Elizabeth Knyihár

Fine structure and fluoride resistant acid phosphatase activity of electron dense sinusoid terminals in the substantia gelatinosa Rolandi of the rat after dorsal root transection.

SummaryFluoride resistant acid phosphatase (FRAP) activity of the rat substantia gelatinosa Rolandi is confined to electron dense sinusoid terminals under normal conditions. Transection of dorsal roots or removal of dorsal root ganglia results in a rapid degeneration of more than half of the electron dense sinusoid axon terminals. First signs of degeneration ensue 20 hours after surgery; at the 24 hours state osmiophilic degeneration bodies develop that are translocated into glial elements in the course of the second postoperative day. At the same time, light microscopically visible FRAP-activity of the Rolando substance disappears. Electron histochemical investigations reveal that decreased enzyme activity is due to degeneration of FRAP-positive terminals. It is concluded that FRAP-positive terminals, representing the majority of electron dense sinusoids in the Rolando substance, are dorsal root collaterals; the origin of non-degenerating FRAP-negative electron dense terminals remains unknown for the time being.

Fluoride-resistant acid phosphatase system of nociceptive dorsal root afferents

Fluorid-resistente saure Phosphatase wird aus den kleinen (dunklen) Nervenzellen des Spinalganglions mittels axoplasmatischer Strömung durch die Hinterwurzeln in die Rolando-Substanz des Rückenmarkes transportiert, wo das Enzym in den Nervendendigungen eine freie axoplasmatische Lokalisation aufweist.

HISTOCHEMICAL AND ULTRASTRUCTURAL ALTERATIONS IN THE ISOLATED ARCHICEREBELLUM OF THE RAT

THOUGH the ultrastructural and the histochemical structure of the central nervous system (CNS) has been studied intensively during recent years, few data are available regarding those ultrastructural and histochemical alterations that follow the degeneration of neural components. In the present paper the ultrastructural and histochemical consequences of degeneration in the cerebellar cortex are discussed, with special reference to the archicerebellar mossy fibre apparatuses.

Regional distribution of acid phosphatase-positive axonal systems in the rat spinal cord and medulla, representing central terminals of cutaneous and visceral nociceptive neurons

In addition to the substantia gelatinosa Rolandi, acid phosphatase active axonal systems are described (1) in the viscerosensory nucleus of the vagus nerve, (2) in Lissauers band, (3) in the fasciculus cornus posterions (Cajal), and (4) in the nucleus basilaris externus (Cajal). Electron microscopically, acid phosphatase is located in between synaptic vesicles of axon terminals; the vesicle population of such terminals in the Rolando substance, however, markedly differs from that in systems 1–4, characterized by the presence of large dense-core vesicles. While acid phosphatase-active axon terminals in the Rolando substance appear to subserve cutaneous nociception, circumstantial evidence suggests participation of systems 1–4 in processing visceral nociception.

Degenerative atrophy of central terminals of primary sensory neurons induced by blockade of axoplasmic transport in peripheral nerves

Perineural colchicine- or vinblastine-treatment results in disappearance of non-lysosomal acid phosphatase activity, characterizing axon terminals in the Rolando substance of the normal spinal cord. Ultrastructural alterations are identical with those seen in the course of degenerative atrophy.

Localizations of inhibitors of the acetylcholine- and GABA-synthesizing systems in the rat brain - An autoradiographic assay on the distribution of 14C-hemicholinium and 14C-thiosemicarbazide

SummaryLight microscopic autoradiographic techniques were employed to detect inhibitors of acetylcholine synthesis and of the GABA-metabolism in the rat nervous system. Sites of acetylcholine synthesis were located by demonstrating deposits of in vivo injected 14C-labelled hemicholinium; sites of GABA-metabolism were located by detecting in vivo injected 14C-labelled thiosemicarbazide. 14C-hemicholinium was concentrated in motor end plates, spinal motoneurons, cerebellar cortex, paleo- and neocortex cerebri, and caudate nucleus. Isotope thiosemicarbazide was found in the hippocampus, medial habenular nucleus, cerebellar cortex, dentate nucleus, substantia nigra and nuclei pontis. Localizations of the above enzyme inhibitors are in accord with biochemically demonstrated activities of choline acetylase and glutamic acid decarboxylase, respectively. It is concluded that the acetylcholine-synthesizing machinery is located partly in neuronal parikarya, but mainly in the neuropil. Sites of GABA-metabolism are more variable; they include neuronal parikarya, neuropil and also glial cells, with special predilection to various brain areas.

Effect of 3-Nitropropionic Acid on Kynurenine Aminotransferase in the Rat Brain

Activation of excitatory amino acid receptors by endogenous excitotoxins results in degenerative changes characteristic of neurodegenerative brain diseases such as Huntingtons disease. Excitatory amino acid receptors are present in the highest concentration in the striatum, the hippocampal region, and the temporal lobe. The most potent, naturally occurring excitatory amino acid receptor antagonist is kynurenic acid (KYNA) which acts preferentially on N-methyl-D-aspartate (NMDA) receptors. KYNA is produced from L-kynurenine, by the action of the enzymes kynurenine aminotransferases (KAT I and KAT II). Several inhibitors of mitochondrial energy metabolism result in an indirect excitotoxic neuronal degeneration. We examined whether systemic administration of the mitochondrial toxin 3-nitroproprionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase, which also acts by an indirect excitotoxic mechanism, would produce alterations in the immunohistochemical pattern of KAT I. Our present investigations demonstrate that after 15 days of administration of 3-NP, an inhibitor of mitochondrial Complex II, the most severe depletion of KAT I occurred in the striatum; less severe depletion occurred in other brain areas investigated, following a striatum > hippocampus > temporal cortex gradient. The alterations induced by 15 days of 3-NP treatment were less conspicuous in 6-week-old (young) animals than in 3-month-old adults. In these adult animals, 3-NP induced necrotic cores in the striatum, characterized by destruction of neuronal and glial elements, similar to that seen in the histologic and neurochemical features of Huntingtons disease. It appears that immunohistochemical depletion of KAT after administration of 3-NP to adult animals may contribute to the pathological processes that characterize Huntingtons disease.

Chemical sympathectomy: Histochemical and submicroscopical consequences of 6-Hydroxydopamine treatment in the rat iris

Eine systematische Verabreichung von 6-Hydroxydopamin bewirkt eine Noradrenalin-Depletion aus terminalen Sympathikusfasern der Ratteniris. Die adrenergischen Nervenfasern werden von einer sekundären Degeneration ergriffen («osmiophobe» Degenerationsform), entsprechend der Degeneration der Nervenfasern nach Exstirpation des Ganglion cervicale superius.

Adrenergic nerve endings in the feline cervical superius ganglion

Fluoreszenzmikroskopische Untersuchungen beweisen die Anwesenheit adrenergischer Terminale im Ganglion cervicale superius der Katze. Die meisten von ihnen stammen aus Axon-Kollateralen. Eine intraganglionäre Hemmung scheint auch im Ganglion c.s. über adrenergische Nervenendigungen zu laufen.

Electron histochemistry of thiamine pyrophosphatase activity in the neuronal Golgi apparatus observed after axotomy and transneuronal deprivation

Thiamine pyrophosphatase activity of the neuronal Golgi apparatus exhibits specific patterns, characterizing nerve cell types of the rat spinal cord at the light microscopal level. Electron histochemistry reveals TPPase activity within cisterns of the internal part of the dictiosomes and in vesicles associated with the Golgi system. According to electron microscopical studies performed on semi-thin (0.5μ) sections, TPPase activity outlines a three-dimensional system of fenestrated cisterns and vesicles. In accord with literature data, axotomy of motoneurones results in a light microscopic decrease of dictiosomal TPPase activity and in an electron microscopic hypertrophy of the Golgi system. Electron histochemically, TPPase in the hypertrophied cisterns exhibits a sporadic, patchy localization, which is completely restored only in the state of restitution. On the contrary, transection of dorsal roots does not induce any light- or electron microscopic alterations in the TPPase activity of cells in the substantia gelatinosa Rolandi. Alterations of the Golgi system evoked by retrograde effects may serve to supply TPPase reserves in synaptic vesicles. Axotomy-induced alterations of neuronal TPPase reaction offer a methodological possibility for hodological studies.