Acetylcholine Receptors

Fambrough, Douglas M.

doi:10.1085/jgp.64.4.468

Cited by 82 publications

(20 citation statements)

References 8 publications

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“…Chronic dysmyelination not only altered the distribution of AChRs within individual junctions but also increased the expression of mRNA encoding the ␣ and ␤ subunit of the AChR at P30 -P90. This increase is consistent with an increase in extrajunctional AChR expression, similar to that observed after denervation or inactivity (Fambrough, 1974;Berg and Hall, 1975;Blondet et al, 1989).…”

Section: Discussionsupporting

confidence: 88%

Dysmyelinated Lower Motor Neurons Retract and Regenerate Dysfunctional Synaptic Terminals

et al. 2004

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Axonal degeneration is the major cause of permanent neurological disability in individuals with inherited diseases of myelin. Axonal and neuronal changes that precede axonal degeneration, however, are not well characterized. We show here that dysmyelinated lower motor neurons retract and regenerate dysfunctional presynaptic terminals, leading to severe neurological disability before axonal degeneration. In addition, dysmyelination led to a decreased synaptic quantal content, an indicator of synaptic dysfunction. The amplitude and rise time of miniature endplate potentials were also increased, but these changes were primarily consistent with an increase in the passive membrane properties of the transgenic muscle fibers. Maintenance of synaptic connections should be considered as a therapeutic target for slowing progression of neurological disability in primary diseases of myelin.

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Section: Discussionsupporting

confidence: 88%

Dysmyelinated Lower Motor Neurons Retract and Regenerate Dysfunctional Synaptic Terminals

et al. 2004

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“…For example, if significant receptor occupation occurred because of the typically lower density of receptors in denervated compared with subsynaptic membrane (Fambrough, 1974;Chang, Chuang & Huang, 1975) both channel lifetime and conductance would be underestimated (Neher & Sakmann, 1976b;Sakmann & Adams, 1976) and the errors would increase with hyperpolarization due to increased receptor occupancy. However, the observations that TN and y at one potential were independent of mean current amplitude in the range studied (5-50 nA) and that the variance of current fluctuations varied in direct proportion to mean current within the same range, indicate that the assumption that a small fraction of available receptors was activated was valid in these experiments.…”

Section: Discussionmentioning

confidence: 99%

Lifetime and conductance of acetylcholine‐activated channels in normal and denervated toad sartorius muscle.

Gage

Hamill

1980

The Journal of Physiology

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SUMMARY1. The average lifetime and conductance of acetylcholine-activated channels were measured in normal and denervated, voltage-clamped toad sartorius muscle fibres at 10 0C.2. The null potential was -4 + 1 mV for subsynaptic channels in normal fibres and -6 + 3 mV for extrasynaptic channels in denervated fibres.3. There was a linear relationship between variance of conductance fluctuations and mean conductance for acetylcholine-induced currents up to 50 nA, in denervated fibres clamped at -50 mV. The ratio gave a channel conductance of 14 pS.4. At the same membrane potential, the average lifetime of extrasynaptic channels in denervated fibres was approximately double, whereas channel conductance was approximately half, that of subsynaptic channels in normal fibres: there was little difference in net charge transfer through the two types of channel under similar conditions. 5. Single channel conductance increased, whereas average channel lifetime decreased, as the membrane potential became more positive (depolarized). The effect of potential on channel lifetime and conductance was more pronounced in denervated than in normal fibres.

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“…To convert the extrajunctional toxin binding to surface binding site densities, the mean fibre circumference was calculated. In some cases this was done by embedding tissue in soft plastic (Fambrough, 1974), cutting cross-sections and determining the mean diameter and circumference of 50-100 fibres on enlarged photomicrographs using a digitizer connected to a desk-top computer (Hewlett-Packard). A more rapid method was used in most cases.…”

Section: Denervated Skeletal Muscles 515mentioning

confidence: 99%

Neuromuscular junctions and alpha‐bungarotoxin‐binding sites in denervated and contralateral cat skeletal muscles.

Steinbach¹

1981

The Journal of Physiology

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SUMMARY1. The distributions of cholinesterase (ChE) activity and acetylcholine (ACh) receptors were studied in normal and denervated cat hind-limb fast-twitch skeletal muscles and in muscles contralateral to denervated muscles.2. On normal muscle fibres almost all receptors were confined to the immediately post-junctional membrane, although a perijunctional gradient of increased ACh receptor density was found on both fast-and slow-twitch fibres. After denervation, the extrajunctional ACh receptor density increased greatly and remained high for at least 10 months. Ectopic regions staining for ChE activity and having a high density of ACh receptors appeared in denervated muscle. The number of junctional ACh receptors decreased slowly after denervation, with a half-time of about 140 days.3. Fast-twitch muscles contralateral to denervated muscles also showed changes, including an increase in junctional size and a small but significant increase in extrajunctional ACh receptor density.

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Acetylcholine Receptors

Cited by 82 publications

References 8 publications

Dysmyelinated Lower Motor Neurons Retract and Regenerate Dysfunctional Synaptic Terminals

Dysmyelinated Lower Motor Neurons Retract and Regenerate Dysfunctional Synaptic Terminals

Lifetime and conductance of acetylcholine‐activated channels in normal and denervated toad sartorius muscle.

Neuromuscular junctions and alpha‐bungarotoxin‐binding sites in denervated and contralateral cat skeletal muscles.

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