Linked Life Data

15281071

Source:http://linkedlifedata.com/resource/pubmed/id/15281071

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-7-28
pubmed:abstractText
Stress-sensitive mutants in Drosophila have been shown to exhibit activity-dependent defects in neurotransmission. Using the neuromuscular junction (NMJ), this study investigates synaptic function more specifically in two stress-sensitive mutants: stress-sensitive B (sesB), which encodes a mitochondrial ADP/ATP translocase (ANT); and Atpalpha(2206), a conditional mutant of the Na+/K+ ATPase alpha-subunit. Mechanical shock induces a period of brief paralysis in both homozygous and double heterozygous mutants, but further analysis revealed distinct activity-dependent neurotransmission lesions in each mutant. Basal neurotransmission appeared similar to wild-type controls in both mutants under low frequency stimulation. High frequency stimulation, however, caused pronounced synaptic fatigue as well as slow and incomplete synaptic recovery in sesB mutants while Atpalpha(2206) mutants displayed an increase (25-fold) in synaptic failures. Perhaps to compensate for these activity dependent defects, the neuromuscular synapse was found to be overgrown in both mutants. Passive electrotonic stimulation, which initiates synaptic transmission independent of action potentials, ameliorated synaptic failures and resulted in increased neurotransmission amplitude in Atpalpha(2206) mutants. In addition, spontaneous synaptic vesicle fusion rates were increased in Atpalpha(2206) mutants, suggesting that, in the absence of action potential requirements, these synaptic terminals are healthy, if not hyperactive. Dye labeling studies revealed aberrant synaptic vesicle cycling in sesB mutants indicating a reduction of functional synaptic vesicles. We therefore postulate that both stress-sensitive mutants harbor unique neurotransmission defects: Atpalpha(2206) mutants are unable to maintain ionic gradients required during repetitive action potential propagation, and sesB mutants cannot maintain synaptic vesicle cycling during periods of high demand.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-3034
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
328-47
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15281071-Animals, pubmed-meshheading:15281071-Behavior, Animal, pubmed-meshheading:15281071-Calcium, pubmed-meshheading:15281071-Drosophila, pubmed-meshheading:15281071-Electrophysiology, pubmed-meshheading:15281071-Evoked Potentials, pubmed-meshheading:15281071-Excitatory Postsynaptic Potentials, pubmed-meshheading:15281071-Genes, Insect, pubmed-meshheading:15281071-Hot Temperature, pubmed-meshheading:15281071-Larva, pubmed-meshheading:15281071-Mitochondria, pubmed-meshheading:15281071-Mutation, pubmed-meshheading:15281071-Neuromuscular Junction, pubmed-meshheading:15281071-Paralysis, pubmed-meshheading:15281071-Physical Stimulation, pubmed-meshheading:15281071-Presynaptic Terminals, pubmed-meshheading:15281071-Pyridinium Compounds, pubmed-meshheading:15281071-Quaternary Ammonium Compounds, pubmed-meshheading:15281071-Stress, Physiological, pubmed-meshheading:15281071-Synaptic Transmission, pubmed-meshheading:15281071-Synaptic Vesicles, pubmed-meshheading:15281071-Time Factors
pubmed:year
2004
pubmed:articleTitle
Cellular bases of activity-dependent paralysis in Drosophila stress-sensitive mutants.
pubmed:affiliation
Department of Biological Sciences, Program in Developmental Biology, Brain Institute, VU Station B, Vanderbilt University, Nashville, Tennessee 37235-1634, USA.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't