Linked Life Data

20392950

Source:http://linkedlifedata.com/resource/pubmed/id/20392950

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
2010-4-15
pubmed:abstractText
Primary afferent neurotransmission is the fundamental first step in the central processing of sensory stimuli. A major mechanism producing afferent presynaptic inhibition is via a channel-mediated depolarization of their intraspinal terminals which can be recorded extracellularly as a dorsal root potential (DRP). Based on measures of DRP latency it has been inferred that this primary afferent depolarization (PAD) of low-threshold afferents is mediated by minimally trisynaptic pathways with GABAergic interneurons forming last-order axoaxonic synapses onto afferent terminals. We used an in vitro rat spinal cord preparation under conditions that restrict synaptic transmission to test whether more direct low-threshold pathways can produce PAD. Mephenesin or high divalent cation solutions were used to limit oligosynaptic transmission. Recordings of synaptic currents in dorsal horn neurons and population synaptic potentials in ventral roots provided evidence that conventional transmission was chiefly restricted to monosynaptic actions. Under these conditions, DRP amplitude was largely unchanged but with faster time to peak and reduced duration. Similar results were obtained following stimulation of peripheral nerves. Even following near complete block of transmission with high Mg(2+)/low Ca(2+)-containing solution, the evoked DRP was reduced but not blocked. In comparison, in nominally Ca(2+)-free or EGTA-containing solution, the DRP was completely blocked confirming that Ca(2+) entry mediated synaptic transmission is required for DRP genesis. Overall these results demonstrate that PAD of low-threshold primary afferents can occur by more direct synaptic mechanisms, including the possibility of direct negative-feedback or nonspiking dendroaxonic pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
14
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5283-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:20392950-Animals, pubmed-meshheading:20392950-Bicuculline, pubmed-meshheading:20392950-Calcium, pubmed-meshheading:20392950-Evoked Potentials, pubmed-meshheading:20392950-GABA Antagonists, pubmed-meshheading:20392950-GABA-A Receptor Antagonists, pubmed-meshheading:20392950-Lumbar Vertebrae, pubmed-meshheading:20392950-Membrane Potentials, pubmed-meshheading:20392950-Neurons, Afferent, pubmed-meshheading:20392950-Peripheral Nerves, pubmed-meshheading:20392950-Posterior Horn Cells, pubmed-meshheading:20392950-Rats, pubmed-meshheading:20392950-Rats, Sprague-Dawley, pubmed-meshheading:20392950-Receptors, GABA-A, pubmed-meshheading:20392950-Sodium Channel Blockers, pubmed-meshheading:20392950-Spinal Cord, pubmed-meshheading:20392950-Synapses, pubmed-meshheading:20392950-Synaptic Transmission, pubmed-meshheading:20392950-Tetrodotoxin, pubmed-meshheading:20392950-Time Factors
pubmed:year
2010
pubmed:articleTitle
Bicuculline-sensitive primary afferent depolarization remains after greatly restricting synaptic transmission in the mammalian spinal cord.
pubmed:affiliation
Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't