Kindern verschiedener Altersstufen benötigte durchschnittliche Dosen werden mitgeteilt. Unter Abbildung von Kontrastdarstellungen des Speichelgangsystems gesunder altersverschiedener Kinder wird das Normalsialogramm der Parotis beschrieben. Im Ergebnis der eigenen Untersuchungen kann die von anderer Seite für das weibliche Geschlecht festgestellte Konstanz einer grobsymmetrischen Entwicklung des Parotisgangsystems für die Mädchen unseres Untersuchungsgutes nicht bestätigt werden. Multiples Vorkommen akzessorischer Drüsen an der Parotis wird im Material des Verfassers auffallend häufig festgestellt. Auch das Normalsialogramm der Submaxillaris wird beschrieben. Im weiteren werden die allgemeinen Indikationen zur Speicheldrüsenkontrastdarstellung beim Kinde erörtert und anschließend die wichtigsten Anzeigen im einzelnen abgehandelt. Die verschiedenen Formen der chronischen unspezifischen Entzündung der Speichelorgane finden in ihrer sialografischen Unterscheidbarkeit hierbei besondere Beachtung und stellen eine hervorragende Indikation der Sialografie im Kindesalter dar. Bei chronisch speicheldrüsenkranken Kindern gewonnene eigene Sialogramme werden in Abbildungen eingefügt. — Die Sialografie ist ein auch beim etwas jüngeren Kinde durchführbarer, unkomplizierter und schadloser diagnostischer Eingriff und wird ihren Platz auch in der kinderärztlichen Speicheldrüsendiagnostik einnehmen.