Search PubMed⌕ Search

Biomedical subjects

B Csillik

Publications and source records attributed to B Csillik.

At least 91 records · Page 5Linked to original sources
PubMed1978

Perineural microtubule inhibitors induce degenerative atrophy of central nociceptive terminals in the Rolando substance.

Short-term perineural application of a microtubule inhibitor around a peripheral nerve induces degenerative atrophy of primary central nociceptive terminals in the Rolando substance. Consequences of the local microtubule inhibitor treatment are identical, both at light- and electron microscopic levels, with those that follow transection of a peripheral nerve. Degenerative atrophy in the Rolando substance is due to arrested axoplasmic transport in, and not to Wallerian degeneration of, the peripheral axons since (1) locally applied vinblastine and vincristone do not induce peripheral degeneration at all and (2) even though local colchicine treatment may cause Wallerian degeneration of thick myelinated axons, thin Adelta and C fibers do not undergo degeneration after colchicine treatment. The intriguing possibility to use this approach in the treatment of intractable pain is discussed.

Animals↗
PubMed1977

Protargol impregnation of plastic-embedded semi-thin sections: a simple method to select degenerative areas for electron microscopy.

0.5 mu plastic-embedded sections, obtained from aldehyde-osmium fixed rat and cat spinal cord, were impregnated in a 0.5% Protargol solution for 24 hours at 56 degrees C. Reduction was performed in a sodium sulphite- (5%) hydroquinone (1%) developer. Terminals undergoing Wallerian degeneration stand out as easily discernible black dots; corresponding osmiophilic degenerative patterns are demonstrated in consecutive thin electron microscopic sections. This simple technique enables successful trimming of blocks to obtain areas with the highest frequency of terminal degeneration.

Animals↗
PubMed1977

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 Lissauer's band, (3) in the fasciculus cornus posterioris (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.

Acid Phosphatase↗
PubMed1976

Effect of peripheral anatomy on the fine structure and histochemistry of the Rolando substance: degenerative atrophy of central processes of pseudounipolar cells.

Disappearance of fluorid-resistant acid phosphatase activity from the ipsilateral Rolando substance after transection of the peripheral nerve, is shown to be due to the cessation of enzyme supply from dorsal root ganglion cells to their central terminals. This is accompanied by (or ensues in consequence of) a fine structural derangement of these terminals ("degenerative atrophy"). Fine structural alterations of axon terminals undergoing degenerative atrophy, though similar to some extent to those seen during early phases of a Wallerian degeneration, are markedly different. Also myelinated nerve fibers, both in the dorsal horn and in dorsal columns, are affected by degenerative atrophy. This important, new trophical feature of sensory ganglion cells suggests a delicate metabolic balance between peripheral and central axonal branches of bipolar (pseudounipolar) cells. Degenerative atrophy raises serious implications in evaluating hodological experiments based upon Wallerian degeneration and offers new perspectives for theoretical and clinical neurology.

Acid Phosphatase↗
PubMed1976

Representation of cutaneous afferents by fluoride-resistant acid phosphatase (FRAP)-active terminals in the rat substantia gelatinosa rolandi.

While transection of the sciatic nerve results in a complete ipsilateral extinction of FRAP activity in respective segments of the rat spinal cord, cutaneous denervation of the hind leg induces a patchy disappearance of this same enzyme in the Rolando substance. The possible participation of FRAP in metabolism of the primary sensory transmitter substance, its relation to substance P and its involvement in gating mechanisms are discussed.

Acid Phosphatase↗
PubMed1976

Axonal labyrinths in the rat spinal cord: a consequence of degenerative atrophy.

Transection, crush or local colchicine treatment of a peripheral nerve induces degenerative atrophy of central terminals of primary sensory neurons in the Rolando substance of the rat spinal cord. In addition to osmiophilic alterations that occur in the course of degenerative processes in general, degenerative atrophy is characterized by the appearance of spectacular labyrinthine formations. Electron-microscopic analysis reveals that these consist of flattened axonal profiles. Axonal labyrinths are interpreted as signs of futile regenerative efforts of axon terminals undergoining degenerative atrophy. Labyrinths disappear from the Rolando substance several months after peripheral nerve injury, when degenerative atrophy of the central terminal is replaced by regenerative proliferation.

Animals↗
PubMed1975

Electron cytochemistry of acetylcholinesterase in the neuromuscular junction during ontogenesis.

Electron histochemical studies were performed on neuromuscular junctions of the diaphragm in early postnatal states of development in rat by means of the acetylthiocholine technique. Presynaptic AChE appears to be derived from perikaryal sources, carried along by means of axonal transport mechanisms. Postsynaptic AChE is synthesized in the sarcotubular system of the underlying muscle fiber and within the perinuclear and endoplasmic reticulum of fundamental cells. Distribution of AChE synthesizing loci parallels with that of acetylcholine sensitive areas.

Acetylcholinesterase↗