Anesthetic-Induced Transformation of Axonal Microtubules

Hinkley, Robert E.; Samson, Frederick E.

doi:10.1083/jcb.53.1.258

Cited by 46 publications

(18 citation statements)

References 11 publications

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“…(See Tyson and Bulger [1973] for a more complete review of the occurrence of macrotubules .) Macrotubules are believed to represent a different conformational state of microtubules since microtubules disappear as macrotubules are formed and vice versa (Tilney and Porter, 1967 ;Hinkley and Samson, 1972), and macrotubules are colchicine sensitive (Hinkley and Samson, 1972 ; also confirmed in this study) . Tilney and Porter (1967) discussed two alternative explanations for this transformation at low temperatures : (a) a direct shortening of microtubules by sliding of adjacent protofilaments, and (b) breakdown of microtubules into subunits and reassembly as macrotubules .…”

Section: Discussionsupporting

confidence: 69%

“…In cells recovering from pressure IPC, macrotubules and microtubules were occasionally observed coexistent and inserting side by side on the same rhizoplast, suggesting an in situ transformation . However, as in all other studies of microtubule-macrotuhule interconversions, no structural intermediates were observed in Ochromonas. On the basis of the experimental evidence (Balasubramanian and Wetlaufer, 1966) that halothane can induce conformational changes in globular proteins, Hinkley and Samson (1972) suggested that macrotubules in anesthetictreated axons are reassembled from halothanemodified microtubular subunit strands. Also, Tyson and Bulger (1973) have hypothesized that the formation of macrotubules in cells exposed to vinblastine may result from a vinblastineinduced conformation change or the stabilization of a particular conformation of microtubule protein .…”

Section: Discussionmentioning

confidence: 99%

“…However, similar transformation has been produced in other organisms by a variety of chemical and physical agents, including : low 534 THE JOURNAL OF CELL BIOLOGY • VOLUME 61,1974 temperature (Tilney and Porter, 1967), digitonin (Hanzely and Olah, 1970), the anesthetic halothane (Allison et al ., 1972 ;Hinkley and Samson, 1972), vinblastine sulfate (Tyson and Bulger, 1972), and the enzyme hyaluronidase (Burton and Fernandez, 1973) . (See Tyson and Bulger [1973] for a more complete review of the occurrence of macrotubules .)…”

Section: Discussionmentioning

confidence: 99%

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MICROTUBULE BIOGENESIS AND CELL SHAPE IN OCHROMONAS

Brown

Bouck

1974

The Journal of Cell Biology

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The role of microtubules and microtubule nucleating sites in the unicell, Ochromonas has been examined through the use of two mitotic inhibitors, isopropyl N-phenylcarbamate (IPC) and isopropyl N-3-chlorophenyl carbamate (CIPC) . Although IPC and CIPC have little or no effect on intact microtubules, the assembly of three separate sets of microtubules in Ochromonas has been found to be differentially affected by IPC and CIPC . The assembly of flagellar microtubules after mechanical deflagellation is partially inhibited ; the reassembly of rhizoplast microtubules after pressure depolymerization is totally inhibited (however, macrotubules may form at the sites of microtubule initiation or elsewhere) ; and, the reassembly of the beak set of microtubules after pressure depolymerization may be unaffected although similar concentrations of IPC and CICP completely inhibit microtubule regeneration on the rhizoplast . These effects on microtubule assembly, either inhibitory or macrotubule inducing, are fully reversible . The kinetics of inhibition and reversal are found to be generally similar for both flagellar and cell shape regeneration . Incorporation data suggest that neither IPC nor CIPC has significant effects on protein synthesis in short term experiments . Conversely, inhibiting protein synthesis with cycloheximide has little effect on microtubule regeneration when IPC or CIPC is removed . Although the exact target for IPC and CIPC action remains uncertain, the available evidence suggests that the microtubule protein pool or the microtubule nucleating sites are specifically and reversibly affected . Comparative experiments using the mitotic inhibitor colchicine indicate some similarities and differences in its mode of action with respect to that of IPC and CIPC on assembly and disassembly of microtubules in these cells .In the first two papers of this series (Bouck and ently independent sets of cytoplasmic microBrown, 1973 ; Brown and Bouck, 1973) evidence tubules which (a) differ from each other in sensiwas presented that the characteristic asymmetric tivity to the microtubule depolymerizing agents shape of Ochromonas is mediated by two appar-colchicine and hydrostatic pressure, (b) are 514

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Section: Discussionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MICROTUBULE BIOGENESIS AND CELL SHAPE IN OCHROMONAS

Brown

Bouck

1974

The Journal of Cell Biology

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“…Propofol (an anesthetic) also changes the cytoskeletal function in cultured neuron. Many scientists have proposed different mechanism for the action of anesthetics [8][9][10]. This paper is in continuation of my already published work [11].…”

Section: Page 2 Ofsupporting

confidence: 69%

Mechanism of Propofol's Action on MAP Rich Tubulin and Actin - An In Vitro Study

Sahni¹,

Kumar²,

Pachauri³

2017

Biochem Anal Biochem

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Despite a century of sustained research, brain scientists remain ignorant of the workings of the three pound organ that is the seat of all conscious human activity. Many have tried to attack the problem by examining the nervous systems of simpler organisms. The difficulty in establishing a link between biology and behaviour in humans is still more acute. There are techniques which are used to record the activity of single neurons in living humans. Such breakthrough methods could, in principle, begin to bridge the gap between the firing of neurons and cognition: perception, emotion, decision making and ultimately, consciousness itself. Deciphering the exact patterns of brain activity that underlie thinking and behavior will also provide critical insights into what happens when neural circuitry malfunctions in psychiatric and neurological disorders-schizophrenia, autism, Alzheimer's or Parkinson's. Anesthetics are also known to inhibit neuronal fast anterograde axoplasmic transport (FAAT) in a reversible and dose-dependent manner, but the precise mechanism by which anesthetic prevent consciousness remains unknown largely because the mechanism by which brain physiology produces consciousness is unexplained. In the present study we have used circular dichroism spectroscopy and confocal laser scanning microscopy to see the effect of propofol on the assembly of neuronal tubulin and actin together and probed into the changes of their secondary structures.

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“…Repolymerization of microtubules in Raphidiophrys (Tilney, 1971) seems to depend on nucleation at the centroplast, and reformation of ciliary microtubules is controlled by the basal body (Renaud and Swift, 1964). However, microtubules can be repolymerized in axons of isolated crayfish ventral cord (Hinkley and Samson, 1972). Similarly, our experiments with lidocaine show that microtubules can be repolymerized in axons cut off from their nerve cell bodies, so that this repolymerization must be independent of the neuronal perikaryon.…”

Section: Discussionmentioning

confidence: 64%

Effects of lidocaine on axonal morphology, microtubules, and rapid transport in rabbit vagus In vitro

et al. 1973

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SUMMARYTreatment with lidocaine, at exposures which completely block impulse conduction and rapid axonal transport, resulted in a sequence of morphological effects on rabbit vagus nerve in uitro. Low exposures (0.3% for 90 min, 0.4% for 45 min, 0.6% for 25 min) caused a reorientation and proliferation of smooth endoplasmic reticulum (SER) ; the number of axonal microtubules either remained normal or was increased. Intermediate exposures (0.4% for 90 min, 0.6% for 45 min) produced a similar effect on the SER, as well as causing a 50% reduction in microtubule number and some swelling of axons and Schwann cells. The highest exposure (0.6% for 75 min) caused over 90% reduction in microtubule number, a partial loss of neurofilaments, and severe swelling of axons, Schwann cells, and mitochondria. Reversibility of these effects was tested in lidocaine-treated nerves that had been washed with fresh culture medium. There was good recovery of nerve structure, rapid transport, and impulse conduction following low exposures. After intermediate exposures, there was only partial return of rapid transport, even though impulse conduction and nerve structure had recovered. After high exposures, there was morphological recovery in half of the axons, occasional return of impulse conduction, and no recovery of rapid transport. Both the disassembly and reassembly of microtubules occured throughout the excised vagus nerve in efferent and afferent axons as well as Schwann cells, and these events did not coincide with changes in the functional state of rapid axonal transport.

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Anesthetic-Induced Transformation of Axonal Microtubules

Cited by 46 publications

References 11 publications

MICROTUBULE BIOGENESIS AND CELL SHAPE IN OCHROMONAS

MICROTUBULE BIOGENESIS AND CELL SHAPE IN OCHROMONAS

Mechanism of Propofol's Action on MAP Rich Tubulin and Actin - An In Vitro Study

Effects of lidocaine on axonal morphology, microtubules, and rapid transport in rabbit vagus In vitro

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